Water
soluble vitamins: structure, properties, biological role
Thiamin (Vitamin B1)
Thiamin (also spelled thiamine) is a water-soluble B vitamin,
previously known as vitamin B1 or aneurine. Isolated and characterized in the 1930s, thiamin was
one of the first organic compounds to be recognized as a vitamin. Thiamin
occurs in the human body as free thiamin and as various phosphorylated forms: thiamin monophosphate (TMP), thiamin triphosphate (TTP), and thiamin pyrophosphate (TPP), which is also
known as thiamin diphosphate.
Deficiency
Beriberi, the disease resulting from severe thiamin deficiency, was
described in Chinese literature as early. Thiamin deficiency affects the
cardiovascular, nervous, muscular, and gastrointestinal systems. Beriberi has been termed dry, wet, or
cerebral, depending on the systems affected by severe thiamin deficiency.
Food sources
A varied diet should provide most individuals with adequate thiamin to
prevent deficiency. In the U.S. the average dietary thiamin intake for young
adult men is about 2 mg/day and 1.2 mg/day for young adult women. A survey of
people over the age of 60 found an average dietary thiamin intake of 1.4 mg/day
for men and 1.1 mg/day for women. However, institutionalization and poverty
both increase the likelihood of inadequate thiamin intake in the elderly.Whole grain cereals, legumes (e.g., beans and lentils), nuts, lean pork, and yeast are rich sources of
thiamin. Because most of the thiamin is lost during the production of white
flour and polished (milled) rice, white rice and foods made from white flour
(e.g., bread and pasta) are fortified with thiamin in many Western countries. A
number of thiamin-rich foods are listed in the table below along with their
thiamin content in milligrams (mg). For more information on the nutrient
content of foods, search the USDA food composition database.
Riboflavin (Vitamin B2)
Riboflavin is a water-soluble B vitamin, also known as vitamin B2. In
the body, riboflavin is primarily found as an integral component of the
coenzymes, flavin adenine dinucleotide (FAD) and flavin mononucleotide (FMN). Coenzymes derived from
riboflavin are termed flavocoenzymes, and enzymes that use a flavocoenzyme are called flavoproteins.
Living organisms derive most of their energy from oxidation-reduction
(redox) reactions, which are processes that involve the
transfer of electrons. Flavocoenzymes participate in redox reactions in numerous metabolic pathways. Flavocoenzymes are critical for the metabolism of carbohydrates, fats, and proteins. FAD is part of the electron transport (respiratory) chain, which is central to
energy production. In conjunction with cytochrome P-450, flavocoenzymes also participate in the metabolism of drugs and
toxins.
Glutathione reductase is a FAD-dependent
enzyme that participates in the redox cycle of glutathione. The glutathione redoxcycle plays a major role in protecting organisms from reactive oxygen species, such as hydroperoxides. Glutathione reductaserequires FAD to regenerate two molecules of reduced
glutathione from oxidized glutathione. Riboflavin deficiency has been
associated with increased oxidative stress. Measurement of glutathione reductase activity in red blood cells is commonly used to assess
riboflavin nutritional status.
Glutathione peroxidase, a
selenium-containing enzyme, requires two molecules of reduced glutathione to
break downhydroperoxides (see diagram).
Xanthine oxidase, another FAD-dependent enzyme, catalyzes the oxidation of hypoxanthine and xanthine to uric acid. Uric acid is one of the most effective
water-soluble antioxidants in the blood. Riboflavin deficiency can result in
decreased xanthine oxidaseactivity, reducing
blood uric acid levels.
Deficiency
Ariboflavinosis is the medical name for clinical riboflavin deficiency.
Riboflavin deficiency is rarely found in isolation; it occurs frequently in
combination with deficiencies of other water-soluble vitamins. Symptoms of
riboflavin deficiency include sore throat, redness and swelling of the lining
of the mouth and throat, cracks or sores on the outsides of the lips (cheliosis) and at the corners of the mouth (angular stomatitis), inflammation and redness of the tongue (magenta
tongue), and a moist, scaly skin inflammation (seborrheic dermatitis). Other symptoms may involve the formation
of blood vessels in the clear covering of the eye (vascularizationof the cornea) and decreased red blood cell count in
which the existing red blood cells contain normal levels of hemoglobin and are
of normal size (normochromic normocytic anemia). Severe riboflavin deficiency may result in decreased conversion of
vitamin B6 toits coenzyme form (PLP) and
decreased conversion of tryptophan to niacin (see Nutrient Interactions).
Food sources
Most plant and animal derived foods contain at least small quantities of
riboflavin. In the U.S., wheat flour and bread have been enriched with
riboflavin (as well as thiamin, niacin, and iron) since 1943. Data from large
dietary surveys indicate that the average intake of riboflavin for men is about
2 mg/day and for women is about 1.5 mg/day; both intakes are well above the
RDA. Intake levels were similar for a population of elderly men and women (1).
Riboflavin is easily destroyed by exposure to light. For instance, up to 50% of
the riboflavin in milk contained in a clear glass bottle can be destroyed after
two hours of exposure to bright sunlight. Some foods with substantial amounts
of riboflavin are listed in the table below along with their riboflavin content
in milligrams (mg). For more information on the nutrient content of foods,
search the USDA food composition database.
Niacin (Vitamin B5)
Niacin exists in two forms, nicotinic acid and nicotinamide. Both forms are readily absorbed from the stomach and
the small intestine. Niacin is stored in small amounts in the liver and
transported to tissues, where it is converted to coenzyme forms. Any excess is
excreted in urine. Niacin is one of the most stable of the B vitamins. It is
resistant to heat and light, and to both acid and alkali environments. The
human body is capable of converting the amino acid tryptophan to niacin when
needed. However, when both tryptophan and niacin are deficient, tryptophan is
used for protein synthesis.
There are two coenzyme forms of niacin: nicotinamide adenine dinucleotide (NAD+) and nicotinamide adenine dinucleotidephophate (NADP+). They both help break down and utilize
proteins, fats, and carbohydrates for energy. Niacin is essential for growth
and is involved in hormone synthesis.
Pellagra results from a combined deficiency of niacin and tryptophan.
Long-term deficiency leads to central nervous system dysfunction manifested as
confusion, apathy, disorientation, and eventually coma and death. Pellagra is
rarely seen in industrialized countries, where it may be observed in people
with rare disorder of tryptophan metabolism (Hartnup's disease), alcoholics, and those with diseases that
affect food intake.
The liver can synthesize niacin from the essential aminoacid tryptophan, but the synthesis is extremely slow; 60 mg of
tryptophan are required to make one milligram of niacin. Dietary niacin
deficiency tends to occur only in areas where people eat corn, the only grain
low in niacin, as a staple food, and that don't use lime during maize (corn)
meal/flour production. Alkali lime releases the tryptophan from the corn so
that it can be absorbed in the gut, and converted to niacin.
Niacin plays an important role in the production of several sex and
stress-related hormones, particularly those made by the adrenal gland. Niacin,
when taken in large doses, increases the level of high density lipoprotein
(HDL) or "good" cholesterol in blood, and is sometimes prescribed for
patients with low HDL, and at high risk of heart attack. Niacin (but not niacinamide) is also used in the treatment of hyperlipidemia because it reduces very low density lipoprotein
(VLDL), a precursor of low density lipoprotein (LDL) or "bad"
cholesterol, secretion from the liver, and inhibits cholesterol synthesis.
The main problem with the clinical use of niacin for dyslipidemia is the occurrence of skin flushing, even with moderate
doses.
Recommended intake is expressed as milligrams of niacin equivalents (NE) to
account for niacin synthesized from tryptophan. High doses taken orally as
nicotinic acid at 1.5 to 2 grams per day can decrease cholesterol and
triglyceride levels, and along with diet and exercise can slow or reverse the
progression of heart disease.
The nicotinamide form of niacin in multivitamin and B-complex tablets
do not work for this purpose. Supplementation should be under a physician's
guidance.
Food sources
Good sources of niacin include yeast, meat, poultry, red fishes (e.g.,
tuna, salmon), cereals (especially fortified cereals), legumes, and seeds. Milk,
green leafy vegetables, coffee, and tea also provide some niacin. In plants,
especially mature cereal grains like corn and wheat, niacin may be bound to
sugar molecules in the form of glycosides, which significantly decrease niacin
bioavailability.
Pantothenic Acid (Vitamin B3)
Pantothenic acid, also called vitamin B3, is a water-soluble
vitamin required to sustain life. Pantothenic acid is needed to form coenzyme-A (CoA), and is critical in the metabolism and synthesis of
carbohydrates, proteins, and fats. Its name is derived from the Greek pantothen meaning "from everywhere" and small
quantities of pantothenic acid are found in
nearly every food, with high amounts in whole grain cereals, legumes, eggs,
meat, and royal jelly
Pantothenic acid is stable in moist heat. It is destroyed by
vinegar (acid), baking soda (alkali), and dry heat. Significant losses occur
during the processing and refining of foods. Pantothenic acid is released from coenzyme A in food in the small
intestine. After absorption, it is transported to tissues, where coenzyme A is resynthesized. Coenzyme A is essential for the formation of energy
as adenosine triphosphate (ATP) from
carbohydrate, protein, alcohol, and fat.
Coenzyme A is also important in the synthesis of fatty acids, cholesterol,
steroids, and the neurotransmitter acetylcholine, which is essential for
transmission of nerve impulses to muscles.
Dietary deficiency occurs in conjunction with other B-vitamin deficiencies. Pantothenic acid is used in the synthesis of coenzyme A
(abbreviated as CoA). Coenzyme A may
act as an acyl group carrier to
form acetyl-CoA and other related
compounds; this is a way to transport carbon atoms within the cell. The
transfer of carbon atoms by coenzyme A is important in cellular respiration, as
well as the biosynthesis of many important compounds such as fatty acids,
cholesterol, and acetylcholine. Dietary deficiency occurs in conjunction with
other B-vitamin deficiencies. In studies, experimentally induced deficiency in
humans has resulted in headache, fatigue, impaired muscle coordination,
abdominal cramps, and vomiting.
In studies, experimentally induced deficiency in humans has resulted
in headache, fatigue, impaired muscle coordination, abdominal cramps, and
vomiting.
Biotin (Vitamin B8)
Biotin is a water soluble vitamin and a member of Vitamin B complex. Also known as Vitamin H, Bios II, Co-enzyme R. Its natural form is D-biotin. It was isolated from liver in 1941 by Dr. Paul Gyorgy.
Biotin is the most stable of B vitamins. It is commonly found in two forms:
the free vitamin and the protein-bound coenzyme form called biocytin. Biotin is absorbed in the small intestine, and it
requires digestion by enzyme biotinidase, which is present in the small intestine. Biotin is
synthesized by bacteria in the large intestine, but its absorption is
questionable. Biotincontaining coenzymes
participate in key reactions that produce energy from carbohydrate and
synthesize fatty acids and protein.
Avidin is a protein in raw egg white, which can bind to the biotin in the stomach
and decrease its absorption. Therefore, consumption of raw whites is of concern
due to the risk of becoming biotin deficient. Cooking the egg white, however,
destroysavidin. Deficiency may
develop in infants born with a genetic defect that results in reduced levels of biotinidase. In the past, biotin deficiency was observed in
infants fed biotin-deficient formula, so it is now added to infant formulas and
other baby foods.
Vitamin B6
Pyridoxal, pyridoxamine and pyridoxine are collectively known as vitamin B6.
All three compounds are efficiently converted to the biologically active form
of vitamin B6, pyridoxal phosphate. This
conversion is catalyzed by the ATP requiring enzyme,pyridoxal kinase.
Vitamin B6 is present in three forms: pyridoxal, pyridoxine, and pyridoxamine. All forms can be converted to the active vitamin-B6
coenzyme in the body. Pyridoxal phosphate (PLP) is the predominant biologically active
form. Vitamin B6 is not stable in heat or in alkaline conditions, so cooking
and food processing reduce its content in food. Both coenzyme and free forms
are absorbed in the small intestine and transported to the liver, where they
are phosphorylated and released into circulation, bound to albumin for
transport to tissues. Vitamin B6 is stored in the muscle and only excreted in
urine when intake is excessive.
Folic Acid, Folate, Folacin (Vitamin B9)
Folacin or folate, as it is usually called, is the form of vitamin B9
naturally present in foods, whereas folic acid is the synthetic form added to
fortified foods and supplements. Both forms are absorbed in the small intestine
and stored in the liver. The folic acid form, however, is more efficiently
absorbed and available to the body. When consumed in excess of needs, both
forms are excreted in urine and easily destroyed by heat, oxidation, and light.
Folic acid is a water soluble vitamin and is a member of the Vitamin B
complex. Also known as Folacin, pteroyl-L-glutamic acid (PGA), vitamin Bc or vitamin M. Folic acid and its derivatives (mostly
the tri and heptaglutamyl peptides) are
widespread in nature. It is a specific growth factor for certain
micro-organisms. Found in yeast and
liver in 1935.
All forms of this vitamin are readily converted to the coenzyme form called tetrahydrofolate (THFA), which plays a key role in transferring
single-carbon methyl units during the synthesis of DNA and RNA, and in interconversions of amino acids. Folate also plays an important role in the synthesis of
neurotransmitters. Meeting folate needs can improve mood and mental functions.
Long term high doses may cause Vitamin B12 losses from the body
Folate deficiency is one of the most common vitamin deficiencies. Early symptoms
are nonspecific and include tiredness, irritability, and loss of appetite.
Severe folate deficiency leads to macrocytic anemia, a condition in which cells in the bone marrow
cannot divide normally and red blood cells remain in a large immature form
called macrocytes. Large immature cells also appear along the length of
the gastrointestinal tract, resulting in abdominal pain and diarrhea.
Pregnancy is a time of rapid cell multiplication and DNA synthesis, which
increases the need for folate. Folate deficiency may lead to neural tube defects such as spina bifida (failure of the spine to close properly during
the first month of pregnancy) and anencephaly (closure of the neural tube
during fetal development, resulting in part of the cranium not being formed). Seventy
percent of these defects could be avoided by adequate folate status before conception, and it is recommended that
all women of childbearing age consume at least 400 micrograms (μg) of folic acid
each day from fortified foods and supplements. Other groups at risk of
deficiency include elderly persons and persons suffering from alcohol abuse or
taking certain prescription drugs.
Vitamin B12
Vitamin B12 is found in its free-vitamin form, called cyanocobalamin, and in two active coenzyme forms. Absorption of
vitamin B12 requires the presence of intrinsic factor,a protein synthesized by acid-producing cells of the
stomach. The vitamin is absorbed in the terminal portion of the small intestine
called the ileum. Most of body's supply of vitamin B12 is stored in the liver.
Vitamin B12
Vitamin B12 is defficiently conserved in the
body, since most of it is secreted into bile and reabsorbed. This explains the
slow development (about two years) of deficiency in people with reduced intake
or absorption. Vitamin B12 is stable when heated and slowly loses its activity
when exposed to light, oxygen, and acid or alkaline environments.
Vitamin B12 coenzymes help recycle folate coenzymes involved in the synthesis of DNA and RNA,
and in the normal formation of red blood cells. Vitamin B12 prevents
degeneration of the myelin sheaths that cover nerves and help maintain normal
electrical conductivity through the nerves.
Active center
of tetrahydrofolate (THF). Note that the N5 position is the site of attachment of
methyl groups, the N10 the site for attachment of formyl and formimino groups and that both N5 and N10 bridge the methylene and methenyl groups
Vitamin-B12 deficiency results in pernicious anemia, which is caused by a
genetic problem in the production of intrinsic factor. When this occurs, folate function is impaired, leading to macrocytic anemia due to interference in normal DNA synthesis.
Unlikefolate deficiency, the anemia caused by vitamin-B12
deficiency is accompanied by symptoms of nerve degeneration, which if left
untreated can result in paralysis and death.
Since vitamin B12 is well conserved in the body, it is difficult to become
deficient from dietary factors alone, unless a person is a strict vegan and
consumes a diet devoid of eggs and dairy for several years. Deficiency is
usually observed when B12 absorption is hampered by disease or surgery to the
stomach or ileum, damage to gastric mucosa by alcoholism, or prolonged use of
anti-ulcer medications that affect secretion of intrinsic factor. Agerelated decrease in stomach-acid production also reduces
absorption of B12 in elderly persons. These groups are advised to consume
fortified foods or take a supplemental form of vitamin B12.
Vitamin C (Ascorbic Acid)
In 1746, James Lind, a British physician, conducted the first nutrition
experiment on human beings in an effort to find a cure for scurvy.
Vitamin C is needed to form and maintain collagen, a fibrous protein that
gives strength to connective tissues in skin, cartilage, bones, teeth, and
joints. Collagen is also needed for the healing of wounds.
When added to meals, vitamin C increases intestinal absorption of
iron from plant-based foods. High concentration of vitamin C in white blood
cells enables the immune system to function properly by providing protection
against oxidative damage from free radicals generated during their action
against bacterial, viral, or fungal infections.
Vitamin C also recycles oxidized vitamin E for reuse in cells, and it helps
folic acid convert to its active form, (THF). Vitamin C helps synthesize carnitine, adrenaline, epinephrine, the neurotransmitter
serotonin, the thyroid hormone thyroxine, bile acids, and steroid hormones.
A deficiency of vitamin C causes widespread connective tissue changes
throughout the body. Deficiencies may occur in people who eat few fruits and
vegetables, follow restrictive diets, or abuse alcohol and drugs. Smokers also
have lower vitamin-C status. Supplementation may be prescribed by physicians to
speed the healing of bedsores, skin ulcers, fractures, burns, and after
surgery. Research has shown that doses up to 1 gram per day may have small
effects on duration and severity of the common cold, but not on the prevention
of its occurrence.
Biological role of ascorbic acid:
acts as a cofactor in the en¬zymatic hydroxylation of proline to hydroxyproline and in other hydroxylation reactions;
inhibits the oxidation of hemoglobin;
accelerates the oxidation of glucose in pentose phosphate pathway;
reduces the disulfide bonds to sulfhydryl bonds;
is necessary for
hydroxylation of cholesterol;
takes part in metabolism of adrenaline;
is necessary for the
metabolism of mineral elements (Fe, Ca);
- accelerates the synthesis of glycogen in liver.
While at sea in May 1747, Lind provided some crewmembers with two oranges
and one lemon per day,
in addition to normal rations, while others continued on cider, vinegar or
seawater, along with their normal rations. In the history of science this is
considered to be the first example of a controlled experiment comparing results
on two populations of a factor applied to one group only with all other factors
the same.
In the hypovitaminosis of vitamin C the
disease scurvy is developed. Main clinical symptoms of scurvy: delicacy,
vertigo, palpitation, tachycardia, pain in the area of heart, dyspnea, petechias, odontorrhagia, dedentition.
Ascorbic acid and products of its decomposition are excreted from the
organism via kidneys. In normal conditions 20-30 mg or 113,5-170,3 mkmol of ascorbic acid is excreted per day with urine.
In animal and plant tissues rather large concentrations of ascorbic acid
are present, in comparison with other water-soluble vitamins; e.g., human blood
plasma contains about 1 mg of ascorbic acid per 100 ml. Ascorbic acid is
especially abundant in citrus fruits, tomatoes, currant, onion, garlic,
cabbage, fruits of wild rose, needles of a pine-tree.
Sources of vitamin C
Vitamin C is obtained through the diet by the vast majority of the world's
population. The richest natural sources are fruits and vegetables, and of
those, the camu camu fruit and the billygoat plum contain the highest concentration of the vitamin.
It is alsopresent in some cuts of meat,
especially liver. Vitamin C as ascorbic acid is the most widely taken
nutritional supplement and is available in a variety of forms from tablets and
drink mixes to pure ascorbic acid crystals in capsules or as plain powder.
Vitamin P (bioflavonoids).
This is the group of compounds (rutin, hesperedin, katecholamines) supporting the elasticity of capillaries, strengthen
their walls and decrease the permeability.
Vitamin P takes part in the oxidative-reduction processes. It oppresses the
activity of enzyme hyaluronidase protecting thehyaluronic acid which is necessary for elasticity of vessel
walls.
The deficiency of vitamin P in organism results in
the petechias (dot hemorrhages on skin).
Day necessity of vitamin P is not clear exactly (about 25-50 mg). In some diseases 1-2 g per day of vitamin P is
administrated.
Investigation of fat soluble vitamins functional role in metabolism and
cell functions realization.
Fat-soluble vitamins
Although fat-soluble vitamins have been studied intensively and widely used
in human nutrition, we know less about their specific biological function than
about the water-soluble vitamins.
Vitamin A.
Vitamin A occurs in two common forms, vitamin A1, or ret¬inol, the form most common in mammalian tissues and marine
fishes, and vitamin, A2, common in freshwater fishes. Both are isoprenoid com¬pounds containing a six-membered carbocyclic ring and an eleven-carbon side chain.
Carotenoids are provitamins of vitamin A. Carotenoids widely distributed in plants, particularly a-, b-, and
g-carotene. The carotenes have no vitamin A activity but are converted into
vitamin A by enzymatic reactions in the intestinal mucosa and the liver. b-Carotene, a symmet¬rical molecule, is cleaved in its center to yield two
molecules of retinol. Retinol occurs in the tissues of mammals and is
transported in the blood.
In vitamin A deficiency young persons fail to grow, the bones and nervous
system fail to develop properly, the skin becomes dry and thick¬ened, the kidneys and various glands degenerate, and both
males and females become sterile.
Detailed information is available on the role of vitamin A in the visual_cycle in vertebrates. The human retina contains two types of
light-sensitive photoreceptor cells. Rod-cells are adapted to sensing low light
intensities, but not colors; they are the cells involved in night vision, whose
function is im¬paired by vitamin A
deficiency. Cone cells, which sense colors, are adapted for high light
intensities.
Retinal rod cells contain many mem¬brane vesicles that serve as light receptors. About one-half
of the protein in the membrane of these vesicles consists of the
light-absorbing protein rhodopsin (visual purple). Rhodopsin consists of a protein, opsin, and tightly bound 11-cis-retinal, the aldehyde of vitamin A. When rhodopsin is exposed to light, the bound 11-cis-retinal
undergoestrans¬formation into
all-trans-retinal, which causes a substantial change in the configuration of
the retinal molecule. This reaction isnonenzymatic. The isomerization of retinal is
followed by a series of other molecular changes, ending in the dissociation of
therhodopsin to yield free opsin and all-trans-retinal, which functions as a trigger
setting off the nerve im-pulse.
In order for rhodopsin to be regenerated
from opsin and all-trans-retinal, the latter must undergo isomerization back to 11-cis-retinal. This appears to occur in a
sequence of en¬zymatic reactions
catalyzed by two enzymes:
The 11-cis-retinal so formed now recombines with opsin to yield rhodopsin, thus completing the visual cycle.
Since vitamin A deficiency affects all tissues of
mammals, not the retina alone, the role of retinal in the visual cycle does not
represent the entire action of vitamin A. It appears possible that vitamin A may play a general
role in:
The vitamin A requirement of man - 1,5-2 milligram per day.
Vitamin A is met in large part by green and yellow vegetables, such as
lettuce, spinach, sweet potatoes, and carrots, which are rich in carotenes.
Fish-liver oils are particularly rich in vitamin A. However, excessive intake
of vitamin A is toxic and leads to easily fractured, fragile bones in children,
as well as abnormal development of the fetus.
Vitamin D
Most important are vitamin D2, or ergocalciferol, and vitamin D3, or cholecalciferol, the form normally found in mammals. These compounds
may be regarded as steroids.
It is now known that 7-dehydrocholesterol in the skin is the natural
precursor of cholecalciferol in man; the
conversion requires irradiation of the skin by sunlight. On a normal unsupplemented diet this is the major route by which people usually
acquire vitamin D.
Rickets, a disease of growing bone, is developed in the deficiency of
vitamin D in organism.
As with vitamin A, excessive intake of vitamin D causes the bones to become
fragile and to undergo multiple fractures, suggesting that both vitamins play a
role in biological transport and deposition of calcium.
Most natural foods contain little of vitamin D; vitamin D in the diet
comes largely from fish-liver oils, liver, yoke of eggs, butter. Vitamin D
preparations available commercially are products of the ultraviolet irradiation
of ergosterol from yeast.
Vitamin E
Vitamin E was first recognized as a factor in vegetable oils that
restores fertility in rats grown on cow's milk alone and otherwise incapable of
bearing young. It was isolated from wheat germ and was given the name tocopherol. Several different tocopherolshaving vitamin E activity have been found in plants;
the most active and abun¬dant is a-tocopherol.
Vitamin K was first discovered
as a nutritional factor required for normal blood-clotting time. At least two
forms of vitamin K are known; vitamin K2 is believed to be the active form.
Vitamin K deficiency cannot readily be produced in rats and other mammals
because the vitamin is synthe-sized by intestinal bacteria.
The only known result of vitamin K deficiency is a failure in the
biosynthesis of the enzyme proconvertin in the liver. This enzyme catalyzes a step in a
complex sequence of reac¬tions involved in the
formation of prothrombin, the pre¬cursor of thrombin, a protein that accelerates the conversion
of fibrinogen into fibrin, the insoluble protein constituting the fibrous
portion of blood clots.
The compound dicumarol, an analog of vitamin K, produces symptoms in animals
resembling vitamin K deficiency; it is believed to block the action of vitamin
K. Dicumarol is used in clinical medicine to prevent clotting in
blood vessels. Dicumarol is theantivitamin of vitamin K.
Some evidence indicates that vitamin K may function as a coenzyme in a
specialized route of electron transport in animal tissues; since vitamin K is a quinone which can be reduced reversibly to a quinol, it may serve as an electron carrier.
Hypovitaminos of vitamin K in man can be developed in liver diseases
when there is the decrease of bile acids amount in intestine and as result the
inhibition of fat soluble substances absorption is observed.
Vitamin K is produced by many microorganisms in the intestine. also Plants (cabbage, tomato, lettuce)are natural sources
of vitamin K.
Adult person requires 200-300 mkg of vitamin K per day.
Vitamins are nutrients required in tiny amounts for essential metabolic
reactions in the body. The term vitamin does not include other essential nutrients
such as dietary minerals, essential fatty acids, or essential amino acids, nor
does it encompass the large number of other nutrients that promote health but
that are not essential for life.
Vitamins are bio-molecules that act both as catalysts and substrates
in chemical reactions. When acting as a catalyst, vitamins are bound to enzymes
and are called cofactors. (For example, vitamin K forms part of the proteases
involved in blood clotting.) Vitamins also act as coenzymes to carry chemical
groups between enzymes. (For example, folic acid carries various forms of
carbon groups–methyl, formyl or methylene–in the cell.).
Vitamins have been produced as commodity chemicals and made widely
available as inexpensive pills for several decades, allowing supplementation of
the dietary intake.
Difference from water soluble vitamins: water soluble vitamins are included
into coenzymes, don't have provitamins, are not included into the membranes, and hypervitaminoses are not peculiar for them.
Thiamin (Vitamin B1)
Thiamin (also spelled thiamine) is a water-soluble B vitamin,
previously known as vitamin B1 or aneurine. Isolated and characterized in the 1930s, thiamin was
one of the first organic compounds to be recognized as a vitamin. Thiamin
occurs in the human body as free thiamin and as various phosphorylated forms: thiamin monophosphate (TMP), thiamin triphosphate (TTP), and thiamin pyrophosphate (TPP), which is also
known as thiamin diphosphate.
Deficiency
Beriberi, the disease resulting from severe thiamin deficiency, was
described in Chinese literature as early. Thiamin deficiency affects the
cardiovascular, nervous, muscular, and gastrointestinal systems. Beriberi has been termed dry, wet, or cerebral,
depending on the systems affected by severe thiamin deficiency.
Food sources
A varied diet should provide most individuals with adequate thiamin to
prevent deficiency. In the U.S. the average dietary thiamin intake for young
adult men is about 2 mg/day and 1.2 mg/day for young adult women. A survey of
people over the age of 60 found an average dietary thiamin intake of 1.4 mg/day
for men and 1.1 mg/day for women. However, institutionalization and poverty
both increase the likelihood of inadequate thiamin intake in the elderly.Whole grain cereals, legumes (e.g., beans and lentils), nuts, lean pork, and yeast are rich sources of
thiamin. Because most of the thiamin is lost during the production of white
flour and polished (milled) rice, white rice and foods made from white flour
(e.g., bread and pasta) are fortified with thiamin in many Western countries. A
number of thiamin-rich foods are listed in the table below along with their
thiamin content in milligrams (mg). For more information on the nutrient
content of foods, search the USDA food composition database.
Riboflavin (Vitamin B2)
Riboflavin is a water-soluble B vitamin, also known as vitamin B2. In
the body, riboflavin is primarily found as an integral component of the
coenzymes, flavin adenine dinucleotide (FAD) and flavin mononucleotide (FMN). Coenzymes derived from
riboflavin are termed flavocoenzymes, and enzymes that use a flavocoenzyme are called flavoproteins.
Living organisms derive most of their energy from oxidation-reduction
(redox) reactions, which are processes that involve the
transfer of electrons. Flavocoenzymes participate in redox reactions in numerous metabolic pathways. Flavocoenzymes are critical for the metabolism of carbohydrates, fats, and proteins. FAD is part of the electron transport (respiratory) chain, which is central to
energy production. In conjunction with cytochrome P-450, flavocoenzymes also participate in the metabolism of drugs and
toxins.
Glutathione reductase is a FAD-dependent
enzyme that participates in the redox cycle of glutathione. The glutathione redoxcycle plays a major role in protecting organisms from reactive oxygen species, such as hydroperoxides. Glutathione reductaserequires FAD to regenerate two molecules of reduced
glutathione from oxidized glutathione. Riboflavin deficiency has been
associated with increased oxidative stress. Measurement of glutathione reductase activity in red blood cells is commonly used to assess
riboflavin nutritional status.
Glutathione peroxidase, a selenium-containing
enzyme, requires two molecules of reduced glutathione to break downhydroperoxides (see diagram).
Xanthine oxidase, another FAD-dependent enzyme, catalyzes the oxidation of hypoxanthine and xanthine to uric acid. Uric acid is one of the most effective
water-soluble antioxidants in the blood. Riboflavin deficiency can result in
decreased xanthine oxidaseactivity, reducing
blood uric acid levels.
Deficiency
Ariboflavinosis is the medical name for clinical riboflavin
deficiency. Riboflavin deficiency is rarely found in isolation; it occurs
frequently in combination with deficiencies of other water-soluble vitamins.
Symptoms of riboflavin deficiency include sore throat, redness and swelling of
the lining of the mouth and throat, cracks or sores on the outsides of the lips
(cheliosis) and at the corners of the mouth (angular stomatitis), inflammation and redness of the tongue (magenta
tongue), and a moist, scaly skin inflammation (seborrheic dermatitis). Other symptoms may involve the formation
of blood vessels in the clear covering of the eye (vascularizationof the cornea) and decreased red blood cell count in
which the existing red blood cells contain normal levels of hemoglobin and are
of normal size (normochromic normocytic anemia). Severe riboflavin deficiency may result in decreased conversion of
vitamin B6 toits coenzyme form (PLP) and
decreased conversion of tryptophan to niacin (see Nutrient Interactions).
Food sources
Most plant and animal derived foods contain at least small quantities of
riboflavin. In the U.S., wheat flour and bread have been enriched with
riboflavin (as well as thiamin, niacin, and iron) since 1943. Data from large
dietary surveys indicate that the average intake of riboflavin for men is about
2 mg/day and for women is about 1.5 mg/day; both intakes are well above the
RDA. Intake levels were similar for a population of elderly men and women (1).
Riboflavin is easily destroyed by exposure to light. For instance, up to 50% of
the riboflavin in milk contained in a clear glass bottle can be destroyed after
two hours of exposure to bright sunlight. Some foods with substantial amounts
of riboflavin are listed in the table below along with their riboflavin content
in milligrams (mg). For more information on the nutrient content of foods,
search the USDA food composition database.
Niacin (Vitamin B5)
Niacin exists in two forms, nicotinic acid and nicotinamide. Both forms are readily absorbed from the stomach and
the small intestine. Niacin is stored in small amounts in the liver and
transported to tissues, where it is converted to coenzyme forms. Any excess is
excreted in urine. Niacin is one of the most stable of the B vitamins. It is
resistant to heat and light, and to both acid and alkali environments. The
human body is capable of converting the amino acid tryptophan to niacin when
needed. However, when both tryptophan and niacin are deficient, tryptophan is
used for protein synthesis.
There are two coenzyme forms of niacin: nicotinamide adenine dinucleotide (NAD+) and nicotinamide adenine dinucleotidephophate (NADP+). They both help break down and utilize
proteins, fats, and carbohydrates for energy. Niacin is essential for growth
and is involved in hormone synthesis.
Pellagra results from a combined deficiency of niacin and tryptophan.
Long-term deficiency leads to central nervous system dysfunction manifested as
confusion, apathy, disorientation, and eventually coma and death. Pellagra is
rarely seen in industrialized countries, where it may be observed in people
with rare disorder of tryptophan metabolism (Hartnup's disease), alcoholics, and those with diseases that
affect food intake.
The liver can synthesize niacin from the essential aminoacid tryptophan, but the synthesis is extremely slow; 60 mg of
tryptophan are required to make one milligram of niacin. Dietary niacin
deficiency tends to occur only in areas where people eat corn, the only grain
low in niacin, as a staple food, and that don't use lime during maize (corn)
meal/flour production. Alkali lime releases the tryptophan from the corn so
that it can be absorbed in the gut, and converted to niacin.
Niacin plays an important role in the production of several sex and
stress-related hormones, particularly those made by the adrenal gland. Niacin,
when taken in large doses, increases the level of high density lipoprotein
(HDL) or "good" cholesterol in blood, and is sometimes prescribed for
patients with low HDL, and at high risk of heart attack. Niacin (but not niacinamide) is also used in the treatment of hyperlipidemia because it reduces very low density lipoprotein
(VLDL), a precursor of low density lipoprotein (LDL) or "bad"
cholesterol, secretion from the liver, and inhibits cholesterol synthesis.
The main problem with the clinical use of niacin for dyslipidemia is the occurrence of skin flushing, even with moderate
doses.
Recommended intake is expressed as milligrams of niacin equivalents (NE) to
account for niacin synthesized from tryptophan. High doses taken orally as
nicotinic acid at 1.5 to 2 grams per day can decrease cholesterol and
triglyceride levels, and along with diet and exercise can slow or reverse the
progression of heart disease.
The nicotinamide form of niacin in multivitamin and B-complex tablets
do not work for this purpose. Supplementation should be under a physician's
guidance.
Food sources
Good sources of niacin include yeast, meat, poultry, red fishes (e.g.,
tuna, salmon), cereals (especially fortified cereals), legumes, and seeds.
Milk, green leafy vegetables, coffee, and tea also provide some niacin. In
plants, especially mature cereal grains like corn and wheat, niacin may be
bound to sugar molecules in the form of glycosides, which significantly
decrease niacin bioavailability.
Pantothenic Acid (Vitamin B3)
Pantothenic acid, also called vitamin B3, is a water-soluble
vitamin required to sustain life. Pantothenic acid is needed to form coenzyme-A (CoA), and is critical in the metabolism and synthesis of
carbohydrates, proteins, and fats. Its name is derived from the Greek pantothen meaning "from everywhere" and small
quantities of pantothenic acid are found in
nearly every food, with high amounts in whole grain cereals, legumes, eggs,
meat, and royal jelly
Pantothenic acid is stable in moist heat. It is destroyed by
vinegar (acid), baking soda (alkali), and dry heat. Significant losses occur
during the processing and refining of foods. Pantothenic acid is released from coenzyme A in food in the small
intestine. After absorption, it is transported to tissues, where coenzyme A is resynthesized. Coenzyme A is essential for the formation of energy
as adenosine triphosphate (ATP) from
carbohydrate, protein, alcohol, and fat.
Coenzyme A is also important in the synthesis of fatty acids,
cholesterol, steroids, and the neurotransmitter acetylcholine, which is
essential for transmission of nerve impulses to muscles.
Dietary deficiency occurs in conjunction with other B-vitamin deficiencies. Pantothenic acid is used in the synthesis of coenzyme A
(abbreviated as CoA). Coenzyme A may
act as an acyl group carrier to
form acetyl-CoA and other related
compounds; this is a way to transport carbon atoms within the cell. The
transfer of carbon atoms by coenzyme A is important in cellular respiration, as
well as the biosynthesis of many important compounds such as fatty acids,
cholesterol, and acetylcholine. Dietary deficiency occurs in conjunction with
other B-vitamin deficiencies. In studies, experimentally induced deficiency in
humans has resulted in headache, fatigue, impaired muscle coordination,
abdominal cramps, and vomiting.
In studies, experimentally induced deficiency in humans has resulted
in headache, fatigue, impaired muscle coordination, abdominal cramps, and
vomiting.
Biotin (Vitamin B8)
Biotin is a water soluble vitamin and a member of Vitamin B complex. Also known as Vitamin H, Bios II, Co-enzyme R. Its natural form is D-biotin. It was isolated from liver in 1941 by Dr. Paul Gyorgy.
Biotin is the most stable of B vitamins. It is commonly found in two forms:
the free vitamin and the protein-bound coenzyme form called biocytin. Biotin is absorbed in the small intestine, and it
requires digestion by enzyme biotinidase, which is present in the small intestine. Biotin is synthesized
by bacteria in the large intestine, but its absorption is questionable. Biotincontaining coenzymes participate in key reactions that produce
energy from carbohydrate and synthesize fatty acids and protein.
Avidin is a protein in raw egg white, which can bind to the biotin in the stomach
and decrease its absorption. Therefore, consumption of raw whites is of concern
due to the risk of becoming biotin deficient. Cooking the egg white, however,
destroysavidin. Deficiency may
develop in infants born with a genetic defect that results in reduced levels of biotinidase. In the past, biotin deficiency was observed in
infants fed biotin-deficient formula, so it is now added to infant formulas and
other baby foods.
Vitamin B6
Pyridoxal, pyridoxamine and pyridoxine are collectively known as vitamin B6.
All three compounds are efficiently converted to the biologically active form
of vitamin B6, pyridoxal phosphate. This
conversion is catalyzed by the ATP requiring enzyme,pyridoxal kinase.
Vitamin B6 is present in three forms: pyridoxal, pyridoxine, and pyridoxamine. All forms can be converted to the active vitamin-B6
coenzyme in the body. Pyridoxal phosphate (PLP) is the predominant biologically active
form. Vitamin B6 is not stable in heat or in alkaline conditions, so cooking
and food processing reduce its content in food. Both coenzyme and free forms
are absorbed in the small intestine and transported to the liver, where they
are phosphorylated and released into circulation, bound to albumin for
transport to tissues. Vitamin B6 is stored in the muscle and only excreted in
urine when intake is excessive.
Folic Acid, Folate, Folacin (Vitamin B9)
Folacin or folate, as it is usually called, is the form of vitamin B9
naturally present in foods, whereas folic acid is the synthetic form added to
fortified foods and supplements. Both forms are absorbed in the small intestine
and stored in the liver. The folic acid form, however, is more efficiently
absorbed and available to the body. When consumed in excess of needs, both
forms are excreted in urine and easily destroyed by heat, oxidation, and light.
Folic acid is a water soluble vitamin and is a member of the Vitamin B
complex. Also known as Folacin, pteroyl-L-glutamic acid (PGA), vitamin Bc or vitamin M. Folic acid and its derivatives (mostly
the tri and heptaglutamyl peptides) are
widespread in nature. It is a specific growth factor for certain
micro-organisms. Found in yeast and
liver in 1935.
All forms of this vitamin are readily converted to the coenzyme form called tetrahydrofolate (THFA), which plays a key role in transferring
single-carbon methyl units during the synthesis of DNA and RNA, and in interconversions of amino acids. Folate also plays an important role in the synthesis of
neurotransmitters. Meeting folate needs can improve mood and mental functions.
Long term high doses may cause Vitamin B12 losses from the body
Folate deficiency is one of the most common vitamin deficiencies. Early symptoms are
nonspecific and include tiredness, irritability, and loss of appetite. Severe folate deficiency leads to macrocytic anemia, a condition in which cells in the bone marrow
cannot divide normally and red blood cells remain in a large immature form
called macrocytes. Large immature cells also appear along the length of
the gastrointestinal tract, resulting in abdominal pain and diarrhea.
Pregnancy is a time of rapid cell multiplication and DNA synthesis, which
increases the need for folate. Folate deficiency may lead to neural tube defects such as spina bifida (failure of the spine to close properly during
the first month of pregnancy) and anencephaly (closure of the neural tube
during fetal development, resulting in part of the cranium not being formed).
Seventy percent of these defects could be avoided by adequate folate status before conception, and it is recommended that
all women of childbearing age consume at least 400 micrograms (μg) of folic acid
each day from fortified foods and supplements. Other groups at risk of
deficiency include elderly persons and persons suffering from alcohol abuse or
taking certain prescription drugs.
Vitamin B12
Vitamin B12 is found in its free-vitamin form, called cyanocobalamin, and in two active coenzyme forms. Absorption of
vitamin B12 requires the presence of intrinsic factor,a protein synthesized by acid-producing cells of the
stomach. The vitamin is absorbed in the terminal portion of the small intestine
called the ileum. Most of body's supply of vitamin B12 is stored in the liver.
Vitamin B12
Vitamin B12 is defficiently conserved in the
body, since most of it is secreted into bile and reabsorbed. This explains the
slow development (about two years) of deficiency in people with reduced intake
or absorption. Vitamin B12 is stable when heated and slowly loses its activity
when exposed to light, oxygen, and acid or alkaline environments.
Vitamin B12 coenzymes help recycle folate coenzymes involved in the synthesis of DNA and RNA,
and in the normal formation of red blood cells. Vitamin B12 prevents
degeneration of the myelin sheaths that cover nerves and help maintain normal
electrical conductivity through the nerves.
Active center
of tetrahydrofolate (THF). Note that the N5 position is the site of attachment of
methyl groups, the N10 the site for attachment of formyl and formimino groups and that both N5 and N10 bridge the methylene and methenyl groups
Vitamin-B12 deficiency results in pernicious anemia, which is caused by a
genetic problem in the production of intrinsic factor. When this occurs, folate function is impaired, leading to macrocytic anemia due to interference in normal DNA synthesis.
Unlikefolate deficiency, the anemia caused by vitamin-B12
deficiency is accompanied by symptoms of nerve degeneration, which if left
untreated can result in paralysis and death.
Since vitamin B12 is well conserved in the body, it is difficult to become
deficient from dietary factors alone, unless a person is a strict vegan and
consumes a diet devoid of eggs and dairy for several years. Deficiency is
usually observed when B12 absorption is hampered by disease or surgery to the
stomach or ileum, damage to gastric mucosa by alcoholism, or prolonged use of
anti-ulcer medications that affect secretion of intrinsic factor. Agerelated decrease in stomach-acid production also reduces
absorption of B12 in elderly persons. These groups are advised to consume
fortified foods or take a supplemental form of vitamin B12.
Vitamin C (Ascorbic Acid)
In 1746, James Lind, a British physician, conducted the first nutrition
experiment on human beings in an effort to find a cure for scurvy.
Vitamin C is needed to form and maintain collagen, a fibrous protein that
gives strength to connective tissues in skin, cartilage, bones, teeth, and
joints. Collagen is also needed for the healing of wounds.
When added to meals, vitamin C increases intestinal absorption of
iron from plant-based foods. High concentration of vitamin C in white blood
cells enables the immune system to function properly by providing protection
against oxidative damage from free radicals generated during their action
against bacterial, viral, or fungal infections.
Vitamin C also recycles oxidized vitamin E for reuse in cells, and it helps
folic acid convert to its active form, (THF). Vitamin C helps synthesize carnitine, adrenaline, epinephrine, the neurotransmitter
serotonin, the thyroid hormone thyroxine, bile acids, and steroid hormones.
A deficiency of vitamin C causes widespread connective tissue changes
throughout the body. Deficiencies may occur in people who eat few fruits and
vegetables, follow restrictive diets, or abuse alcohol and drugs. Smokers also
have lower vitamin-C status. Supplementation may be prescribed by physicians to
speed the healing of bedsores, skin ulcers, fractures, burns, and after
surgery. Research has shown that doses up to 1 gram per day may have small
effects on duration and severity of the common cold, but not on the prevention
of its occurrence.
Biological role of ascorbic acid:
acts as a cofactor in the en¬zymatic hydroxylation of proline to hydroxyproline and in other hydroxylation reactions;
inhibits the oxidation of hemoglobin;
accelerates the oxidation of glucose in pentose phosphate pathway;
reduces the disulfide bonds to sulfhydryl bonds;
is necessary for
hydroxylation of cholesterol;
takes part in metabolism of adrenaline;
is necessary for the
metabolism of mineral elements (Fe, Ca);
- accelerates the synthesis of glycogen in liver.
While at sea in May 1747, Lind provided some crewmembers with two oranges
and one lemon per day,
in addition to normal rations, while others continued on cider, vinegar or
seawater, along with their normal rations. In the history of science this is
considered to be the first example of a controlled experiment comparing results
on two populations of a factor applied to one group only with all other factors
the same.
In the hypovitaminosis of vitamin C the
disease scurvy is developed. Main clinical symptoms of scurvy: delicacy,
vertigo, palpitation, tachycardia, pain in the area of heart, dyspnea, petechias, odontorrhagia, dedentition.
Ascorbic acid and products of its decomposition are excreted from the
organism via kidneys. In normal conditions 20-30 mg or 113,5-170,3 mkmol of ascorbic acid is excreted per day with urine.
In animal and plant tissues rather large concentrations of ascorbic acid
are present, in comparison with other water-soluble vitamins; e.g., human blood
plasma contains about 1 mg of ascorbic acid per 100 ml. Ascorbic acid is
especially abundant in citrus fruits, tomatoes, currant, onion, garlic,
cabbage, fruits of wild rose, needles of a pine-tree.
Sources of vitamin C
Vitamin C is obtained through the diet by the vast majority of the world's
population. The richest natural sources are fruits and vegetables, and of
those, the camu camu fruit and the billygoat plum contain the highest concentration of the vitamin.
It is alsopresent in some cuts of meat,
especially liver. Vitamin C as ascorbic acid is the most widely taken
nutritional supplement and is available in a variety of forms from tablets and
drink mixes to pure ascorbic acid crystals in capsules or as plain powder.
Vitamin P (bioflavonoids).
This is the group of compounds (rutin, hesperedin, katecholamines) supporting the elasticity of capillaries, strengthen
their walls and decrease the permeability.
Vitamin P takes part in the oxidative-reduction processes. It oppresses the
activity of enzyme hyaluronidase protecting thehyaluronic acid which is necessary for elasticity of vessel
walls.
The deficiency of vitamin P in organism results in
the petechias (dot hemorrhages on skin).
Day necessity of vitamin P is not clear exactly (about 25-50 mg). In some diseases 1-2 g per day of vitamin P is
administrated.
Investigation of fat soluble vitamins functional role in metabolism and
cell functions realization.
Fat-soluble vitamins
Although fat-soluble vitamins have been studied intensively and widely used
in human nutrition, we know less about their specific biological function than
about the water-soluble vitamins.
Vitamin A.
Vitamin A occurs in two common forms, vitamin A1, or ret¬inol, the form most common in mammalian tissues and marine
fishes, and vitamin, A2, common in freshwater fishes. Both are isoprenoid com¬pounds containing a six-membered carbocyclic ring and an eleven-carbon side chain.
Carotenoids are provitamins of vitamin A. Carotenoids widely distributed in plants, particularly a-, b-, and
g-carotene. The carotenes have no vitamin A activity but are converted into
vitamin A by enzymatic reactions in the intestinal mucosa and the liver. b-Carotene, a symmet¬rical molecule, is cleaved in its center to yield two
molecules of retinol. Retinol occurs in the tissues of mammals and is transported
in the blood.
In vitamin A deficiency young persons fail to grow, the bones and nervous
system fail to develop properly, the skin becomes dry and thick¬ened, the kidneys and various glands degenerate, and both
males and females become sterile.
Detailed information is available on the role of vitamin A in the visual_cycle in vertebrates. The human retina contains two types of
light-sensitive photoreceptor cells. Rod-cells are adapted to sensing low light
intensities, but not colors; they are the cells involved in night vision, whose
function is im¬paired by vitamin A
deficiency. Cone cells, which sense colors, are adapted for high light
intensities.
Retinal rod cells contain many mem¬brane vesicles that serve as light receptors. About one-half
of the protein in the membrane of these vesicles consists of the
light-absorbing protein rhodopsin (visual purple). Rhodopsin consists of a protein, opsin, and tightly bound 11-cis-retinal, the aldehyde of vitamin A. When rhodopsin is exposed to light, the bound 11-cis-retinal
undergoestrans¬formation into
all-trans-retinal, which causes a substantial change in the configuration of
the retinal molecule. This reaction isnonenzymatic. The isomerization of retinal is
followed by a series of other molecular changes, ending in the dissociation of
therhodopsin to yield free opsin and all-trans-retinal, which functions as a trigger
setting off the nerve im-pulse.
In order for rhodopsin to be regenerated
from opsin and all-trans-retinal, the latter must undergo isomerization back to 11-cis-retinal. This appears to occur in a
sequence of en¬zymatic reactions
catalyzed by two enzymes:
The 11-cis-retinal so formed now recombines with opsin to yield rhodopsin, thus completing the visual cycle.
Since vitamin A deficiency affects all tissues of
mammals, not the retina alone, the role of retinal in the visual cycle does not
represent the entire action of vitamin A. It appears possible that vitamin A may play a general
role in:
The vitamin A requirement of man - 1,5-2 milligram per day.
Vitamin A is met in large part by green and yellow vegetables, such as
lettuce, spinach, sweet potatoes, and carrots, which are rich in carotenes.
Fish-liver oils are particularly rich in vitamin A. However, excessive intake
of vitamin A is toxic and leads to easily fractured, fragile bones in children,
as well as abnormal development of the fetus.
Vitamin D
Most important are vitamin D2, or ergocalciferol, and vitamin D3, or cholecalciferol, the form normally found in mammals. These compounds
may be regarded as steroids.
It is now known that 7-dehydrocholesterol in the skin is the natural
precursor of cholecalciferol in man; the
conversion requires irradiation of the skin by sunlight. On a normal unsupplemented diet this is the major route by which people usually
acquire vitamin D.
Rickets, a disease of growing bone, is developed in the deficiency of
vitamin D in organism.
As with vitamin A, excessive intake of vitamin D causes the bones to become
fragile and to undergo multiple fractures, suggesting that both vitamins play a
role in biological transport and deposition of calcium.
Most natural foods contain little of vitamin D; vitamin D in the diet
comes largely from fish-liver oils, liver, yoke of eggs, butter. Vitamin D
preparations available commercially are products of the ultraviolet irradiation
of ergosterol from yeast.
Vitamin E
Vitamin E was first recognized as a factor in vegetable oils that restores
fertility in rats grown on cow's milk alone and otherwise incapable of bearing
young. It was isolated from wheat germ and was given the name tocopherol. Several different tocopherolshaving vitamin E activity have been found in plants;
the most active and abun¬dant is a-tocopherol.
Vitamin K was first discovered
as a nutritional factor required for normal blood-clotting time. At least two
forms of vitamin K are known; vitamin K2 is believed to be the active form.
Vitamin K deficiency cannot readily be produced in rats and other mammals
because the vitamin is synthe-sized by intestinal bacteria.
The only known result of vitamin K deficiency is a failure in the
biosynthesis of the enzyme proconvertin in the liver. This enzyme catalyzes a step in a complex
sequence of reac¬tions involved in the
formation of prothrombin, the pre¬cursor of thrombin, a protein that accelerates the conversion
of fibrinogen into fibrin, the insoluble protein constituting the fibrous
portion of blood clots.
The compound dicumarol, an analog of vitamin K, produces symptoms in animals
resembling vitamin K deficiency; it is believed to block the action of vitamin
K. Dicumarol is used in clinical medicine to prevent clotting in
blood vessels. Dicumarol is theantivitamin of vitamin K.
Some evidence indicates that vitamin K may function as a coenzyme in a
specialized route of electron transport in animal tissues; since vitamin K is a quinone which can be reduced reversibly to a quinol, it may serve as an electron carrier.
Hypovitaminos of vitamin K in man can be developed in liver diseases
when there is the decrease of bile acids amount in intestine and as result the
inhibition of fat soluble substances absorption is observed.
Vitamin K is produced by many microorganisms in the intestine. also Plants (cabbage, tomato, lettuce)are natural sources
of vitamin K.
Adult person requires 200-300 mkg of vitamin K per day.