• hydrophilic vitamins
  • complex
    chemical formula, important chemical group(s) and modification(s) by human enzyme(s) 
    derived coenzymes and their role(s)
    dietary reference intake (DRI)
    hypovitaminosis / vitanition 
    recommended dietary allowance (RDA)
    adequate intake (AI)
    estimated average requirement (EAR)
    tolerable upper intake level (UL)
    symptoms & signs 
    laboratory examinations
    vitamin B complex vitamin B1 / thiamine / aneurine (the first vitamin, discovered by K.Funk in 1912) 
    • acethiamine hydrochloride
    • benfotiamine / S-benzoylthiamine  O-monophosphate
    • bisbentiamine / O-benzoylthiamine disulphide
    • bisbutiamine / O-butyrylthiamine disulphide
    • cetotiamine hydrochloride / dicethiam hydrochloride
    • cycotiamine / cyclorcabolthiamine
    • fursultiamine / thiamine tetrahydrofurfuryl disulphide
    • octotiamine / hioctothiamine
    • prosultiamine / thiamine propyl disulphid
    • sulbutiamine / bisibutiamine / O-isobutyrylthiamine disulphide
    • thiamine hydrochloride
    • thiamine nitrate
    The recent 3-month nationwide shortage of intravenous formulations of vitamin B1 (thiamine) in 2005 highlights the fact that only one company, American Pharmaceutical Partners, is manufacturing this lifesaving drug. This shortage was the second in the past few years, and the company has not provided a reason for the shortages. The retail cost of parenteral thiamine can be as low as 89 cents for 100 mg with collective purchases, so it is no wonder there was a shortage of this medication when blockbuster drugs hold more commercial promiseref
    pyrimidine + thiazole 
    + ATP ==thiamine diphosphokinase==> AMP + thiamine pyrophosphate (TPP) (prosthetic group) : a-ketoacid decarboxylases and aminotransferases SLC19A2 frequent vomiting beri-beri / rice disease / dietetic neuritis / neuritis multiplex endemica / endemic polyneuritis (maladie des jambes : a disease of rice growers in Louisiana, probably beriberi) : polyneuritis in individuals defective for transketolase, cardiac pathology, and edema. The epidemic form is found primarily in areas in which white (polished) rice is the staple food, as in Japan, China, the Philippines, India, and other countries of Southeast Asia. The onset of symptoms is often rapid and the fatality rate can be high.  The neurological form often begins with symptoms that include apathy, irritability, sleep disturbances, vomiting, and constipation. Later symptoms include convulsions and loss of consciousness. There are 8 clinically recognizable syndromes (often a patient has features of more than one of the syndromes) : 
  • 5 in adults :
    • dry beriberi / atrophic beriberi / paralytic beriberi : a form of beriberi in which flaccid paralysis, muscular atrophy, and areflexia are the prominent signs; cardiac enlargement and tachycardia may be present
    • wet beriberi : a form marked by cardiac failure and edema, but without extensive nervous system involvement.
    • Wernicke's encephalopathy
    • Korsakoff's psychosis
    • temporal atrophy
  • 3 in children : infantile beriberi : a disease of breast-fed infants whose mothers have thiamine deficiency or artificially fed with thiamine-poor preparations; it is characterized by diminished urine secretion, progressive edema, and often by acute cardiac failure, which may terminate in sudden death. Vomiting, aphonia, opisthotonos, and convulsions may occur.
    • infantile encephalitic beri-beri (sometimes called "pseudomeningeal" beri-beri) -- This usually occurs in 6-12 month-old infants and is the equivalent of Wernicke's encephalopathy in adults. The patient appears to have meningoencephalitis. There is nystagmus, muscle twitching, a bulging fontanelle, convulsions, and loss of consciousness. This can be confused with all forms of encephalitis and meningitis, malaria, and even acute vitamin A intoxication.
    • infantile acute cardiac beri-beri : peak prevalence of this form occurs in breast-fed infants aged 1-3 months.  The first signs appear like colic with screaming bouts, restlessness, anorexia, and nausea and vomiting. This progress to edema, cyanosis, and shortness of breath with signs of heart failure. Tachycardia, enlargement of the heart, systolic murmurs, pulmonary edema, liver enlargement, and oliguria. Pneumonia and septicemia are commonly confused with this form of beri-beri.
    • aphonic beri-beri : peak prevalence is in 4-6 month-old children. The child's voice changes so that the cry gets more and more hoarse until no sound is produced. These children appear to be crying without any noise. Without treatment they progress over a few days to restlessness, edema, breathlessness, and then death.
    The treatment for beri-beri is thiamine supplementation.  Infants may be safely treated with adult doses (it is not toxic in very large quantities).  For severely ill children, give 50 mg of thiamine hydrochloride slowly, and watch for response; if no response in several hours consider a repeat dose. I.v. treatment should be followed by a daily p.o. or i.m. dose of 10 mg of thiamine for 1-2 weeks. The response to acute cardiac beri-beri may be rapid, with a diuresis starting between 4 and 48 hours after the thiamine, with visible resolution of much of the edema over the next 4 to 8 hours, followed by complete loss over the next 48 hours. The convulsions and delirium in encephalitic patients respond rapidly to treatment.  However, the cranial nerve lesions can take months to recover and may be permanent. Aphonia gradually resolves over 2 to 3 weeks
    vitamin B2 or G / riboflavin / E101 / lactoflavin isoalloxazine (4n+2 = 14) = dimethylbenzene + pteryn flavin mononucleotide (FMN) / E101a / riboflavin phosphate
    and flavine adenine dinucleotide (FAD) (prostethic groups) : transport of 2 hydride ions (H2) in flavoproteins 
    quinone <=> semiquinone / semiquinol <=> quinol   photophobia, angular cheilitis, increased production of sebum, cobble-stone tongue, magenta tongue
    vitamin B3 or PP / niacin / nicotinic acid / E375 (Niaspan®) pyridine It is an agonist on HM74 or can be converted to : 
    nicotinamide adenine dinucleotide (NAD+) and nicotinamide adenine dinucleotide phosphate (NADP+) (cosubstrates) : 

    transport of H- ; CD38 catalyze conversions of ... 
    • ... NAD+ to cyclic ADP ribose (cADPR) 
    • ... NADP+ to NAADP
    insufficient endogenous synthesis via Trp ; it decreases [VLDL] by competing with phosphocholine for methyl moieties in choline ; nicotinic acid + PRPP => PPi + nicotinic acid ribonucleotide =+ ATP=> PPi + desamido-NAD =+ Gln + ATP=> ADP + Pi + Glu + NAD =+ATP=> ADP + NADP normal pyridoxine plasma range, 5-30 ng/ml [20-121 nmol/l]

    normal niacin serum range =  0.5-15 ng/ml [4-122 nmol/l] 

    3 D's : dermatitis (pellagra), injuries of intestinal mucosa => diarrhea, and CNS impairment => dementia, degeneration of posterolateral cords, Sandwith's bald tongue, and death if untreated. Casal's necklace (i.e., erythema, hyperpigmentation, and scales around the neck)
    vitamin B4 adenine (no longer considered a vitamin !) purine (pyrimidine + imidazole)
  • FMN 
  • FAD 
  • NAD 
  • NADP 
  • CoA 
  • S-AdoMet 
  • PAPS 
  • ATP
  • vitamin B5pantothenic acid 4-phosphopantetheine : 
    • b-mercaptoethylamine / cysteamine
    • b-alanine
    • pantoic acid 
    • phosphate
  • CoA (prosthetic group) : activates acyl group to thioester groups ; 
  • acyl carrier protein (ACP : prosthetic group) : acyl carrier
  • partly produced from intestinal flora ; antagonist is w-methyl pantothenate neuromotor and cardiovascular impairment
    vitamin B6 pyridine 
    • pyridoxine
    • pyridoxal
    • pyridoxamine
    pyridoxal phosphate (prosthetic group) : aminotransferases, amino acid decarboxylases, d-ALA synthetase, racemases, glycogen phosphorylase  dermatitis and gyrate atrophy from pyridoxal kinase inhibitors (e.g. hydrazones resulting from  isoniazid reaction with pyridoxal or pyridoxal phosphate), cycloserine, hydralazine, and antimetabolites (4-deoxypyridoxine, which forms in vivo4-deoxypyridoxine-5-phosphate, a competitive inhibitor of several pyridoxal phosphate-dependent enzymes) 

    tryptophan load test : a single large dose of tryptophan is administered orally and a 24-hour urine sample is analyzed for xanthurenic acid, and sometimes also kynurenine, hydroxykynurenine, and kynurenic acid. If vitamin B6 deficiency exists, kynureninase activity will be decreased and these metabolites will accumulate in the urine.

    Randomized, double-blind, controlled trials suggest that this vitamin combination lowers serum homocysteine levels and the risk of myocardial infarction.

    vitamin B7, B8 or H / biotin / CoR sature analogs of imidazole and thiophene prosthetic group : pyruvate, acetylCoA, propyionyl-CoA, and b-methylcrotonyl-CoA decarboxylases it may arise from liocithinase action on biocytin ; it is chelated by avidine found in egg white squamous dermatitis
    vitamin B8, B9, M, Bc, folate or folic acid (Folvite®) and the 5-formylderivative of tetrahydrofolic acid folinic acid (leucovorin (LV) calcium, citrovorum factor (CF) (Isorvorin®, Wellcovorin®) / pteroyl glutamate / NSC 3073 / USAF C313 / B11 / L / U (for ulcer) factor / Lactobacillus casei factor / P-factor Streptococcus ( SRL) / folacine Glun
    pteroic acid 
    • p-aminobenzoic acid (PABA)
    • pterine
      • pyrimidine
      • pyrazine
    tetrahydrofolate (THF : cosubstrate) : carries monocarbon units (except CO2) synthetyzed from GTP; inhibitors of bacterial dihydropteroate synthetase are antibiotics; bacterial DHF reductase is inhibited by trimethoprim ; inhibitors of human DHF reductase are cytostatic drugs; lysosomal folate hydrolase 1 and 2 eliminate Glun => decrease of negativce charge => can cross lamina propria of enterocytes. Enter cells via:  Transporters :  Enzymes  normal plasma concentration : 3-17 ng/mL or 6.8-38.5 nmol/l  megaloblastic anemia
    Rates of neural tube defects are significantly diminished if the diet is supplemented with folic acid during pregnancy.
    vein occlusion in posterior eye segment 
    Randomized, double-blind, controlled trials suggest that this vitamin combination lowers serum homocysteine levels and the risk of myocardial infarction.

    deoxyuridine suppression test : a test for folate or cobalamin deficiency, in which lack of 5,10-methylene tetrahydrofolate inhibits incorporation of deoxyuridine into DNA, so that deoxyuridine fails to inhibit incorporation of 3H-thymidine. 

    histidine loading or formiminoglutamic acid (FIGLU) excretion test : a loading dose of histidine is given, and the resultant urinary excretion of excess FIGLU, secondary to decreased amounts of tetrahydrofolic acid, is measured

    The widespread practice of fortifying food with folic acid could be slowly changing the genetic make-up of the population - and perhaps creating future generations more vulnerable to fatal diseasesref. It is added by law to flour and grain products in some countries, including the USA, to ensure that pregnant women, who are often unaware of their pregnancy early on, eat enough folic acid to reduce the risk of their babies developing defects in the brain and spine. Folic-acid fortification, which bumps up the entire population's intake of the nutrient, could slowly and inadvertently change the genetic make-up of the population and potentially make us unhealthier as a whole. The babies of women on diets rich in folic acid are 4 times more likely to carry the 677T MTHFR allele than were fetuses that were miscarried, suggesting that fetuses carrying this gene variant are more likely to survive to birth, if their mothers are getting an adequate or abundant intake of folic acidref. And because widespread folic-acid fortification and vitamin supplements ensure that more and more mothers do indeed get high levels of the nutrient, the number of children carrying this variant could be climbing. This change of genetics could have a negative effect on health over time : several studies have shown that this same form of the gene, 677T MTHFR, may increase the risk of various conditions in adults, including heart disease, certain forms of cancer and complications of pregnancy. Some studies suggest that these harmful effects of the gene are more common when people's diets are low in folic acid. It's not clear why this might be, but as long as people's diets remain high in folic acid this would compensate for any adverse impacts of 677T MTHFR. However  widespread fortification could effectively create a future population that is artificially dependent on copious quantities of the vitamin - and one that would be more vulnerable to certain fatal diseases if that supply vanished. At present, the health benefits of folic-acid fortification for pregnant women outweigh the potential future risk. But until the potential health risks of fortification are clearer, governments could consider lowering their recommendation on how much folic acid should be added to food. They might, for example, aim for women to obtain 200 mg per day rather than the 400 mg currently recommended in the USA. There is not yet enough evidence to say whether or not this genetic selection is taking place. Folic-acid fortification would change the genetics of the population so slowly that the effects would never be seen. Besides preventing spinal-cord defects in babies, some studies suggest that folic acid also protects against heart disease and stroke. But the long-term safety implications of boosting folic acid are unknown. There are fears that high doses might accelerate the progression of certain cancers, for example. Concerns such as these have prevented many countries, such as the UK, from mandating that the nutrient be added to flour

    biopterin tetrahydrobiopterin (THB : prosthetic group) : phenylalanine hydroxylase and NO synthase
    vitamin B10 or Bx / p-aminobenzoic acid (PABA) / H1 inhibitors of bacterial dihydropteroate synthetase are PABA analogs
    vitamin B11 or Bt (growth factor for Tenebrio molitor) / L-carnitine / b-hydroxy-g-trimethylammonium butyrate (Carnitor® SF and oral solution (sugar-free; source : Sigma-Tau Pharmaceuticals); and Carnitene®). 
    • acetyl-L-carnitine (Branigen®, Ceredor®, Nicetile®, Normobren® and Zibren®)
    partly synthetized in liver and kidney from Lys residues in various proteins, beginning with formation of 6-N-trimethyllysine by a sequence of reactions involving S-AdoMet
    vitamin B12 / cobalamine / extrinsic factor / dibencozide (Dobetin®)
  • cyanocobalamine 
  • aquocobalamine 
  • hydroxycobalamine 

  • dimethylbenz- (o-xylen-) imidazole ribonucleotide ;
  • corrhinic ring
  • 5'dA-B12 (prosthetic group) 
  • methyl-B12 (prosthetic group) : it carries H and alkyl groups (including CH3 groups) 
  • cofactor for 
  • R binder / haptocorrin / transcobalamin I is produced in salivary glands and in secondary granules of neutrophils; it is the carrier for vitamin B12 from mouth through stomach (protecting it from degradation) to duodenum, where pancreatic proteases cleave it) : here it binds to protease-resistant Castle's gastric intrinsic factor (IF) (GIF) produced by parietal / oxyntic cells of gastric glands in stomach mucosa, that acts as a carrier for vitamin B12 from duodenum to ileum, where the complex undergoes RME. It is carried in plasma by R binder / transcobalamin 2. Absent in vegetables. It is accumulated in liver (storage : 4 mg) and undergoes enterohepatic circulation.

    Plants do not contain cobalamin because they have no cobalamin-dependent enzymes. In contrast, many algae are rich in vitamin B12, with some species, such as Porphyra yezoensis (Nori), containing as much cobalamin as liver. Despite this, the role of the cofactor in algal metabolism remains unknown, as does the source of the vitamin for these organisms. A survey of 326 algal species revealed that 171 species require exogenous vitamin B12 for growth, implying that more than half of the algal kingdom are cobalamin auxotrophs. The role of vitamin B12 in algal metabolism is primarily as a cofactor for vitamin B12-dependent methionine synthase, and that cobalamin auxotrophy has arisen numerous times throughout evolution, probably owing to the loss of the vitamin B12-independent form of the enzyme. The source of cobalamin seems to be bacteria, indicating an important and unsuspected symbiosisref

    1-3 mg / day (normal plasma concentration : 205-876 pg/mL = 150-674 pmol/L). As liver storage = 1 mg/g weight = 1.5 g, deficiency occurs after 3-4 years of malabsorptions
    > 20% among elderly people 
  • insufficient ingestion :
    • alcoholism
    • anorexia nervosa
    • extremely imbalanced diet (vegetarianism)
  • impaired intestinal absorption 
  • essential pernicious (megaloblastic) anemia
    posterolateral sclerosis / subacute combined degeneration of the spinal cord
    methylmalonic acidemia, temporal atrophy 

    Randomized, double-blind, controlled trials suggest that this vitamin combination lowers serum homocysteine levels and the risk of myocardial infarction.

    vitamin B13orotic acid (no longer considered a  vitamin !)
    vitamin B15 (B16 ?) / pangamic acid / dimethylglycine although widely used as doping agent, it is rather an hepatotoxic agent whose sale has been forbidden by FDA
    vitamin B17 (B19 ?) / amygdalin
    • L-mandelonitrile-b-glucuronoside (Laetrile®)
    cyanogenetic O-glucoside
    vitamin C / L-ascorbic acid / hygnose / 3-oxo-L-gulofuranoacetone / E300 enediol <=> dehydroascorbic acid (DHA) 
    hydroxylases (proline, lysine, biliary acids), reduction of Cu+ and Fe3+ synthesis from glucuronic acid doesn't occur in Primates. Upping your intake of vitamin C to ward off the common cold makes sense if you're an extreme skiier or mountaineer. But a review of 55 studies carried out over 65 years shows that prophylactic use of this vitamin in everyday circumstances has little effect. This latter find clashes with the conviction held by many that vitamin C supplements boost the immune system and ward off illness, an idea that gained great popularity during the 1970s thanks to famous chemist and Nobel laureate Linus Pauling. Pauling advocated the consumption of megadoses of this vitamin. Unlike most animals, humans can't produce their own vitamin C. In many countries, including the USA, the current recommended daily allowance of vitamin C ranges between 60 and 90 mg. But Pauling calculated that the average adult should eat > 1,000 mg. Recently, large-scale scientific studies have cast doubt over how much vitamin C supplements protect people against the common cold. Many of the studies in their review asked whether vitamin C reduces the incidence of the common cold. Pooling the data, no significant protective effect was found overall. But marathon runners, skiers and soldiers exposed to icy conditions or physical stress experienced a 50% reduction in colds thanks to the vitamin. Use of the vitamin reduced the duration of colds by only 8% in adults and 14% in children. This provides poor justification for everyday mega doses of the nutrient. Most adults catch only 1 common cold a year : taking supplements every day to avoid this makes little sense. Tthere is little doubt that vitamin C has some biological impact. : although in the main it is nothing like what Pauling predicted and has little place in therapy, it remains the possibility that a very high dose very early after the onset of cold symptoms could be shown in the future to have a useful effect on reducing the severity of illnessref 30-40 mmol/l scurvy (a.k.a. scorbuto in Italy) : fragile collagen, decreased Ca2+ absorptionref => 
    • hemorrhagic diathesis
    • stomatitis scorbutica ( gingivitis), ...)
    • cardiorespiratory sign : a change in the normal pulse-respiration ratio from 4:1 to 2:1; seen in infantile scurvy. 
    • cataract
    • scorbutic beads
    • scorbutic position : a pseudoparalytic position characteristic of advanced infantile scurvy, in which the infant lies quietly with the legs flexed at the knees and the hips flexed and externally rotated.
    • Trümmerfeld line : a zone of metaphyseal degeneration sometimes seen in the bones in infantile scurvy
    choline / trimethylethanolamine (no longer considered a  vitamin !) (CH3)3N+CH2CH2OH
    myo-inositol / B (no longer considered a  vitamin !) inositol (hexahydroxycyclohexane) is an isomer of glucose with 7 optically inactive and 2 optically active stereoisomers, of which only one, the optically inactive myo-inositol, is nutritionally active.
    P (for permeability) or citrus factor 
    bioflavonoids (Szent-Györgyi)
    oligomeric proantocyanidin (OPC) 
    => calchones (reducing agents that protect vitamin C and epinephrine from oxidation)
    T coagulation deficits
    U allantoine (?), methylmethionine sulfochloride ulcers
  • lipophilic or terpenic vitamins : they are absorbed thanks to biliary acids and transported in bloodstream thanks to carrier proteins. They can undergo accumulation, so hypervitaminosis syndromes can occur.
  • chemical formula, important chemical groups and modifications by human enzymes 
    derived coenzymes and their role(s)
    dietary reference intake (DRI)
    hypovitaminosis / vitanition 
    symptoms / signs
    hypervitaminosis symptoms / signs
    recommended dietary allowance (RDA)
    adequate intake (AI)
    estimated average requirement (EAR)
    tolerable upper intake level (UL)
    A complex vitamin A1 / axerophthol / all-trans retinol (prosthetic group) : opsins b-caroten / provitamin A => all-trans-retinol bound to retinol-binding proteins : 
    • intracellular
    • interstitial
      • RBP3 (interphotoreceptor matrix of the retina,  transporting retinoids between the retinal pigment epithelium and the photoreceptors)
      • RBP4 (plasma : delivers retinol from the liver stores to the peripheral tissues. In plasma, the RBP-retinol complex interacts with transthyretin which prevents its loss by filtration through the kidney glomeruli)
    STRA6 is a receptor for retinol-binding protein (RBP)ref

    <=> all-trans-retinal

    international unit of vitamin A : an older unit of vitamin A activity, equal to the activity of 0.3 mg retinol or 0.6 mg b-carotene; because the provitamin A carotenoids are absorbed less efficiently than is retinol, the source must be specified. When the source is retinol, the unit is officially vitamin A unit : the specific biological activity of 0.3 mg of the all-trans isomer of retinol. Now it has been  largely supplanted by retinol equivalent (RE) (the specific biological activity of 1.0 mg of all-trans retinol, 6.0 mg of b-carotene, or 12.0 mg of other provitamin A carotenoids; it is equivalent to 3.3 international units of vitamin A activity from retinol (10 from b-carotene)), the unit is still used in labeling 

    carotenoid normal plasma concentration : 0.8-4.0 mg/mL; vitamin A : 0.15-0.6 mg/mL

    squamous metaplasia of epithelia, Bitot's spots, => corneal xerosis => keratomalacia, xerosis, xerophthalmia => night blindness / nyctalopia (ophtalmia Brasiliana), hypopigmentation of retinal pigment epithelium, keratitis punctata
    Friderichsen's test : determination of the weakest light stimulus which will give rise to an oculomotor reflex. A variation from normal indicates vitamin A deficiency 
    dark-adaptation test : a test based on the fact that with a deficient intake of vitamin A the ability to see a dimly illuminated object in a dark room is diminished.

    A large, randomized controlled trial showed that in association with zinc and vitamin E it reduces the progression of age-related macular degeneration.

    Massive studies in a number of developing nations proved that vitamin A deficiency is prevalent and associated with increased risks of mortality in young children. Prospective trials showed that 100,000 to 200,000 IU of vitamin A twice a year can reduce the overall death rate significantly.

    autolysis, dizziness, alopecia, skin desquamation, metaplasias

    2 large controlled trials of b-carotene for prevention of cancer or retinal diseases found increased rates of lung cancer in those randomized to the supplement. 

    vitamin A2 / 3,4-didehydroretinol
    vitamin A3
    D complex (see Vitamin D Home Page at University of California, Riverside) vitamin D1 / calciferol mix of ergosterol and other steroids (e.g. lumisterol, ...) hypovitaminosis 1a,25-(OH)2-vitamin D3 hypervitaminosis 1a,25-(OH)2-vitamin D3
    vitamin D2 / 9,10-seco(5Z,7E)-5,7,10(19), 22-ergostatetraene-3b-ol / ergocalciferol / viosterol (for (ultra)vio(let ergo)sterol) (Drisdol®) arise from UVB-induced photolysis of 9,10 bond in ergosterol (yeast steroid) and 180° rotation of 6,7 bond added to milk and some cereals, but 71% of milk samples don't contain the vitamin quantity described on the label and 15% of decreamed milk don't contain any dosable amount
    vitamin D3 / previtamin D3 / cholecalciferol / 9,10-seco(5Z,7E)-5,7,10(19)cholestatriene-3b-ol previtamin D3 comes from : 
    • dietary intake : herring, salmon, sardines, and fatty fish liver oils > eggs, veal, beef, butter, and vegetable oils >> plants, fruits, and nuts ; artificial fortification of foods such as milk (both fresh and evaporated : one cup of fortified milk contains about half of the estimated adult daily need.), margarine and butter, cereals, and chocolate 
    • photobiogenesis : UVB-induced photoconversion (photolysis) of the 9,10 bond in ring B of the endogenous metabolite 7-dehydrocholesterol (7-DHC) / provitamin D3 and 180° rotation of the 6,7 bond in keratinocytes occurs for many hours after a single exposure. When Sun zenith angle increases (during Winter in Northern hemisphere) most UVB photons are absorbed by O3 in ozonosphere. If the entire BSA is exposed to sunlight untile erythema, it equates with oral assumption of 10,000-25,000 UI. The daily dose can be achieved by soaking up bright sunshine on the face and hands for 15', 3 times a week - weather permitting. Epidermal melanins compete with 7-DHC for UVB photons. Photochemical isomerization of previtamin D3 and vitamin D3 in biologically inert compounds seems to be the most important mechanism to prevent excessive accumulation during long-lasting sunlight exposure
    Then previtamin D3 can :  1a,25-(OH)2-vitamin D3 is converted to 1a,24,25-(OH)3-vitamin D3 which is less active. 
    1.0 IU of vitamin D3 = 1.0 IU of  1,25-(OH)2-vitamin D3 / calcitriol = 0.025 mg =  65.0 pM 

    RDA = 

    • 200 IU/day (5 mg/day) before age 50
    • 400 IU/day (10 mg/day) after age 51
    • 600 IU/day (15 mg/day)  for people with inadequate sunlight exposure
    vitamin D4 / 22,24-dihydrovitamin D3
    vitamin D5 precursor for the drug 1a-OH-D5
    vitamin E / tocopherols
    RRR-a-tocopherol / d-a-tocopherol / E307 (allrac-a-tocopherol / d,l-a-tocopherol), a-tocopheryl acetate or succinate (Aquasol E®, Ephynal®,  ...): methyl groups at C-5 and C-7 
    b-tocopherol : methyl group at C-5 
    g-tocopherol / E308 : methyl group at C-7 
    d-tocopherol / E309 : no methyl group at C-5 and C-7
    antioxidant (a-form is the most active; even for progesterone) international unit of vitamin E : the specific biological activity of 0.671 mg of d-a-tocopherol or 1.0 mg of dl-a-tocopherol acetate 
    alpha-tocopherol equivalent : the specific biological activity of 1.0 mg of d-a-tocopherol 

    found naturally in vegetable oils, leafy vegetables, and nuts 

    RDA : 10-20 mg (or 15-30 IU) ; guard limit is 1,000 IU/day

    PUFA peroxidation, sterility in both genders, macular degeneration (a large, randomized controlled trial showed that in association with vitamin A and zinc reduces the progression of age-related macular degeneration);  daily doses of 150 IU or less have no adverse effects, and might even offer health benefits. Risk of death starts to increase above this level, and becomes significant for individuals taking daily doses of 400 IU, the amount of vitamin E in common off-the-shelf supplements, are 10% more likely to die than they would have been if they had not taken the supplement at allref
    vitamin F / essential fatty acids (EFA) linoleic acid
    linolenic acid
    phenobarbital-induced hypoprothrombinemia, hemorrhages (conjunctiva, retina,  ...), hyphema
    vitamin K (for koagulation) complex / naphthoquinones vitamin K1 / phylloquinone / phytonadione / 2-methyl-3-phytyl-1,4-naphthoquinone (component of photosystem I in plants) (Aquamephyton®, Konakion®, Mephyton®) cofactor for g-glutamyl carboxylase Ansbacher unit : a unit of vitamin K dosage. 
    vitamin K2 / menaquinones (2-13 prenyl units replacing the phytyl side chain of phylloquinone) 
    • farnoquinone
    • ...
    (in animal and symbiont intestinal bacterial flora, killed by antimicrobial treatments)
    vitamin K3 / menadione / 2-methyl-1,4-naphthoquinone (synthetic, precursor for endogenous synthesis of menaquinone-4)
    vitamin K4 / acetomenadione
    vitamin K5 / 4-amino-2-methyl-1-naphtol

    ubiquinone / CoQ  (usually n = 10) 
    cosubstrate quinone <=> semiquinone <=> semiquinol
    lipoic acid / internal disulfur of 6,8-dithiooctanoic acid biotin-like structure with sulfur replacing the imidazole ring lipoyl-Lys / lipoamide (prosthetic group) : transport of acyl groups and electrons
    adenosine triphosphate (ATP4-)  (cosubstrate) : transport of PO32- (as creatine phosphate or arginine phosphate) and potential (chemical) energy RBCs =crenation => echinocytes
    S-adenosylmethionine (S-AdoMet (SAM)) (cosubstrate) : transport of CH3 moieties
    3-phosphoadenosine-5'-phosphosulfate (PAPS4-) (cosubstrate) : transport of SO32-
    ferroprotoporphyrins porphyrine / tetrapyrrole (4n+2 = 18 e-p) : 
    protoporphyrin IX / protoheme IX or other protoporphyrin + Fe2+ =protoheme lyase / ferrochelatase=> ferroprotoporphyrin IX / heme ... : 
    • chlorocruoroheme (globin : Hb and Mb)
    • heme a (cytochrome a in cytochrome c oxidase)
    • heme b (cytochrome b, catalse, globins, guanylate cyclase, peroxidase)
    • heme c (cytochrome c) : the only one covalently bound
    • heme d (catalase)
    • heme d1
    • heme o
    • heme P460
    • siroheme
    ... or other ferroprotoporphyrin
    prosthetic group in hemoproteins (hemoglobin, myoglobin, cytochromes, catalase, peroxidases, leghemoglobin)  : carries O2, CN-, CO 
    • in globins Fe2+ is oxidized to Fe3+ only in methemoglobin and metamyoglobin
    • in cytochromes iron cycles from Fe2+ <=> Fe3+ and they can accept only 1 e- per time
    dithiotreitol (DTT) / Cleland's reagent disulfide reducers
    biliary acids
    F420 in methanogens
    glutathione Glu-g-Cys-Gly
    tryptophanyl-tryptophan quinone (TTQ)
    reduced flavin
    pyrroloquinolin quinone (PQQ) first discovered in bacteria;  in mice a PQQ-dependent dehydrogenase enzyme is crucial for the degradation of the amino acid Lysref. However, this claim was dependent on a sequence analysis using databases that inappropriately label b-propeller sequences as PQQ-binding motifs. What the evidence actually suggests is that the enzyme is an interesting novel protein that has a 7-bladed b-propeller structure, but there is nothing to indicate that it is a PQQ-dependent dehydrogenaseref. The activity of a-aminoadipic acid-a-semialdehyde (AAS) dehydrogenase in liver and plasma levels of d-aminoadipic acid (AAA), both of which act as indicators of lysine degradation in mammals, are not affected by changes in PQQ dietary statusref. Whether or not PQQ provides nutritional benefit for humans has yet to be determined. The dietary requirements of PQQ may vary between species in the same way as ascorbic acid (vitamin C), which is essential for humans but not miceref
    multivitamin integrators :  COFACTORS
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