B1 = Thiamine (IV), C = Ascorbic acid (I)
D = Calciferol (II), K = Phylloquinone (III)
Answer: A-IV, B-I, C-II, D-III
Vitamins are organic compounds required in small amounts for normal physiological function that cannot be synthesised by the body in sufficient quantities and must be obtained from the diet. The word "vitamin" was coined by Casimir Funk in 1912 (from "vital" + "amine," reflecting his initial belief that all vitamins were amines — a belief quickly disproved). Vitamins are classified into two broad groups based on their solubility: Fat-soluble vitamins (A, D, E, K): absorbed with dietary lipids via the lymphatic system, transported in the blood associated with lipoproteins, and stored in the liver and adipose tissue. Their storage in the body means that dietary intake does not need to be daily, but it also means that excessive intake (from supplements) can lead to accumulation to toxic levels (hypervitaminosis A causes liver damage; hypervitaminosis D causes hypercalcaemia and soft tissue calcification). Water-soluble vitamins (B complex and C): absorbed directly into the portal blood, distributed throughout the aqueous compartments of the body, and excess is readily excreted in urine. They generally cannot be stored in significant quantities, so regular dietary intake is more important. However, this also means that toxicity from excess dietary intake is rare (though pharmacological doses of niacin cause flushing and liver damage, and excess pyridoxine causes peripheral neuropathy).
The B vitamins are a group of structurally unrelated water-soluble compounds that share the common feature of functioning as coenzymes (or precursors to coenzymes) in metabolic reactions. Vitamin B1 (thiamine): contains a pyrimidine ring and a thiazole ring connected by a methylene bridge. As thiamine pyrophosphate (TPP), it functions as a coenzyme for decarboxylase enzymes: pyruvate decarboxylase (pyruvate → acetyl-CoA in aerobic metabolism and → acetaldehyde in fermentation), alpha-ketoglutarate dehydrogenase (TCA cycle), and transketolase (pentose phosphate pathway). Deficiency causes beri-beri: thiamine is not stored well, and diets high in polished rice (from which thiamine has been milled away) lead to deficiency. Neurological symptoms (Wernicke's encephalopathy, Korsakoff syndrome) occur in alcoholics who have poor diets and impaired thiamine absorption. Vitamin B2 (riboflavin): contains a ribose sugar attached to isoalloxazine ring. Functions as FAD (flavin adenine dinucleotide) and FMN (flavin mononucleotide) coenzymes in oxidoreductase reactions: the succinate dehydrogenase reaction (TCA cycle), fatty acid beta-oxidation, glutathione reductase (antioxidant defence). Riboflavin is bright yellow-green fluorescent — urine appears bright yellow when riboflavin supplements are taken (harmless). Vitamin B3 (niacin, nicotinic acid or nicotinamide): functions as NAD+ and NADP+ (nicotinamide adenine dinucleotide), the most important electron carriers in metabolism. Involved in >400 enzyme reactions. Deficiency causes pellagra. Can be synthesised from tryptophan (60 mg tryptophan → 1 mg niacin), so pellagra occurs in maize-dependent populations where tryptophan is limiting. Niacin at pharmacological doses (1-3 g/day) lowers LDL cholesterol and raises HDL cholesterol — used as a lipid-lowering drug.
Vitamin C (L-ascorbic acid) is a six-carbon lactone (cyclic ester) with an enediol structure that makes it a powerful reducing agent and antioxidant. The L-form (L-ascorbic acid) is biologically active; the D-form is not. L-Ascorbic acid is oxidised readily to dehydroascorbic acid (DHAA) by donating two electrons; this oxidation is reversible, making ascorbic acid an effective redox buffer in biological systems. Key biochemical functions: Collagen biosynthesis: ascorbic acid is an essential cofactor for prolyl hydroxylase and lysyl hydroxylase, the enzymes that hydroxylate specific proline and lysine residues in procollagen to 4-hydroxyproline and hydroxylysine respectively. These hydroxyl groups are required for: (a) stable hydrogen bonding in the collagen triple helix, (b) galactosylation of hydroxylysine (required for collagen-collagen crosslinking in the extracellular matrix). Without adequate Vitamin C, hydroxylation is impaired, the collagen triple helix is unstable, procollagen accumulates intracellularly and is degraded, and existing connective tissue structures weaken. This explains the manifestations of scurvy: bleeding gums (capillaries rupture due to weakened vessel walls), poor wound healing, joint and muscle pain (collagen-dependent structures weaken), corkscrew hairs (hair follicle collagen), and perifollicular haemorrhages. Antioxidant function: scavenges reactive oxygen species (ROS) including superoxide radical, hydroxyl radical, and peroxyl radicals; regenerates vitamin E from the tocopheroxyl radical. Iron absorption: reduces dietary non-heme iron from Fe3+ to Fe2+ in the intestinal lumen; Fe2+ is absorbed 2-3× more efficiently than Fe3+. Therefore, consuming Vitamin C with iron-containing foods or iron supplements significantly improves iron absorption. Immune function: concentrated in phagocytes (neutrophils, monocytes) where it enhances killing of pathogens; required for T-cell development and function.
Vitamin D is unique among vitamins in that it is not truly a dietary vitamin in the conventional sense — it can be synthesised in adequate quantities in the skin upon exposure to ultraviolet B (UVB) radiation (wavelength 290-315 nm) from sunlight. Vitamin D2 (ergocalciferol): found in plant foods, especially UV-irradiated yeast and fungi. Vitamin D3 (cholecalciferol): synthesised in human skin from 7-dehydrocholesterol upon UVB exposure; also found in fatty fish (salmon, mackerel, sardines), fish liver oils, egg yolks, and fortified foods. The conversion of 7-dehydrocholesterol to pre-vitamin D3 in the skin is a photochemical (not enzymatic) reaction driven by UVB. Pre-vitamin D3 undergoes thermal isomerisation to vitamin D3 over 2-3 days. Both D2 and D3 are biologically inactive prodrugs that must undergo sequential hydroxylation: 25-hydroxylation in the liver (by 25-hydroxylase, CYP2R1) to form 25-hydroxyvitamin D (calcidiol, the major circulating form, measured to assess vitamin D status); 1alpha-hydroxylation in the kidney (by 1alpha-hydroxylase, CYP27B1, tightly regulated by PTH and serum phosphate) to form 1,25-dihydroxyvitamin D3 (calcitriol, the biologically active hormone). Calcitriol functions as a steroid hormone: it binds the vitamin D receptor (VDR), a nuclear receptor, which then acts as a transcription factor regulating the expression of hundreds of genes. Classical functions: intestinal absorption of calcium and phosphate (upregulates TRPV6 calcium channels, calbindin, and PMCA); renal calcium reabsorption; bone mineralisation (together with PTH). Modern understanding of Vitamin D: VDR is expressed in virtually every tissue. Vitamin D has roles in immune function (upregulates antimicrobial peptides like cathelicidin, modulates T-cell responses), cell differentiation and proliferation, cardiovascular function, and muscle function.
Vitamin A (retinol and its derivatives) plays critical roles in vision, immune function, cell differentiation, and reproduction. Retinol is the alcohol form; retinal is the aldehyde; retinoic acid is the acid. Beta-carotene (in orange/yellow/red vegetables) is a precursor ("pro-vitamin A") cleaved by intestinal enzymes to yield retinal. Vision: 11-cis-retinal is the chromophore of rhodopsin (the visual pigment of rod photoreceptors), covalently attached to the protein opsin via a Schiff base. Absorption of a photon causes isomerisation of 11-cis-retinal to all-trans-retinal, triggering a conformational change in rhodopsin that activates the visual phototransduction cascade (involving G-protein transducin and phosphodiesterase), ultimately generating a nerve impulse. Night blindness (difficulty seeing in dim light) is the earliest sign of Vitamin A deficiency, resulting from inadequate rhodopsin synthesis. Severe deficiency causes xerophthalmia (corneal drying and ulceration, leading to blindness), one of the leading causes of preventable blindness in developing countries. Vitamin A (as all-trans-retinoic acid) is also used therapeutically in dermatology (tretinoin for acne and photoaging) and oncology (all-trans-retinoic acid causes differentiation and clinical remission in acute promyelocytic leukaemia). Vitamin E (tocopherols, primarily alpha-tocopherol): the major lipid-soluble antioxidant in cell membranes. Protects polyunsaturated fatty acids (PUFAs) in membrane phospholipids from lipid peroxidation by quenching peroxyl radicals (LOO•). The tocopheroxyl radical produced is reduced back to tocopherol by ascorbic acid (Vitamin C) or glutathione — demonstrating the cooperative antioxidant network. Deficiency causes haemolytic anaemia in premature infants (red blood cell membranes are damaged by oxidative stress), peripheral neuropathy, and ataxia in severe cases.
The relationship between vitamins, health, and disease has been one of the most extensively studied areas in nutritional science, generating both important medical advances and considerable controversy. Historically, the discovery and identification of vitamins in the first half of the 20th century explained previously mysterious deficiency diseases and provided simple cures: Lind's discovery that citrus fruit prevented scurvy (1747), Takaki's observation that beriberi was a dietary disease (1884), Eijkman's chicken model showing polished rice causes beriberi (1897), Hopkins' "accessory food factors" concept (1906), Funk's vitamin hypothesis (1912), and the chemical isolation and synthesis of individual vitamins from the 1920s-1940s represented a triumph of nutritional science. Modern supplementation and fortification: mandatory fortification of flour with thiamine, riboflavin, and niacin (to replace what's removed in milling), iodisation of salt, vitamin D fortification of milk, and folic acid fortification of grain products (to prevent neural tube defects) represent public health interventions of immense impact. Vitamin B9 (folic acid) supplementation before conception and in early pregnancy dramatically reduces the incidence of spina bifida and anencephaly (neural tube defects), one of the clearest examples of nutritional prevention of a birth defect. Controversial areas: whether megadoses of Vitamins C, D, or E provide health benefits beyond preventing deficiency has been extensively studied but remains controversial. High-dose beta-carotene supplementation in smokers was found in the ATBC and CARET trials (1994-1996) to INCREASE (not decrease) lung cancer risk — a sobering reminder that physiological dosing and pharmacological dosing have completely different biological effects, and that food contains not just isolated vitamins but complex mixtures of bioactive compounds that act synergistically.