Coenzymes & Vitamins
Most coenzymes are derived from vitamins. Memorizing the vitamin-coenzyme-enzyme-deficiency connections lets you reason about a lot of MCAT biochemistry at once.
Water-Soluble Vitamins (B Complex and C)
| Vitamin | Coenzyme / Role | Key enzymes | Deficiency |
|---|---|---|---|
| B1 (Thiamine) | TPP | PDH, α-KG dehydrogenase, branched-chain KG dehydrogenase, transketolase | Beriberi, Wernicke-Korsakoff |
| B2 (Riboflavin) | FAD, FMN | Succinate dehydrogenase, acyl-CoA dehydrogenase, many oxidases | Cheilosis, corneal vascularization |
| B3 (Niacin) | NAD+, NADP+ | All dehydrogenases using NAD+/NADP+ | Pellagra: 3 D’s (dermatitis, diarrhea, dementia) |
| B5 (Pantothenate) | CoA, ACP | Fatty acid synthesis, TCA, fatty acid oxidation | Rare, paresthesias |
| B6 (Pyridoxine) | PLP (pyridoxal phosphate) | Transaminases, decarboxylases, glycogen phosphorylase | Sideroblastic anemia, peripheral neuropathy |
| B7 (Biotin) | Biotin cofactor | Carboxylases: pyruvate carb., ACC, propionyl-CoA carb. | Rare; egg whites (avidin) can cause it |
| B9 (Folate) | THF (tetrahydrofolate) | 1-carbon transfers, thymidine synthesis | Megaloblastic anemia, NTDs in pregnancy |
| B12 (Cobalamin) | Methylcobalamin, adenosylcobalamin | Methionine synthase, methylmalonyl-CoA mutase | Pernicious anemia, neurological deficits |
| C (Ascorbate) | Cofactor for hydroxylases | Prolyl/lysyl hydroxylase (collagen), dopamine beta-hydroxylase | Scurvy |
Fat-Soluble Vitamins (ADEK)
| Vitamin | Role | Deficiency |
|---|---|---|
| A (Retinol) | Vision (as retinal), growth, immunity | Night blindness, xerophthalmia |
| D (Cholecalciferol) | Ca2+ absorption, bone mineralization | Rickets (kids), osteomalacia (adults) |
| E (Tocopherol) | Membrane antioxidant | Hemolytic anemia (rare) |
| K (Phylloquinone) | Gamma-carboxylation of clotting factors II, VII, IX, X | Bleeding; newborns given K at birth |
B12 and Folate
Both are needed for DNA synthesis, and deficiency of either causes megaloblastic anemia. But B12 deficiency additionally causes neurological problems (peripheral neuropathy, subacute combined degeneration) because it is needed for methylmalonyl-CoA mutase in nerve myelin synthesis. Folate replacement alone can mask B12 deficiency and allow the neurological damage to progress - hence the caution about folate supplementation without B12 checking.
Which vitamin is the coenzyme for transaminases and glycogen phosphorylase?
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Vitamin B6 (pyridoxine), as pyridoxal phosphate (PLP). PLP is required by all aminotransferases (ALT, AST, etc.) and by glycogen phosphorylase. B6 deficiency impairs both amino acid metabolism and glycogen breakdown, with clinical features including sideroblastic anemia and peripheral neuropathy.
Why should thiamine (B1) be given before glucose in a chronic alcoholic presenting with altered mental status?
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Thiamine is the cofactor for PDH and α-KG dehydrogenase. Alcoholics are often thiamine-deficient. Glucose loads drive glycolysis and produce more pyruvate that requires PDH to proceed. Without thiamine, pyruvate cannot be oxidized, lactic acid accumulates, and Wernicke encephalopathy is precipitated (confusion, ataxia, ophthalmoplegia). Giving thiamine first prevents this catastrophe.
Why does B12 deficiency cause both megaloblastic anemia and neurological symptoms, while folate deficiency causes only anemia?
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Both B12 and folate are needed for DNA synthesis (thymidine synthesis in particular), and deficiency of either causes megaloblastic anemia. But B12 is additionally required for methylmalonyl-CoA mutase (important for myelin integrity). B12 deficiency causes demyelination (peripheral neuropathy, subacute combined degeneration of the spinal cord). Folate alone does not have this neurological role.