Energy Releasing Vitamins MCQs

Ans. is 'c' i.e.,PLP [Ref Guyton 12thie p. 854]

Option A: NADPH is never used to produce ATP in oxidative phosphorylation, instead it is used for reductive biosynthesis of many compounds. Option B: The oxidation of one molecule FADH2 in oxidative phosphorylation produces 1.5 ATPs. Option C: The oxidation of one molecule NADH in oxidative phosphorylation produces 2.5 ATPs. Option D: It was believed that the oxidation of one molecule NADH in oxidative phosphorylation produces 3 ATPs earlier, but recently it is corrected to 2.5. Reference: Harper's illustrated biochemistry 32nd edition CH 11 PN 108

Many steps in fatty acid synthesis, cholesterol synthesis and steroid hormone required NADPH. NADPH helps in the reductive biosynthesis of fatty acids, Cholesterol and steroid hormones. Reference: Harper's illustrated biochemistry 32 nd edition, page 269

Ans. is 'a' i.e., NADP [Rep Harper 29t5/e p. 201-204] Gulonate dehydrogenase is an enzyme in glucuronic acid pathway (uronic acid pathway) that requires NADP'.

The PDH Complex contains five coenzymes that act as carriers or oxidants for the intermediates of the reactions. E1 requires thiamine pyrophosphate (TPP), E2 requires lipoic acid and CoA, and E3 requires FAD and NAD+. [Note: TPP, lipoic acid, and FAD are tightly bound to the enzymes and function as coenzymes–prosthetic groups][Note: Lipoic acid linked to a lysine residue in E2 functions as a “swinging arm” that allows interaction with E1 and E3.] The PDHC catalyzes an irreversible reaction that is inhibited when the decarboxylase component (E1) is phosphorylated. The PDHC is located in the mitochondrial matrix. Biotin is utilized by carboxylases, not decarboxylases. Reference: Lippincott SAE, page no. 207-208 Reference: Harper's 32 nd edition, chapter - 17

Option B: The main clinical manifestation of pyridoxine-dependent epilepsy is generalized seizures, which usually occur in the first days of life and are unresponsive to conventional anticonvulsant therapies. Some mothers of affected fetuses report abnormal intrauterine fluttering movements. The seizures are usually tonic-clonic in nature but can be almost any type. Other manifestations such as dystonia, respiratory distress, and abdominal distention with vomiting, hepatomegaly, hypoglycemia and hypothermia may be present. Learning problems and speech delay are common sequelae. Late-onset forms of the condition (as late as 5 years of age) have been reported. Consequently, a trial with vitamin B6 is recommended in any infant with intractable convulsions Option A, Option C & Option D: Thiamine, Riboflavin & Pantothenic acid deficiency not reported to cause neonatal seizures.

Ans. is 'b' i.e.,Oxidative decarboxylation [Ref Harper 29th/e p. 534] * Active form (coenzyme form) of thiamine is thiamine pyrophosphate (TPP), also called thiamine diphosphate (TDP). * TPP acts as coenzyme for - Oxidative decarboxylation:- Pyruvate dehydrogenase, a- ketoglutarate dehydrogenase, brached-chain keto acid dehydrogenase. - Transketolase in PPP.

Ans. is 'c' i.e., 0.03 mg/kg [Ref. Park 22"d/e p. 572] Vitamin A→ 600 mcg retinol Vitamin B7 (Thiamine)--> 0.5 mg per 1000 Kcal of energy intake Vitamin B, (Riboflavin) → 0.6 mg per 1000 Kcal of energy intake Vitamin B, (Niacin) → 6.0 mg per 1000 Kcal of energy intake Vitamin 135 (Pantothenic Acid) → 10 mg Vitamin B6 (Pyridoxine) →2 mg Vitamin B, (Folic Acid) →200 mcg Vitamin B12(Cobalamin) →1 mcg Vitamin D 100 IU (2.5 mcg calciferol) Vitamin E (Tocopherol) ⇒ → 0.8 mg per gm of essential fatty acids Vitamin K → 0.03 mg per kg