HNF 462Final Exam Study GuideExam 4 Material1. What’s the disease caused by vitamin C deficiency?a. Scurvy: hemorrhagic signs, hyperkeratosis of hair follicles, hypochondriasis, and hematologic abnormalities2. What are the reduced and oxidized forms of vitamin C?a. Reduced form: Ascorbic acid (AA)b. Oxidized form: Dehydroascorbic acid (DHAA)3. How stable is vitamin C? What is it sensitive to?a. Not very stableb. Sensitive to heat, light, and oxygenc. Can be destroyed by long storage or cooking4. Do all mammals need vitamin C from diet?a. Not all mammals need vitamin C from dietb. Only human and all other higher species are unable to self-synthesize vitamin C5. What do most animals use to synthesize vitamin C?a. Most animals use gulonolactone oxidase to synthesize vitamin C6. What Na-dependent transporter is responsible for AA absorption?a. AA is absorbed by SVCT1 and SVCT2 Na-dependent transporters7. Why are vitamin C deficient patients often iron deficient?a. AA enhances the intestinal absorption of nonheme iron, so a deficiency in vitamin C will decrease the absorption of iron8. Which form of vitamin C is found in blood?a. AA is found in blood9. How are AA and DHAA absorbed by cells? What transporters do they use?a. AA: absorbed into cells by Na-dependent SVCT1 and 2 transportersb. DHAA: absorbed into cells by GLUT1, 3, and 4 transporters10. AA transport into cells can happen against AA gradient. Why?a. AA is transported by a Na-dependent transporterb. AA can be transported into cells against the gradient due to the Na/K active transport pump11. Know the synthetic reactions vitamin C participates in and the mechanism of vitamin C function in these reactions.a. Collagen Synthesis: hydroxylation reactions require vitamin Ci. Vitamin C converts oxidized iron to its reduced stateii. Hydroxylation forms hydrogen bonds between collagen strandsb. Carnitine Synthesis (Carnitine transports long-chain fatty acids into mitochondria)i. Last step is a hydroxylation reaction that requires vitamin C, which maintains the iron in a reduced statec. Tyrosine Synthesis and Catabolismi. Last step requires vitamin C to convert oxidized copper and iron atoms to their reduced statesd. Neurotransmitter Synthesisi. AA acts as a reducing agent in a hydroxylase reaction12. Why does scurvy have hemorrhagic symptoms?a. Collagen synthesis is disturbed, which causes hemorrhagic symptoms13. How is vitamin C excreted?a. Vitamin C is absorbed by the kidney until the kidney is completely saturated, then excess is excreted via urine14. Can vitamin C concentration in blood increase indefinitely in response to increased intake? Why?a. No, excess vitamin C will be digested by intestinal florab. High doses of vitamin C can cause diarrhea 15. High vitamin C supplementation may increase the risk of kidney stones. Why?a. Oxidized form of vitamin C (oxalic acid) is not soluble in water and can cause kidney stones. High intakes of vitamin C can cause oxalic build up, and therefore, kidney stones16. What are free radicals?a. A molecule with an unpaired electronb. Vitamin C acts as an antioxidant by reducing free radicals by donating electrons to them17. How does vitamin C decrease the risk of plaque formation and CVD?a. Prevents LDL oxidation, so macrophages absorb LDL less efficiently decreased risk of plaque formation and CVD18. Know the names of the B vitamins. a. B1 = Thiaminb. B2 = Riboflavinc. B3 = Niacind. B5 = Pantothenic Acid e. Biotinf. Folateg. B12h. B619. What is the disease caused by B1 deficiency?a. Beriberi (wet, dry, and acute forms)b. Loss of appetite, cardiovascular abnormalities, neurological symptoms20. Know the four enzymes discussed in class that require B1 and what kind of reaction is catalyzed by these enzymes.a. Pyruvate Dehydrogenase Complex (Pyruvate Decarboxylation)i. Pyruvate Acetyl CoAii. B1 temporarily holds acetyl group from pyruvate and then transfers it to the intermediate product lipoamideb. Alpha-Ketoglutarate Dehydrogenase Complexi. Alpha-KetoglutarateSuccinyl-CoAii. Similar mechanism to PDHc. Transketolase (key enzyme in PPP)i. B1 acts as coenzyme to transketolase for the generation of NADPHd. Branched-Chain Alpha-Keto Acid Dehydrogenase Complexi. Similar mechanism to pyruvate decarboxylatione. *Involved in decarboxylation reactions21. IS white rice or refined grain a good source of B1? How about brown rice? Why?a. White/refined grains are not good sources of B1b. Brown rice is a good source of B1 because the bran layer contains B122. Which form of B1 is absorbed? Phosphorylated or unphosphorylated? Which enzyme removes P?a. Unphosphorylated form of thiamin is absorbed23. What form of riboflavin is absorbed by enterocytes and liver cells?a. Free riboflavin is absorbed into peripheral cells24. What is riboflavin converted to once in the cells?a. Riboflavin is converted to FMN or FAD in the cells25. What’s the color of riboflavin?a. Fluorescent yellowb. Causes yellow color of urine26. What are the coenzyme forms of riboflavin? Are they both involved in ETC?a. FMN—involved in ETCi. Coenzyme for complex 1 in ETCb. FAD—involved in ETCi. FADH2 FAD in complex 2 in ETC27. The activity of which enzyme in RBCs is measured to assess riboflavin status? What is AC?a. Measurement of glutathione reductase activity to assess riboflavin statusb. AC = (Enzyme Activity + FAD) / (Enzyme Activity – FAD)i. Lower than 1.2: adequate statusii. Higher than 1.2: deficient status28. What is the disease caused by niacin deficiency? Why is it associated with corn or maize based diet?a. Pellagra: dermatitis, diarrhea, dementia, and deathb. Niacin is poorly absorbed when it is bound to a complex carbohydrate or a small peptide, which is how it is found in corn. Therefore, deficiency is common in corn-based diets29. What are the coenzyme forms of niacin?a. NADb. NADP30. What form of niacin is absorbed? Are NAD and NADP absorbed directly intact?a. Digestion required for absorption of nicotinic acid and nicotinamide b. NADP NAD nicotinamide31. Is niacin transported as nicotinamide or nicotinic acid? Which one is the direct precursor of NAD and NADP? Which form is used to treat hypercholesterolemia? Which form causes niacin flush?a. Primarily transported in the blood as nicotinamideb. Nicotinamide is the direct precursor of NAD and NADPc. Nicotinic acid is used to treat hypercholesterolemiad. Nicotinic acid causes niacin flush; nicotinamide does not have this effect32. What is niacin