The E vitamins consist of eight naturally occurring tocopherols, of which αtocopherol is the most active (Fig. 28.28). Vitamin E functions as an antioxidant in prevention of nonenzymic oxidations (for example, oxidation of LDL (see p.
232) and peroxidation of polyunsaturated FA by O2 and free radicals). [Note: Vitamin C regenerates active vitamin E.]
A. Distribution and requirements
Vegetable oils are rich sources of vitamin E, whereas liver and eggs contain moderate amounts. The RDA for α-tocopherol is 15 mg/day for adults. The vitamin E requirement increases as the intake of polyunsaturated FA increases to limit FA peroxidation.
B. Deficiency
Newborns have low reserves of vitamin E, but breast milk (and formulas) contain the vitamin. Very-low-birth-weight infants may be given supplements to prevent the hemolysis and retinopathy associated with vitamin E deficiency. When observed in adults, deficiency is usually associated with defective lipid absorption or transport. [Note: Abetalipoproteinemia, caused by a defect in the formation of chylomicrons (and VLDL), results in vitamin E deficiency (see p. 231).]
C. Clinical indications for vitamin E
Vitamin E is not recommended for the prevention of chronic disease, such as CVD or cancer. Clinical trials using vitamin E supplementation have been uniformly disappointing. For example, subjects in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study trial who received high doses of vitamin E not only lacked cardiovascular benefit but also had an increased incidence of stroke. [Note: Vitamins E and C are used to slow the progression of age-related macular degeneration.]
D. Toxicity
Vitamin E is the least toxic of the fat-soluble vitamins, and no toxicity has been observed at doses of 300 mg/day (UL = 1,000 mg/day).
Populations consuming diets high in fruits and vegetables show decreased incidence of some chronic diseases. However, clinical trials have failed to show a definitive benefit from supplements of folic acid; vitamins A, C, or E; or antioxidant combinations for the prevention of cancer or CVD.
XV. CHAPTER SUMMARY
The vitamins are summarized in Figure 28.29 on pp. 396–397.
Choose the ONE best answer.
For Questions 28.1–28.5, match the vitamin deficiency to the clinical consequence.
8.1. Bleeding 8.2. Diarrhea and dermatitis 8.3. Neural tube defects 8.4. Night blindness (nyctalopia) 8.5. Sore, spongy gums and loose teeth
Correct answers = H, B, A, C, E. Vitamin K is required for formation of the γcarboxyglutamate residues in several proteins required for blood clotting. Consequently, a deficiency of vitamin K results in a tendency to bleed. Niacin deficiency is characterized by the three Ds: diarrhea, dermatitis, and dementia (and death, a fourth D, if untreated). Folic acid deficiency can result in neural tube defects in the developing fetus. Night blindness is one of the first signs of vitamin A deficiency. Rod cells in the retina detect white and black images and work best in low light, for example, at night. Rhodopsin, the visual pigment of the rod cells, consists of 11-cis retinal bound to the protein opsin. Vitamin C is required for the hydroxylation of proline and lysine during collagen synthesis.
Severe vitamin C deficiency (scurvy) results in defective connective tissue, characterized by sore and spongy gums, loose teeth, capillary fragility, anemia, and fatigue.