Vitamin E Supplementation Decreases Basal Levels of F2-Isoprostanes and Prostaglandin F2α in Rats

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Abstract
Lipid peroxidation is thought to be an important factor in the pathophysiology of a number of diseases and in the process of aging. We investigated the effects of supplementation with vitamin E on lipid peroxidation in rats. Both free radical-induced nonenzymatic- and cyclooxygenase-catalyzed enzymatic lipid peroxidation were investigated by measuring the levels of F2-isoprostanes (8-iso-PGF2α) and PGF2α-metabolite (15-K-DH-PGF2α), respectively, in blood, urine and liver. Samples were collected from control rats (n = 6) and from rats supplemented with vitamin E in the diet for 3 wk (n = 8, 20 g/kg diet of dl-α-tocopherol hydrogen succinate). Plasma α-tocopherol concentration and antioxidative capacity were greater in the vitamin E-supplemented rats than in the control rats (17.9 ± 1.7 vs. 50.4 ± 10.4 μmol/L, P < 0.001 and 181 ± 6 vs. 275 ± 27 μmol/L trolox equivalents, P < 0.001). Urine 8-iso-PGF2α tended to be lower in the vitamin E-supplemented rats (0.72 ± 0.40 vs. 0.34 ± 0.19 nmol/mmol creatinine, P = 0.056). Urine 15-K-DH-PGF2α was lower due to vitamin E supplementation (0.97 ± 0.38 vs. 0.56 ± 0.21 nmol/mmol creatinine, P < 0.05), as was liver-free 8-iso-PGF2α concentration (0.47 ± 0.11 vs. 0.18 ± 0.04 nmol/g, P < 0.001). Supplementation with vitamin E did not affect plasma 8-iso-PGF2α or 15-K-DH-PGF2α concentrations, liver total 8-iso-PGF2α or plasma malondialdehyde levels. Thus, vitamin E supplementation reduced urine basal levels of biomarkers of both nonenzymatic and enzymatic lipid peroxidation. In liver, vitamin E reduced the basal level of free 8-iso-PGF2α but not total 8-iso-PGF2α.