EFFECT OF SELENIUM AND VITAMIN-E SUPPLEMENTS ON TISSUE-LIPIDS, PEROXIDES, AND FATTY-ACID DISTRIBUTION IN EXPERIMENTAL DIABETES

The protective role of selenium (Se), given as a Se-rich yeast, seleno methionine or selenomethionine + vitamin E supplement, toward changes in lipid, peroxide, and fatty acid distribution in tissues of streptoz otocin-induced diabetic rats, was investigated, after 24 wk of disease . Diabetes increased liver thiobarbituric acid-reactive substances and conjugated dienes; Se supplement completely corrected these changes. In kidney, as in heart, the peroxide levels were not significantly cha nged by diabetes. In diabetic rat liver, a significant drop in triglyc erides and phospholipids (P < 0.05) was observed; this was modulated b y Se + vitamin E supplementation. Se + vitamin E supplementation also inhibited the decrease in 18:2n-6 and the increase in 22:6n-3 observed in liver of diabetic rats, changes which reflect altered glycemic con trol. In kidney, heart, and aorta, diabetes produced some changes in l ipid content and fatty acid distribution, especially an increase in he art triglycerides which was also corrected by the Se supplement. Se su pplementation to diabetic rats also increased 18:0 ether-linked alcoho l, 20:4 n-6, and 22:5 n-3 in cardiac lipids. In aorta, Se + vitamin E significantly increased 20:5 n-3. These polyunsaturated fatty acids ar e precursors, in situ, of prostaglandin l(2) (PGl(2)) and PGl(3) which may protect against cardiovascular dysfunction. In kidney, conversely , Se decreased 20:4 n-6, the precursor of thromboxane A(2) Implicated in diabetic glomerular injury. Thus Se, and more efficiently Se + Vita min E supplementation, in experimental diabetes could play a role in c ontrolling oxidative status and altered lipid metabolism in liver, the reby maintaining favorable fatty acid distribution in the major tissue s affected by diabetic complications.