Selenium deficiency-induced alterations in the vascular system of the rat

To enunciate the mechanisms whereby Se protects against cardiovascular dise ases, weanling male Wistar rats were fed deficient (0.022 mg/kg diet) and a dequate (0.159 mg/kg diet) Se diets for 14 and/or 39 wk. As the Se content and glutathione peroxidase activity were decreased and the Lipid peroxide l evel was increased, the plasma -keto-PGF(1 alpha) concentration of the Se-d eficient group was markedly decreased in blood and tissues of the Se-defici ent rats, as compared with the Se-adequate animals. Furthermore, the Se-def icient group had significantly lower plasma nitric oxide content and vascul ar nitric oxide synthase activity, higher erythrocyte sedimentation equatio n K value and aggregation index, and lower erythrocyte deformability than t he Se-adequate group. Experimental Se deficiency also resulted in significa nt increases in serum total cholesterol and low-density lipoprotein cholest erol levels and a significant decrease in serum high-density lipoprotein ch olesterol level. These results give some experimental supports to the hypot hesis that low Se status and Lipid peroxidation are involved in the etiolog y of cardiovascular diseases.