A comparative study on effect of dietary selenium and vitamin E on some antioxidant enzyme activities of liver and brain tissues

TURAN B., Acan N., Ulusu N., Tezcan E.

Biological Trace Element Research, vol.81, no.2, pp.141-152, 2001 (Peer-Reviewed Journal) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 81 Issue: 2
  • Publication Date: 2001
  • Doi Number: 10.1385/bter:81:2:141
  • Journal Name: Biological Trace Element Research
  • Journal Indexes: Science Citation Index Expanded, Scopus
  • Page Numbers: pp.141-152
  • Keywords: sodium selenite, selenium deficiency, vitamin E, selenium toxicity, glutathione reductase, glutathione peroxidase, EXPERIMENTAL ATHEROSCLEROSIS, GLUTATHIONE-REDUCTASE, RABBIT-TISSUES, E-DEFICIENT, RAT, TOXICITY, DYSFUNCTION, ENDOTOXIN, DISEASE, LAMBS


Since selenium and vitamin E have been increasingly recognized as an essential element in biology and medicine, current research activities in the field of human medicine and nutrition are devoted to the possibilities of using these antioxidants for the prevention or treatment of many diseases. The present study was aimed at investigating and comparing the effects of dietary antioxidants on glutathione reductase and glutathione peroxidase activities as well as free and protein-bound sulfhydryl contents of rat liver and brain tissues. For 12-14 wk, both sex of weanling rats were fed a standardized selenium-deficient and vitamin E-deficient diet, a selenium-excess diet, or a control diet. It is observed that glutathione reductase and glutathione peroxidase activities of both tissues of the rats fed with a selenium-deficient or excess diet were significantly lower than the values of the control group. It is also shown that free and bound sulfhydryl concentrations of these tissues of both experimental groups were significantly lower than the control group. The percentage of glutathione reductase and glutathione peroxidase activities of the deficient group with respect to the control were 50% and 47% in liver and 66% and 61% in the brain, respectively; while these values in excess group were 51% and 69% in liver and 55% and 80% in brain, respectively. Free sulfhydryl contents of the tissues in both experimental groups showed a parallel decrease. Furthermore, the decrease in protein-bound sulfhydryl values of brain tissues were more pronounced than the values found for liver. It seems that not only liver but also the brain is an important target organ to the alteration in antioxidant system through either a deficiency of both selenium and vitamin E or an excess of selenium alone in the diet.