Effects of some probable antioxidants on selenite-induced cataract formation and oxidative stress-related parameters in rats


Orhan H., Marol S., Hepsen I., Sahin G.

TOXICOLOGY, cilt.139, sa.3, ss.219-232, 1999 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 139 Sayı: 3
  • Basım Tarihi: 1999
  • Doi Numarası: 10.1016/s0300-483x(99)00128-6
  • Dergi Adı: TOXICOLOGY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.219-232
  • İnönü Üniversitesi Adresli: Hayır

Özet

The effect of several natural and synthetic compounds on selenite-induced cataract was investigated in rat pups. Simultaneous determination of glutathione S-transferase (GST), selenium dependent glutathione peroxidase (Se-GPx), catalase (CAT), superoxide dismutase (SOD) activities and malondialdehyde (MDA) levels were carried out in the lens, erythrocyte and plasma. The results showed that propolis, diclofenac, vitamin C (Vit-C) and quercetin prevented cataract formation to the extent of 70, 60, 58.4, and 40%, respectively. Standardized extract of Ginkgo biloba (Egb 761) did not affect the cataract formation. Selenite treatment caused a significant decrease in the activity of erythrocyte SOD. This was accompanied by a simultaneous increase in the levels of MDA either in lens and in plasma. A significant increase was shown in erythrocyte GST (substrate ethacrynic acid; eaa), and GPx activities and lens GST (substrate chlorodinitro benzene; cdnb) activity. Antioxidant treatment caused significant changes in enzyme activities and MDA levels. There was no effect of selenite and antioxidants on total body weight increase during the course of the study. Blood parameters did not correlate to lens parameters following selenite treatment. Our results suggest that antioxidant supplementation following selenite exposure may prevent the cataract formation and may enhance antioxidant defence of blood and lens. (C) 1999 Elsevier Science Ireland Ltd. All rights reserved.