Influence of kolaviron and vitamin E on ethylene glycol monoethyl ether-induced haematotoxicity and renal apoptosis in rats

被引:17
作者
Adedara, Isaac A. [1 ]
Farombi, Ebenezer O. [1 ]
机构
[1] Univ Ibadan, Coll Med, Dept Biochem, Drug Metab & Toxicol Res Labs, Ibadan, Nigeria
关键词
ethylene glycol monoethyl ether (EGEE); nephrotoxicity; oxidative stress; apoptosis; rat; GARCINIA-KOLA SEEDS; GERM-CELL APOPTOSIS; LIPID-PEROXIDATION; OXIDATIVE STRESS; PROTECTIVE ROLE; DAMAGE; ANTIOXIDANT; LIVER; GLUTATHIONE; MECHANISMS;
D O I
10.1002/cbf.2968
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The present study investigated the protective effects of kolaviron, a biflavonoid from the seed of Garcinia kola, and vitamin E on ethylene glycol monoethyl ether (EGEE)-induced haematotoxicity and renal apoptosis in male rats. EGEE was administered at a dose of 200mgkg-1 alone or simultaneously administered with kolaviron (100 and 200mgkg-1) and vitamin E (50mgkg-1) for 14days. Results of haematological examination showed that white blood cells, platelets, neutrophils and mean corpuscular haemoglobin concentration were significantly lower, whereas lymphocytes were increased in EGEE-exposed rats compared with those in the control. Administration of EGEE caused a significant decrease in the superoxide dismutase and catalase activities as well as in the glutathione level but significantly increased glutathione Stransferase activity and levels of hydrogen peroxide and lipid peroxidation in kidneys of rats compared with those in the control. Also, EGEE-treated rats showed significant elevation in the serum urea and creatinine with marked increase in the frequency of terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling assay-positive apoptotic cells in the tubular epithelial cells in comparison with the control. Co-administration with kolaviron or vitamin E exhibited chemoprotective effects against EGEE-mediated haematotoxicity, augmented renal antioxidant status and prevented the induction of renal apoptosis. Copyright (c) 2013 John Wiley & Sons, Ltd.
引用
收藏
页码:31 / 38
页数:8
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