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Protective effects of boron on cyclophosphamide induced lipid peroxidation and genotoxicity in rats

•B reduces cyclophosphamide (CYC) induced toxicity.•B inhibits lipid peroxidation and DNA damage in rats.•B regenerates CYC-induced histopathological changes in rat tissues.•B attenuates NO and restores SOD, CAT, and GSH in rats. The aim of the present study was to evaluate the possible protective e...

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Published in:Chemosphere (Oxford) 2014-08, Vol.108, p.197-204
Main Authors: Ince, Sinan, Kucukkurt, Ismail, Demirel, Hasan Huseyin, Acaroz, Damla Arslan, Akbel, Erten, Cigerci, Ibrahim Hakki
Format: Article
Language:English
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Summary:•B reduces cyclophosphamide (CYC) induced toxicity.•B inhibits lipid peroxidation and DNA damage in rats.•B regenerates CYC-induced histopathological changes in rat tissues.•B attenuates NO and restores SOD, CAT, and GSH in rats. The aim of the present study was to evaluate the possible protective effect of boron (B) on cyclophosphamide (CYC) induced oxidative stress in rats. Totally, thirty Wistar albino male rats were fed standard rodent diet and divided into 5 equal groups: physiological saline was given intraperitoneally (i.p.) to the control group (vehicle treated), to the second group only 75mgkg−1 CYC was given i.p. on the 14th d, and boron was administered (5, 10, and 20mgkg−1, i.p.) to the other groups for 14 d and CYC (75mgkg−1, i.p.) on the 14th d. CYC caused increase of malondialdehyde and decrease of glutathione levels, decrease of superoxide dismutase activities in erythrocyte and tissues, decrease of erythrocyte, heart, lung, and brain catalase, and plasma antioxidant activities. Also, CYC treatment caused to DNA damage in mononuclear leukocytes. Moreover, B exhibited protective action against the CYC-induced histopathological changes in tissues. However, treatment of B decreased severity of CYC-induced lipid peroxidation and genotoxicity on tissues. In conclusion, B has ameliorative effects against CYC-induced lipid peroxidation and genotoxicity by enhancing antioxidant defence mechanism in rat.
ISSN:0045-6535
1879-1298
DOI:10.1016/j.chemosphere.2014.01.038