Evidence of oxidative damage and reproductive dysfunction accompanying 4-vinylcyclohexene diepoxide exposure in female Wistar rats

被引：13

作者：

Abolaji, Amos O. ^{[1
]}

Adedara, Isaac A. ^{[1
]}

Abajingin, Ayodeji O. ^{[1
]}

Fatunmibi, Ore J. ^{[1
]}

Ladipo, Emmanuel O. ^{[1
]}

Farombi, Ebenezer O. ^{[1
]}

机构：

[1] Univ Ibadan, Drug Metab & Mol Toxicol Res Labs, Dept Biochem, Fac Basic Med Sci,Coll Med, Ibadan, Nigeria

来源：

REPRODUCTIVE TOXICOLOGY | 2016年 / 66卷

关键词：

4-Vinylcyclohexene diepoxide; Oxidative damage; Endocrine disruption; Infertility; Apoptosis; Inflammation; GLUTATHIONE-S-TRANSFERASE; VCD-INDUCED OVOTOXICITY; 4-VINYL-1-CYCLOHEXENE DIEPOXIDE; OVARIAN; STRESS; APOPTOSIS; ACTIVATION; ENZYMES; INVOLVEMENT; EXPRESSION;

D O I：

10.1016/j.reprotox.2016.09.009

中图分类号：

Q [生物科学];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

4-Vinylcyclohexene diepoxide (VCD) is an occupational chemical widely reported to deplete ovarian follicles in rodents. Here, we investigated VCD-induced reproductive dysfunction in female Wistar rats. The rats were orally administered with VCD (100, 250 and 500 mg/kg) for twenty-eight days. Thereafter, we evaluated selected biomarkers of oxidative damage, inflammation, endocrine disruption, and apoptosis. We observed that VCD increased ovarian and uterine malondialdehyde (MDA) level, and catalase, glutathione peroxidase (GPx) and glutathione S-transferase (GST) activities in rats (p<0.05). Also, VCD induced hormonal imbalance, increased ovarian superoxide dismutase (SOD) activity, and depleted uterine SOD activity and ovarian glutathione (GSH) level in rats (p<0.05). Lastly, VCD markedly increase immunohistochemical expressions of ovarian cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), Caspase-9 and Caspase-3. Overall, VCD induced reproductive dysfunctions in rats via ovarian and uterine oxidative damage, hormonal imbalance, as well as inflammation and apoptosis in the ovary of rats. (C) 2016 Elsevier Inc. All rights reserved.

引用

页码：10 / 19

页数：10

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