<i>N</i>‐acetyl‐cysteine protects chicken growth plate chondrocytes from T‐2 toxin‐induced oxidative stress

Journal of Applied Toxicology - Tập 32 Số 12 - Trang 980-985 - 2012
S He1, Jiafa Hou1,2,3, Yu‐yi Dai1, Zhenlei Zhou1, Yifeng Deng1
1College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095, People's Republic of China
2*Email: [email protected]
3Jia-fa Hou, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095, People's Republic of China.

Tóm tắt

ABSTRACT

T‐2 toxin is now considered to be related to bone malformation such as incomplete ossification, absence of bones and fused bones. In this study, primary cultures of chicken tibial growth plate chondrocytes (GPCs) were treated with various concentrations of T‐2 toxin (5, 50, and 500 n m) in the absence and presence of N‐acetyl‐cysteine (NAC) to investigate the effects of the antioxidant NAC on T‐2 toxin‐induced toxicity. Our results showed that T‐2 toxin markedly decreased cell viability, alkaline phosphatase activity and glutathione content (P < 0.05). In addition, T‐2 toxin significantly increased reactive oxygen species levels and malondialdehyde in a dose‐dependent manner. However, the T‐2 toxin‐induced cytotoxicity was reversed, in part, by the antioxidant NAC (P < 0.05). These results suggest that T‐2 toxin inhibits the proliferation and differentiation of GPCs in vitro by altering cellular homeostasis and NAC can protect GPCs against T‐2 toxin cytotoxicity by reducing the T‐2 toxin‐induced oxidative stress. Copyright © 2011 John Wiley & Sons, Ltd.

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Thông tin xuất bản

Journal of Applied Toxicology

Tập 32 Số 12

980-985

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