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N ‐acetyl‐cysteine protects chicken growth plate chondrocytes from T‐2 toxin‐induced oxidative stress
Author(s) -
He Shaojun,
Hou Jiafa,
Dai Yuyi,
Zhou Zhenlei,
Deng Yifeng
Publication year - 2012
Publication title -
journal of applied toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.784
H-Index - 87
eISSN - 1099-1263
pISSN - 0260-437X
DOI - 10.1002/jat.1697
Subject(s) - toxin , oxidative stress , glutathione , reactive oxygen species , alkaline phosphatase , cytotoxicity , malondialdehyde , chemistry , viability assay , toxicity , antioxidant , biochemistry , in vitro , pharmacology , microbiology and biotechnology , biology , enzyme , organic chemistry
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.