College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, 210095, People's Republic of China.
J Appl Toxicol. 2012 Dec;32(12):980-5. doi: 10.1002/jat.1697. Epub 2011 Jul 28.
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.
T-2 毒素现在被认为与骨骼畸形有关，如不完全骨化、骨缺失和骨融合。在这项研究中，鸡胫骨生长板软骨细胞（GPC）的原代培养物在无和存在 N-乙酰半胱氨酸（NAC）的情况下用不同浓度的 T-2 毒素（5、50 和 500 nM）处理，以研究抗氧化剂 NAC 对 T-2 毒素诱导的毒性的影响。我们的结果表明，T-2 毒素显著降低细胞活力、碱性磷酸酶活性和谷胱甘肽含量（P<0.05）。此外，T-2 毒素以剂量依赖性方式显著增加活性氧水平和丙二醛。然而，抗氧化剂 NAC 部分逆转了 T-2 毒素诱导的细胞毒性（P<0.05）。这些结果表明，T-2 毒素通过改变细胞内稳态抑制 GPC 的增殖和分化，而 NAC 可以通过减少 T-2 毒素诱导的氧化应激来保护 GPC 免受 T-2 毒素的细胞毒性。
