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N-acetylcysteine protects against cadmium-induced oxidative stress in rat hepatocytes
Jicang Wang,Huali Zhu,Xue-Zhong Liu,Zong-Ping Liu 대한수의학회 2014 Journal of Veterinary Science Vol.15 No.4
Cadmium (Cd) is a well-known hepatotoxic environmentalpollutant. We used rat hepatocytes as a model to studyoxidative damage induced by Cd, effects on the antioxidantsystems, and the role of N-acetylcysteine (NAC) in protectingcells against Cd toxicity. Hepatocytes were incubated for 12and 24 h with Cd (2.5, 5, 10 μM). Results showed that Cd caninduce cytotoxicity: 10 μM resulted in 36.2% mortality after12 h and 47.8% after 24 h. Lactate dehydrogenase, aspartate aminotransferase, and alanine aminotransferase activitiesincreased. Additionally, reactive oxygen species (ROS)generation increased in Cd-treated hepatocytes along withmalondialdehyde levels. Glutathione concentrationssignificantly decreased after treatment with Cd for 12 h butincreased after 24 h of Cd exposure. In contrast, glutathioneperoxidase activity significantly increased after treatmentwith Cd for 12 h but decreased after 24 h. superoxidedismutase and catalase activities increased at 12 h and 24 h. glutathione S-transferase and glutathione reductase activitiesdecreased, but not significantly. Rat hepatocytes incubatedwith NAC and Cd simultaneously had significantly increasedviability and decreased Cd-induced ROS generation. Ourresults suggested that Cd induces ROS generation that leads to oxidative stress. Moreover, NAC protects rat hepatocytes from cytotoxicity associated with Cd.
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