N-acetylcysteine protects against cadmium-induced oxidative stress in rat hepatocytes
Journal of Veterinary Science
;
: 485-493, 2014.
Article
in English
| WPRIM
| ID: wpr-24552
ABSTRACT
Cadmium (Cd) is a well-known hepatotoxic environmental pollutant. We used rat hepatocytes as a model to study oxidative damage induced by Cd, effects on the antioxidant systems, and the role of N-acetylcysteine (NAC) in protecting cells against Cd toxicity. Hepatocytes were incubated for 12 and 24 h with Cd (2.5, 5, 10 microM). Results showed that Cd can induce cytotoxicity 10 microM resulted in 36.2% mortality after 12 h and 47.8% after 24 h. Lactate dehydrogenase, aspartate aminotransferase, and alanine aminotransferase activities increased. Additionally, reactive oxygen species (ROS) generation increased in Cd-treated hepatocytes along with malondialdehyde levels. Glutathione concentrations significantly decreased after treatment with Cd for 12 h but increased after 24 h of Cd exposure. In contrast, glutathione peroxidase activity significantly increased after treatment with Cd for 12 h but decreased after 24 h. superoxide dismutase and catalase activities increased at 12 h and 24 h. glutathione S-transferase and glutathione reductase activities decreased, but not significantly. Rat hepatocytes incubated with NAC and Cd simultaneously had significantly increased viability and decreased Cd-induced ROS generation. Our results suggested that Cd induces ROS generation that leads to oxidative stress. Moreover, NAC protects rat hepatocytes from cytotoxicity associated with Cd.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Acetylcysteine
/
Cadmium
/
Cell Survival
/
Cells, Cultured
/
Reactive Oxygen Species
/
Rats, Sprague-Dawley
/
Oxidative Stress
/
Hepatocytes
/
Environmental Pollutants
/
Antioxidants
Limits:
Animals
Language:
English
Journal:
Journal of Veterinary Science
Year:
2014
Type:
Article
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