N-acetylcysteine protects against cadmium-induced oxidative stress in rat hepatocytes
Journal of Veterinary Science
; : 485-493, 2014.
Article
em En
| WPRIM
| ID: wpr-24552
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WPRO
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.
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Assunto principal:
Acetilcisteína
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Cádmio
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Sobrevivência Celular
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Células Cultivadas
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Espécies Reativas de Oxigênio
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Ratos Sprague-Dawley
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Estresse Oxidativo
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Hepatócitos
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Poluentes Ambientais
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Antioxidantes
Limite:
Animals
Idioma:
En
Revista:
Journal of Veterinary Science
Ano de publicação:
2014
Tipo de documento:
Article