Chronic-Binge Ethanol Drinking Exacerbates Liver Damage through Oxidative/Nitrosative Stress
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Chronic binge alcohol drinking is a major cause of liver disease including steatosis,chronic hepatitis, and liver cirrhosis. The purpose of this study is to examine the change of oxidative/nitrosative stress in the chronic-binge ethanol model. Using wildtype (WT) mice, we show that chronic binge alcohol drinking develops steatosis and apoptotic cells. Furthermore, the activities of anti-oxidant and mitochondrial enzymes including catalase (CAT), superoxide dismutase 1 (SOD1) and glutathione peroxidase (GPx) were decreased in chronic binge alcohol-treated mice. Protein nitration was also increased in a chronic-binge group compared to pair-fed control counterpart. These findings suggest that chronic binge alcohol drinking plays a critical role in hepatic injury through oxidative/nitrosative stress.
Abstract
Chronic binge alcohol drinking is a major cause of liver disease including steatosis,chronic hepatitis, and liver cirrhosis. The purpose of this study is to examine the change of oxidative/nitrosative stress in the chronic-binge ethanol model. Using wildtype (WT) mice, we show that chronic binge alcohol drinking develops steatosis and apoptotic cells. Furthermore, the activities of anti-oxidant and mitochondrial enzymes including catalase (CAT), superoxide dismutase 1 (SOD1) and glutathione peroxidase (GPx) were decreased in chronic binge alcohol-treated mice. Protein nitration was also increased in a chronic-binge group compared to pair-fed control counterpart. These findings suggest that chronic binge alcohol drinking plays a critical role in hepatic injury through oxidative/nitrosative stress.
참고문헌 (10)
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