Effects of Shark Hepatic Stimulator Substance on the Function and Antioxidant Capacity of Liver Mitochondria in an Animal Model of Acute Liver Injury
Article first published online: 11 AUG 2005
DOI: 10.1111/j.1745-7270.2005.00081.x
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How to Cite
FAN, Q.-L., HUANG, C.-G., JIN, Y., FENG, B., MIAO, H.-N., LI, W.-J., JIAO, B.-H. and YUAN, Q.-S. (2005), Effects of Shark Hepatic Stimulator Substance on the Function and Antioxidant Capacity of Liver Mitochondria in an Animal Model of Acute Liver Injury. Acta Biochimica et Biophysica Sinica, 37: 507–514. doi: 10.1111/j.1745-7270.2005.00081.x
Publication History
- Issue published online: 11 AUG 2005
- Article first published online: 11 AUG 2005
- Received: January 5, 2005 Accepted: June 20, 2005
- Abstract
- References
- Cited By
Keywords:
- shark hepatic stimulator substance;
- acute liver injury;
- mitochondrion;
- respiratory function;
- antioxidant capacity
Abstract This study was carried out to investigate whether shark hepatic stimulator substance (HSS) can prevent acute liver injury and affect mitochondrial function and antioxidant defenses in a rat model of thioacetamide (TAA)-induced liver injury. The acute liver injury was induced by two intraperitoneal injections of TAA (400 mg/kg) in a 24 h interval. In the TAA plus shark HSS group, rats were treated with shark HSS (80 mg/kg) 1 h prior to each TAA injection. In this group, serum liver enzyme activities were significantly lower than those in the TAA group. The mitochondrial respiratory control ratio was improved, and the mitochondrial respiratory enzyme activities were increased in the TAA plus shark HSS group. The mitochondrial antioxidant enzyme activities and glutathione level were higher in the TAA plus shark HSS group than in the TAA group. These results suggest that the protective effect of shark HSS against TAA-induced acute liver injury may be a result of the restoration of the mitochondrial respiratory function and antioxidant defenses and decreased oxygen stress.
Edited by Ming-Hua XU

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