Acute liver toxicity by carbon tetrachloride in HSP70 knock out mice

• Published in: Experimental and toxicologic pathology : official journal of the Gesellschaft für Toxikologische Pathologie 2007-09, Vol.59 (1), p.29-34
• Main Authors: Song, Ji-Ye, Li, Lan, Ahn, Jae-Bum, Park, Jong-Gil, Jo, Ji-Sang, Park, Dae-Hun, Jang, Hyung-Kwan, Jang, Ja June, Lee, Min-Jae
• Format: Article
• Language: English
• Subjects: Acute Disease; Acute liver toxicity; Alanine Transaminase - metabolism; Animals; Biological and medical sciences; Carbon tetrachloride (CCl 4); Carbon Tetrachloride - toxicity; Carbon Tetrachloride Poisoning - enzymology; Carbon Tetrachloride Poisoning - pathology; Chemical and Drug Induced Liver Injury - enzymology; Chemical and Drug Induced Liver Injury - pathology; Disease Models, Animal; HSP70; HSP70 Heat-Shock Proteins - biosynthesis; HSP70 Heat-Shock Proteins - deficiency; HSP70 Heat-Shock Proteins - genetics; Injections, Intraperitoneal; Investigative techniques, diagnostic techniques (general aspects); Knock out; Liver - drug effects; Liver - enzymology; Liver - pathology; Medical sciences; Mice; Mice, Inbred C57BL; Mice, Knockout; Necrosis - chemically induced; Necrosis - pathology; Neutrophil Infiltration - drug effects; Olea; Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques
• ISSN: 0940-2993; 1618-1433
• DOI: 10.1016/j.etp.2007.02.005

The effects of carbon tetrachloride (CCl 4) treatment on acute liver damage in knock out (heat shock proteins—HSP70−/−) mice and wild-type (C57BL/6) mice were examined. Acute liver injury was induced by a single intraperitoneal injection of 0.3 ML/kg CCl 4 in olive oil. Mice were sacrificed at 12, 24, 48 and 72 h after treatment. To assess hepatotoxicity, alanine transaminase, neutrophil infiltration and degree of necrosis were measured. Western blot analysis was employed for heat shock proteins. The result revealed that HSP70−/− mice showed higher alanine transaminase levels and a more severe degree of neutrophilic infiltration and necrosis than those of wild-type mice. Furthermore, HSP70−/− mice recovered more slowly from CCl 4 treatment. In HSP70−/− mice, HSP47 was overexpressed. Therefore, HSP70−/− mice could be an adequate model of acute liver toxicity study.