Mollusc C-reactive protein crosses species barrier and reverses hepatotoxicity of lead in rodent models.
Indian J Exp Biol
;
2013 Aug; 51(8): 623-634
Article
in English
| IMSEAR
| ID: sea-149365
ABSTRACT
Achatina fulica C-reactive protein (ACRP) reversed the toxic effects of lead nitrate both in vivo in mice and in vitro in rat hepatocytes restoring the basal level of cell viability, lipid peroxidation, reduced glutathione and superoxides. Cytotoxicity was also significantly ameliorated in rat hepatocytes by in vitro pre-treatments with individual subunits (60, 62, 90 and 110 kDa) of ACRP. Annexin V-Cy3/CFDA dual staining showed significant reduction in the number of apoptotic hepatocytes pre-treated with ACRP. ACRP induced restoration of mitochondrial membrane potential was remarkable. ACRP pre-treatment prevented Pb-induced apoptosis mediated by caspase activation. The antagonistic effect of ACRP may be due to scavenging of reactive oxygen species which maintained the homeostasis of cellular redox potential as well as reduced glutathione status. The results suggest that ACRP crosses the species barrier and it may be utilized as a viable exogenous agent of cytoprotection against heavy metal related toxicity.
Full text:
Available
Index:
IMSEAR (South-East Asia)
Main subject:
Rats
/
Male
/
C-Reactive Protein
/
Mitochondria, Liver
/
Hazardous Substances
/
Lipid Peroxidation
/
Cell Survival
/
Blotting, Western
/
Reactive Oxygen Species
/
Rats, Sprague-Dawley
Type of study:
Prognostic study
Language:
English
Journal:
Indian J Exp Biol
Year:
2013
Type:
Article
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