Identification of the Toxicity Pathways Associated With Thioacetamide-Induced Injuries in Rat Liver and Kidney.
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Abstract
Ingestion or exposure to chemicals poses a serious health risk Early detection of cellular changes induced by such events is vital to identify appropriate countermeasures to prevent organ damage We hypothesize that chemically induced organ injuries are uniquely associated with a set module of genes exhibiting significant changes in expression We have previously identified gene modules specifically associated with organ injuries by analyzing gene expression levels in liver and kidney tissue from rats exposed to diverse chemical insults Here we assess and validate our injury associated gene modules by analyzing gene expression data in liver kidney and heart tissues obtained from Sprague Dawley rats exposed to thioacetamide a known liver toxicant that promotes fibrosis The rats were injected intraperitoneally with a low 25 mg kg or high 100 mg kg dose of thioacetamide for 8 or 24 h and definite organ injury was diagnosed by histopathology Injury associated gene modules indicated organ injury specificity with the liver being most affected by thioacetamide The most activated liver gene modules were those associated with inflammatory cell infiltration and fibrosis Previous studies on thioacetamide toxicity and our histological analyses supported these results signifying the potential of gene expression data to identify organ injuries