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Published on: April 28, 2020
Identification of the Toxicity Pathways Associated With Thioacetamide-Induced Injuries in Rat Liver and Kidney
Patric Schyman1, Richard L Printz2, Shanea K Estes2
1DoD Biotechnology High Performance Computing Software Applications Institute, Telemedicine and Advanced Technology Research Center, U.S. Army Medical Research and Materiel Command, Fort Detrick, MD, United States.
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.
Insights
Chemically induced organ injuries can be detected early using specific gene expression patterns. This study validates gene modules for identifying liver, kidney, and heart damage from chemical exposure, aiding in timely interventions.
Area of Science:
- Toxicology
- Molecular Biology
- Genomics
Background:
- Chemical exposure poses significant health risks, necessitating early detection of cellular damage.
- Identifying specific biomarkers for chemically induced organ injuries is crucial for effective countermeasures.
- Previous research identified gene modules associated with liver and kidney injuries.
Purpose of the Study:
- To validate previously identified gene modules for detecting chemical-induced organ injuries.
- To assess the specificity of these gene modules in liver, kidney, and heart tissues.
- To investigate the utility of gene expression data in identifying thioacetamide-induced organ damage.
Main Methods:
- Gene expression analysis in Sprague-Dawley rats exposed to varying doses and durations of thioacetamide.
- Histopathological examination to confirm organ injury.
- Analysis of gene expression data to identify injury-associated gene modules.
Main Results:
- Gene modules accurately indicated organ injury specificity, with the liver being most affected.
- Activated liver gene modules were significantly associated with inflammation and fibrosis.
- Results were consistent with known thioacetamide toxicity and histological findings.
Conclusions:
- Validated gene modules show potential for early detection of chemical-induced organ injuries.
- Gene expression profiling can serve as a valuable tool for identifying specific organ damage.
- This approach aids in understanding toxicological mechanisms and developing targeted interventions.
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