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Published on: July 3, 2013
Early alterations in protein and gene expression in rat kidney following bromate exposure
Gene J Ahlborn1, Don A Delker, Barbara C Roop
1United States Environmental Protection Agency, National Health and Environmental Effects Research Laboratory, Environmental Carcinogenesis Division, B143-06, 109 T.W. Alexander Drive, Research Triangle Park, NC 27711, United States.
Abstract:
Bromate, a common disinfectant byproduct of drinking water ozonation, has been linked to human and animal renal toxicity, including renal cell carcinomas in multiple animal species. Here, we evaluate changes in protein and gene expression through two-dimensional difference gel electrophoresis (2D-DIGE) and Affymetrix arrays to identify potential modes of action involved in potassium bromate carcinogenicity. Male rats were exposed to potassium bromate in drinking water at concentrations of 0, 1, 20 and 400 ppm for two weeks. Differential expression of glycolytic proteins including enolase 1 (Eno1), triosephosphate isomerase 1 (Tpi1) and glyceraldehyde-3-phosphate dehydrogenase (Gapdh) suggests that bromate toxicity is associated with changes in energy consumption and utilization in renal cells involving up-regulation of glycolytic processes that may be the result of altered mitochondrial function. Several alterations in glycolysis and mitochondrial gene transcripts were also observed to be consistent with this mode of action. These studies provide insight into early events in renal cell physiology altered by bromate exposure.
Insights
Potassium bromate, a drinking water contaminant, alters renal cell energy metabolism and protein expression. This study identifies early physiological changes in kidney cells linked to bromate toxicity and carcinogenicity.
Area of Science:
- Environmental toxicology
- Molecular biology
- Biochemistry
Background:
- Bromate is a disinfection byproduct in ozonated drinking water.
- Bromate exposure is associated with renal toxicity and carcinogenicity in animal models.
Purpose of the Study:
- To investigate the molecular mechanisms underlying potassium bromate-induced renal carcinogenicity.
- To identify early changes in protein and gene expression in response to bromate exposure.
Main Methods:
- Male rats were exposed to varying concentrations of potassium bromate in drinking water for two weeks.
- Two-dimensional difference gel electrophoresis (2D-DIGE) was used to analyze protein expression.
- Affymetrix arrays were employed to assess gene expression profiles.
Main Results:
- Differential expression of key glycolytic proteins (enolase 1, triosephosphate isomerase 1, glyceraldehyde-3-phosphate dehydrogenase) was observed.
- Up-regulation of glycolytic processes and alterations in mitochondrial gene transcripts suggest changes in cellular energy metabolism.
- These findings indicate potential alterations in mitochondrial function.
Conclusions:
- Bromate exposure significantly impacts renal cell energy metabolism, particularly glycolysis.
- Altered mitochondrial function may play a role in bromate-induced renal toxicity and carcinogenicity.
- The study provides insights into the early physiological events involved in bromate carcinogenicity.
