Abstract

Background. Exposure to environmental toxicants including endocrine disruptor bisphenol A (BPA) during early life can be detrimental to the immune system. To our knowledge, a few research has looked at the effects of developing BPA exposures on spleen. Objective. The murine model was developed to investigate the underlying molecular mechanisms and mode of BPA actions on the spleen subsequent to prolonged early-life exposure to BPA. Methods. Immature (3 weeks old) male and female Swiss Albino mice were intraperitoneally injected with 50μg/kg BPA in corn oil or corn oil alone for 6 weeks. At 10 weeks old (adulthood) mouse spleens were harvested and examined histologically. Results. We observed neurobehavioral impairments and a significant increase in peripheral monocyte and lymphocyte counts in mice (males and females). Moreover, several spleen abnormalities in both male and female mice were observed in adulthood. BPA-treated mice's histopathological results revealed toxicity in the form of significantly active germinal centers of the white pulp and few apoptotic cells. There was also a noticeable invasion of the red pulp by eosinophils and lymphocytes that were significantly higher than normal. Agarose gel electrophoresis provided further evidence of internucleosomal DNA fragmentation and apoptosis in the splenic tissues of BPA-treated mice compared to controls. In addition, there were increased levels of the lipid peroxidation malondialdehyde end-product, a marker of oxidative lipid damage, in the spleens of BPA-treated mice compared to controls. Conclusion. Our study provides evidence for oxidative stress injury induced by BPA exposures early-life could contribute to a range of splenic tissue damage during adulthood.

Key words: Apoptosis; Bisphenol A; DNA Damage; MDA; Murine model; Oxidative stress; Spleen damage