Gaseous pollutants and PM2.5 Co-exposure induces BCL2/Bax apoptosis pathway activation in rat Sertoli cells: Implication of GATA4 and GATA6 interaction

Document Type : Research Paper

Authors

1 Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran

2 Department of Environmental Health Engineering, School of Public Health and Safety, Shahid Beheshti University of Medical Sciences, Tehran, Iran

3 Department of Pathobiology, Science and Research Branch, Islamic Azad University, Tehran, Iran

4 Department of Physiology, Faculty of Medicine, Tehran Medical Sciences, Islamic Azad University of Medical Sciences, Shariati St., Tehran, Iran

10.22124/cjes.2023.7102

Abstract

Exposure of males to particulate matter and gaseous air pollution poses a serious threat to spermatogenesis. However, the specific molecular mechanism underlying this effect remains unclear. In this in-vivo study on Wistar albino rats, we investigated the impact of combined exposure to ambient fine particulate matter (PM2.5) and gaseous pollutants on the BCL2/BAX signaling pathway, as well as GATA4 and GATA6 gene and protein expression in Sertoli cells. A total of twenty-one male rats were randomly assigned to one of three groups: a control group exposed to standard air conditions, a Gas group exposed to gaseous pollutants alone, and a Gas+PM2.5 group exposed to both PM2.5 and gaseous pollutants. All groups were exposed for four days a week, five hours per day, for three months. Sertoli cells were isolated and analyzed for gene and protein expression. The findings revealed a significant reduction in BCL2, GATA4, and GATA6 gene and protein expression in the Sertoli cells of the Gas+ PM2.5 group, accompanied by an elevation in the Bax gene and protein expression compared to the control group. Consequently, the combined exposure to ambient PM2.5 and gaseous pollutants is likely to trigger the upraised Sertoli cell apoptosis via activation of the BCL2/BAX pathway and possible interaction with GATA 4 and GATA 6 proteins.
 

Keywords


 
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