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Bisphenol A induces reproductive toxicity by antagonizing cholesterol uptake at the StAR mitochondrial transmembrane transporter in C. elegans


Endocrine-disrupting compounds (EDCs) are found in numerous products and due to their structural similarity to endogenous hormones, they can interfere with many aspects of the endocrine system. Bisphenol A (BPA) is one such EDC commonly used as an intermediate in the production of several plastic polymers, including polycarbonate and epoxy resins. Here, we examined the role of BPA as a reproductive toxicant using three strains of Caenorhabditis elegans: N2 (wild-type), Strl-1 F52F12.7(ok3347) I (StAR) and tspo-1 C41G7.9(tm5526) (TSPO). The StAR and TSPO mutants have a mutation that inactivated the StAR or TSPO mitochondrial membrane transporter respectively. A combination of one cholesterol concentration (0 μg/ml cholesterol, 0.5 μg/ml cholesterol or 5 μg/ml cholesterol) with a BPA concentration (0 �M BPA, 100 �M BPa or 500 �M BPA) allowed us to analyze how varying cholesterol and BPA concentrations affect fertility, the germline and cholesterol uptake in the mitochondria. We found that cholesterol antagonizes the reproductive toxicity of BPA in wild-type (N2) C. elegans and BPA may induce its reproductive toxicity through the StAR transporter as the StAR mutants did not show signs of reproductive toxicity with increased exposure to BPA. These results indicate that cholesterol rescues the reproductive effects of BPA and that StAR may be an important component of this mechanism.

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