Bisphenol A-induced renal metabolic disruption: Insights into MAPK-mediated steroid hormone dysregulation from transcriptomic and metabolomic analyses
After long-term exposure of BPA, human is probably suffering from invisible renal injury and metabolic disruption, while its linked intricate gene transcriptional mechanisms warrant more conclusive evidence.  Comprehensive analysis utilizing transcriptomics and metabolomics were used to elucidate the transcriptional mechanisms regulating metabolic homeostasis involved in BPA-induced nephrotoxicity. Here, six-week-old male ICR (CD1) mice were randomly divided into vehicle group with 10 mice and BPA exposure group with 10 mice (five mice per cage). The mice in the exposure group received a daily gavage of BPA dissolved in an aqueous solution containing 0.1% ethanol at the dose of 50 µg/kg/d, which is the tolerable daily intake (TDI) dose of BPA. The mice in the vehicle group received the same dose of aqueous solution containing 0.1% ethanol. After 6-week exposure, the mice were euthanized and left kidney were tissues were frozen with liquid nitrogen and used for RNA transcriptome sequencing. Overall design: RNA-seq profiling of kidney after BPA exposure