Bisphenol‐A Exposure Induces Anemia and Alters Antioxidant, Apoptotic, and Anti‐Inflammatory Pathways in Mouse Erythrocytes

Bisphenol A (BPA) is an endocrine disruptor (EDC) that causes a variety of human disorders. The current study investigates the mechanism of BPA‐induced anemia in Swiss mice. Mice were given repeated low doses (LD, 1 mg/kg of body weight) and high doses (HD, 5 mg/kg of body weight) of BPA on alternate days for four months. The impacts of BPA on reticulocyte proportion, reactive oxygen species (ROS) production, and apoptotic responses were studied using flow cytometry. BPA exposure decreases body weight and causes chronic haemolytic anemia at different time points at HD. The reticulocyte and ROS production were significantly increased in the LD as well as the HD‐treated group. The apoptotic cell percentages were almost similar in LD but significantly increased in HD. The qRT‐PCR revealed that relative expressions of antioxidant gene, SOD1, CAT, GPX1, and cellular response regulators AKT, PI3K, and NRF2 were increased, but FOXO3 and SOD2 expression were decreased. The expression of proapoptotic gene BAX was increased, but anti‐apoptotic BCL2 and Cyt C were significantly decreased. The expressions of anti‐inflammatory genes, IFN‐γ, NF‐κB, and TGF‐β were increased, but TNF‐α was reduced at LD as well as HD.