Bisphenol A disrupts epithelial homeostasis in the midgut of the freshwater shrimp Neocaridina davidi

Bisphenol A (BPA) is commonly used in the production of plastics and epoxy resins. Hence, it is used to produce many everyday items. It is classified as a hazardous chemical due to its potential to cause serious eye damage, allergic skin reactions, and respiratory irritation or can affect reproductive function, cognitive function, and metabolism. Furthermore, BPA, due to its ability to mimic the human hormone estrogen, is an endocrine disruptor. However, aquatic organisms are most vulnerable to BPA. While changes in the abundance and fecundity of freshwater invertebrates have been analysed, data on the cytotoxic effects of BPA are scarce. Cytotoxicity triggers numerous degenerative or regenerative processes that attempt to maintain homeostasis in the body. Thus, to determine which cytotoxicological processes could be activated after BPA exposure, we used the freshwater shrimp Neocaridina davidi, a species widely cultured worldwide. Individuals of N. davidi were exposed to three concentrations of BPA: 1, 5, and 10 mg/L for 24, 48, and 72 h. Isolated from the specimens, the intestine and hepatopancreas were prepared for qualitative and quantitative analysis. The present findings demonstrate that BPA disrupts multiple cytotoxicity pathways, triggering a cascade of cellular interactions, including damage to mitochondria, nuclei, and DNA. We conclude that the oxidant-antioxidant imbalance induced by BPA compromises epithelial cell homeostasis, leading to midgut barrier dysfunction and impairing the regenerative capacity of the digestive system.