BPA disrupts crustacean reproduction: Tissue-specific accumulation, oxidative stress, and gene dysregulation in Macrobrachium nipponense.

Bisphenol A (BPA), a pervasive environmental endocrine disruptor, increasingly threatens aquatic ecosystems due to its reproductive toxicity. This study investigates how BPA disrupts ovarian development in Macrobrachium nipponense - by analyzing its tissue-specific bioaccumulation (ovaries, hepatopancreas, fertilized eggs), antioxidant responses, and developmental gene regulation. Experimental results demonstrated that after 10-day exposure to 10, 100, and 1000 μg/L BPA, significant BPA accumulation was observed in both ovaries and hepatopancreas, while fertilized eggs showed notable accumulation only at the highest concentration (1000 μg/L) (P < 0.05). The ovarian glutathione peroxidase (GSH-Px) activity displayed a concentration-dependent increase, contrasting with the inverse pattern observed in fertilized eggs. Gene expression analysis revealed that cytochrome P450 49A1 (CYP49a1) in both ovaries and hepatopancreas reached peak levels at the highest BPA concentration, whereas cathepsin D (CTSD) and catalase (CAT) expression peaked at the intermediate concentration (100 μg/L) in both tissues (P < 0.05), while female sterile homeotic (fsh) in ovaries remained steady but significantly decreased in hepatopancreas upon BPA exposure (P < 0.05). These results provide preliminary evidence that BPA may disrupt ovarian development in M. nipponense through interfering with antioxidant systems and altering the expression of key developmental genes, highlighting its potential endocrine-disrupting effects in this commercially important crustacean species.