Abstract

Bisphenol A (BPA) is a well-known endocrine disruptor that negatively impacts reproductive physiology, barrier function, and overall metabolic health in aquatic organisms. Melatonin, a hormone secreted by the pineal gland, possesses antioxidant and chronobiotic properties and has been proposed as a potential protective agent against BPA-induced toxicity. However, evidence supporting efficacy in teleost models remains limited. In this study, zebrafish (Danio rerio) were exposed to BPA and melatonin for 21 days to assess alterations in circadian rhythm-associated genes (Clock1a, Cry3a, Per1b, Mt1), tight junction proteins (Claudin, Occludin), inflammatory cytokines (Interleukin-6, Tumor Necrosis Factor-alpha), antioxidant enzymes, and histopathological changes in the gut and ovary. BPA exposure resulted in significant downregulation of circadian genes and tight junction markers, accompanied by elevated levels of inflammatory mediators and oxidative stress. In contrast, melatonin administration alone enhanced gene expression, antioxidant capacity, and tissue integrity. Moreover, co-treatment with melatonin effectively mitigated the adverse effects of BPA, restoring gene expression and reducing inflammation and oxidative damage. These findings highlight the role of melatonin in counteracting BPA-induced toxicity and support its potential application as a therapeutic agent in aquatic toxicology.

Key words: Bisphenol A, Melatonin, Reproduction, Endocrine disruption, Zebra fish, Gut, Ovary