Monitoring aquatic health from environmental pollutants is critical, none more so than bisphenol-A (BPA), a ubiquitous endocrine-disrupting chemical (EDC). The present study brings out the responses of selected transcripts, hormone levels, and tissue histomorphology in a widely distributed fish species Cyprinus carpio (Linn.), following exposure to environmentally relevant (10, 100 ng/L) and higher (1000 ng/L) concentration of BPA. The response of cyp19a1a, cyp19a1b, and c3 significantly decreased, while that of vtg increased in their respective tissue domains. The hematological parameters TEC, Hb, and Hct decreased significantly in contrast to TLC (p < 0.05) at all exposure concentrations, whereas none of the erythrocytic indices (MCV, MCH, and MCHC) was perturbed. The steroidogenic hormone levels, such as estradiol and progesterone, increased significantly with increasing BPA concentrations. In contrast, the testosterone and all the thyroid hormones (T3, T4, and TSH) were suppressed significantly (p < 0.05). At the histological level, the BPA induced chondrocyte proliferation, which was accompanied by hemorrhage of the gill lamellae, increased melanomacrophagic centers (MMCs), and degeneration of tubules and fluid accumulation in the kidney. In parallel, binucleated hepatocytes and inflammations were prominent in the liver. Collectively, the histomorphology confirmed induction of degenerative effects in all the tissues investigated, while the cyclic responses of biochemical markers suggest an ability to regulate the impacts. However, a chronic exposure could result in overriding the endemic reproductive pathways with potential population-level effects. In conclusion, the study identified multiple molecular, cellular, and physiological markers that could be employed to detect early signs of BPA and more broadly EDC exposures. These markers in combination with a wide distribution of C. carpio should allow comparative studies of pollutants at environmental concentrations.
Keywords: BPA; Hematology; Histomorphology; Hormone disruption; Molecular response.
© 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.