Molecular insights: zebrafish embryo damage linked to hospital effluent.

Abstract

This study addresses the pressing issue of pollutants, particularly heavy metals and pharmaceuticals, infiltrating aquatic ecosystems due to untreated hospital effluents. These contaminants, known for their toxicity and bioaccumulative potential, adversely affect water quality and ecosystem health. The research focuses on the intricate relationship between oxidative stress and embryonic damage in Danio rerio exposed to hospital effluent, offering a detailed understanding of the underlying mechanisms. Concentrations of pharmaceutical residues (ng L^-1) such as NSAIDs, corticosteroids, proton pump inhibitors, H2-receptor antagonists, and heavy metals (mg L^-1) like Cd, As, Cu, Cr, Hg, Ni, Pb, and Zn were meticulously quantified. The effluent exhibited a significant embryolethal potential with an LC₅₀ of 2.328% and an EC₅₀ for malformation at 2.607%. Notable embryonic malformations included yolk sac edema, tail abnormalities, pericardial edema, scoliosis, craniofacial deformities, eye hypopigmentation, developmental delays, and body malformations. Zebrafish embryos were exposed to varying concentrations of the effluent (0.5% to 4.0%) and assessed for lethality and malformations at specific intervals (12, 24, 48, 72, and 96 h post-fertilization). The study also scrutinized oxidative damage and monitored the expression of genes central to antioxidant processes, detoxification, and apoptosis (sod, cat, nrf2, cyp1a1, bax, casp3, casp6, casp7, and casp9) at 48-, 72-, and 96-h post-fertilization across all concentrations. Findings consistently revealed lipid and protein damage, heightened antioxidant activity, and altered gene expression at all time points and effluent concentrations. These results highlight the environmental threat posed by untreated hospital effluent, emphasizing the need for comprehensive effluent treatment measures to protect aquatic ecosystems from the detrimental impacts of pharmaceuticals and heavy metals. The study underscores the critical role of oxidative stress in embryonic damage and advocates for improved environmental stewardship and regulatory measures.