Ecotoxicological risk assessment of endocrine- disrupting compounds in freshwater ecosystems using tropical cladocerans Moina micrura (Kurz, 1875)

Despite the global recognition of the adverse effects of endocrine-disrupting compounds (EDCs) on human health and the environment, comprehensive regulations addressing these contaminants in water sources are lacking worldwide, including in Malaysia. Furthermore, the absence of a regulatory framework impedes systematic research and ecotoxicological risk assessment data on the effects of EDCs, complicating the development of effective mitigation strategies. This study employed tropical zooplankton (Moina micrura) as a model species to elucidate the toxicity pathway and establish adverse effects at different organizational levels (molecular, organ, individual, and population). The study focused on nine EDCs: bisphenol A (BPA), bisphenol F (BPF), bisphenol S (BPS), perfluorooctanoic acid (PFOA), perfluorooctanesulfonic acid (PFOS), diclofenac (DCF), propranolol (PROP), 17α-ethinylestradiol (EE2), and 17β-estradiol (E2). Besides EDCs, the study also revealed that climate change significantly impacted the life-history traits of M. micrura. Lifespan, total number of offspring, heart rate, individual size, and total molting of M. micrura were significantly reduced (p < 0.05) under acidic (pH 5) and basic (pH 9) water conditions. Male offspring were observed only under conditions of no food supply and low food concentration (1 × 102 cells/mL). In the molecular evaluation, the study observed significant up-regulation of 15 genes that can serve as biomarkers under unfavorable environmental conditions. Hemoglobin (HBB), glutathione S-transferase (GST), doublesex (DSX), and juvenile hormone analog (JHA) gene expression levels were used to evaluate the molecular impact of EDCs on M. micrura. The results indicated significant upregulation (p < 0.05) of HBB and GST genes by at least 2-fold during all acute EDC exposures. DSX and JHA were only significantly upregulated (p < 0.05) by two-fold during exposure to EE2 and E2. At the organ and individual levels, significant reductions (p < 0.05) in the heart rate of M. micrura were observed. Subsequently, significant differences (p < 0.05) were noted in the individual sizes of M. micrura under the exposure to PFOS, PFOA, EE2, and E2. The adverse effects of EDCs at the population level were determined using the lethal concentration (LC50) and predicted no-effect concentration (PNEC) to evaluate the risk associated with EDCs. Based on the LC50 values, the most hazardous EDCs to M. micrura were DCF (66.5 μg/L), followed by PROP (90.4 μg/L), EE2 (312.0 μg/L), E2 (374.8 μg/L), PFOA (474.7 μg/L), PFOS (549.6 μg/L), BPA (611.6 μg/L), BPF (632.0 μg/L), and BPS (819.1 μg/L). However, when utilizing the species sensitivity distribution to calculate PNEC (PNECSSD), the most toxic chemical was E2, followed by DCF, PROP, BPF, EE2, BPA, PFOS, and PFOA. Overall, the results of the toxicity pathway indicated that alterations in GST and HBB genes affected reactive oxygen species (ROS) production in M. micrura. ROS serve as a potential mechanism for EDCs, primarily through oxidative stress pathways, leading to outcomes such as mortality, growth reduction, and reproductive failure. Furthermore, the induction of HBB, JHA, and DSX contributes to the increase in male offspring. This comprehensive study is crucial for informed decision-making in environmental monitoring, effective water pollution mitigation, and the sustainability of riverine ecosystems.

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