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The increasing concentration of Antimony (Sb) in ecological environments has raised serious concerns about its potential biotoxicological impact. This study investigated the toxicokinetics, Global DNA Methylation (GDM), biomarker expression, and Integrated Biological Response (IBR) of Sb at different concentrations in zebrafish. The toxic mechanism of Sb exposure was simulated using molecular dynamics (MD). The results showed that significant differences effect existed (BCFk: liver > ovary > gut > brain) and uptake saturation phenomenon of Sb among zebrafish tissues. Over a 54-day exposure period, the liver emerged as the main target site for Sb-induced GDM, and the restoration was slower than in other tissues during the 54-day recovery period. Moreover, the concentration of Sb had a significant impact on the normally expression of biomarkers, with GSTM1 inhibited and MTF2, MT1, TET3, and p53 showing varying degrees of activation at different Sb concentrations. This could be attributed to Sb3+ potentially occupying the active site or tightly binding to the deep cavity of these genes. The IBR and MD results highlighted DNMT1 as the most sensitive biomarker among those assessed. This heightened sensitivity can be attributed to the stable binding of Sb3+ to DNMT1, resulting in alterations in the conformation of DNMT1's catalytic domain and inhibition of its activity. Consequently, this disruption leads to damage to the integrity of GDM. The study suggests that DNA methylation could serve as a valuable biomarker for assessing the ecotoxicological impact of Sb exposure. It contributes to a better understanding of the toxicity mechanisms in aquatic environments caused potential pollutants.

Water pollution caused by widely used agricultural pesticide chlorpyrifos (CPF) has aroused extensive public concern. While previous studies have reported on toxic effect of CPF on aquatic animal, little is known about its effect on common carp (Cyprinus carpio L.) livers. In this experiment, we exposed common carp to CPF (11.6 μg/L) for 15, 30, and 45 days to establish a poisoning model. Histological observation, biochemical assay, quantitative real-time polymerase chain reaction (qRT-PCR), Western blot, and integrated biomarker response (IBR) were applied to assess the hepatotoxicity of CPF in common carp. Our results displayed that CPF exposure damaged histostructural integrity and induced liver injury in common carp. Furthermore, we found that CPF-induced liver injury may be associated with mitochondrial dysfunction and autophagy, as evidenced by swollen mitochondria, broken mitochondrial ridges, and increased the number of autophagosomes. Moreover, CPF exposure decreased the activities of ATPase (Na+/K+-ATPase, Ca2+-ATPase, Mg2+-ATPase, and Ca2+Mg2+-ATPase), altered glucose metabolism-related genes (GCK, PCK2, PHKB, GYS2, PGM1, and DLAT), and activated energy-sensing AMPK, indicating that CPF caused energy metabolism disorder. The activation of AMPK further induced mitophagy via AMPK/Drp1 pathway, and induced autophagy via AMPK/mTOR pathway. Additionally, we found that CPF induced oxidative stress (abnormal levels of SOD, GSH, MDA, and H2O2) in common carp livers, which further contributed to the induction of mitophagy and autophagy. Subsequently, we confirmed a time-dependent hepatotoxicity caused by CPF in common carp via IBR assessment. Our findings presented a new insight into molecular mechanism of CPF induced-hepatotoxicity in common carp, and provided a theoretical basis for evaluating CPF toxicity to aquatic organisms.

Pharmaceuticals are emerging pollutants of concern for aquatic ecosystems where they are occurring in complex mixtures. In the present study, the chronic toxicity of an environmentally relevant pharmaceutical mixture on juvenile rainbow trout (Oncorhynchus mykiss) was investigated. Five pharmaceuticals (paracetamol, carbamazepine, diclofenac, naproxen and irbesartan) were selected based on their detection frequency and concentration levels in the Meuse river (Belgium). Fish were exposed for 42 days to three different concentrations of the mixture, the median one detected in the Meuse river, 10-times and 100-times this concentration. Effects on the nervous, immune, antioxidant, and detoxification systems were evaluated throughout the exposure period and their response standardized using the Integrated Biomarker Response (IBRv2) index. IBRv2 scores increased over time in the fish exposed to the highest concentration. After 42 days, fish exposed to the highest concentration displayed significantly higher levels in lysozyme activity (p

Lead (Pb) is a non-essential metal. Its occurrence in the environment is related principally to anthropogenic contamination. Pb is toxic to aquatic organisms and can provoke damage to membranes and inhibit the activity of essential enzymes. The filter-feeding, Manila clam Ruditapes philippinarum is widely used as a biomonitor organism to assess metal toxicity. Among biomarkers related to the Pb toxicity, the enzymatic activity of δ-aminolevulinic acid dehydratase (δ-ALAD) has been adopted as a specific tool. Metallothionein (MT), lipid peroxidation (LPO) and antioxidant enzymes activities, such as catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione S-transferase (GST) and superoxidase dismutase (SOD) have also been employed to assess the toxic effect of metals. Two target tissues, the gills and the digestive gland, were selected to examine biomarker responses. In order to assess the effects of Pb accumulation and the mechanisms involved in the recovery from it, clams were exposed at two Pb levels (10 and 100 µg/L) for 7 days and were later maintained in clean water for 7 days as a depuration period. Pb accumulation was dependent on the exposure concentration and higher Pb levels were observed in the gills compared to the digestive gland. Inhibition of δ-ALAD, GST and SOD and the induction of MT and LPO over the exposure period were observed in the gills and the digestive gland of R. philippinarum. The depuration period showed a continuous inhibition of the δ-ALAD activity and induction of MT and LPO in both tissues. These results demonstrate that lead induced an exposure effect and the 7 days of depuration were not sufficient to recover the basal health status of the clams., (Copyright © 2018 Elsevier Inc. All rights reserved.)