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Metformin is one of the most extensively used drugs, making it one of the most likely endocrine disruptors in the environment, which may negatively affect fish and other freshwater animals. Still, there is a dearth of studies examining metformin's impact on freshwater creatures, like fish. This research aimed to identify the biochemical and genotoxicity effects of the endocrine disruptor metformin in the freshwater fish Labeo rohita at ecologically appropriate doses. Metformin's toxicity was evaluated by subjecting L. rohita to the drug over 28 days at two dosages (40 µg/L to 80 µg/L). The results indicated that 40 µg/L and 80 µg/L of metformin caused an increase in reactive oxygen species and the generation of free radicals in the body of L. rohita, which in turn caused impairment and alterations in total hemoglobin, red blood corpuscles, white blood corpuscles, oxidative stress, lipid peroxidation, protein carbonyl activity, respiratory burst activity, myeloperoxidase activity, and lysozyme activity. In addition, animals treated with the maximum metformin dose (80 µg/L) demonstrated substantial DNA damage in the genotoxicity experiment. Metformin's endocrine-disrupting actions may have unintended ramifications for the well-being of aquatic species in their natural habitats. Results of the study demonstrated a serious concern that metformin exposure might be harmful to aquatic life. [ABSTRACT FROM AUTHOR]

Bacterial fish disease outbreaks are a key concern for aquaculture. Complementary feed additives such as immunostimulants can serve as an ideal solution for disease prevention. Herein, we scrutinized the efficacy of exopolysaccharides (EPSs) from probiotic Bacillus licheniformis and EPS-mediated zinc oxide nanoparticles (EPS-ZnO NPs) for a diet to evaluate growth parameters, antioxidant enzyme activities, and immune stimulation together with disease resistance against Aeromonas hydrophila and Vibrio parahaemolyticus in Mozambique tilapia Oreochromis mossambicus. Fish were separated into seven groups, with six experimental groups fed with EPS and EPS-ZnO NPs at 2, 5, and 10 mg/g and a control fed a basal diet. The fish ingesting feed supplemented with EPS and EPS-ZnO NPs at 10 mg/g showed improved growth performance. Cellular and humoral-immunological parameters were tested in serum and mucus after 15 and 30 days of feeding. These parameters were substantially enriched with a 10 mg/g diet (p < 0.05) of EPS and EPS-ZnO NPs in comparison with the control. Furthermore, the EPS and EPS-ZnO NP supplemental diet actively enhanced the antioxidant response (glutathione peroxidase, superoxide dismutase, and catalase). In addition, the supplemental diet of EPS and EPS-ZnO NPs lowered the death rate and improved the disease resistance of O. mossambicus following assessment with A. hydrophila and V. parahaemolyticus at 50 µL. Hence, the overall results suggest that the supplemental diet of EPS and EPS-ZnO NPs might be used to ensure aquaculture feed additives. [ABSTRACT FROM AUTHOR]

In recent years, polypropylene microplastic has persisted in freshwater ecosystems and biota, forming ever-growing threats. This research aimed to prepare polypropylene microplastics and evaluate their toxicity to the filter feeder Oreochromis mossambicus. In this research, fish were given a dietary supplement of polypropylene microplastics at 100, 500, and 1000 mg/kg for acute (96 h) and sub-acute (14 days) durations to assess toxic effects on liver tissues. FTIR results revealed the presence of polypropylene microplastic in their digestion matter. The ingestion of microplastics in O. mossambicus led to fluctuations in homeostasis, an upsurge in reactive oxygen species (ROS) levels, an alteration in antioxidant parameters, including superoxide dismutase (SOD), catalase (CAT), glutathione-S–transferase (GST), and glutathione peroxidase (GPx); a promotion in the oxidation of lipid molecules; and a denaturation in the neurotransmitter enzyme acetylcholinesterase (AChE). Our data indicated that sustained exposure to microplastics (14 days) produced a more severe threat than acute exposure (96 h). In addition, higher apoptosis, DNA damage (genotoxicity), and histological changes were found in the liver tissues of the sub-acute (14 days) microplastics-treated groups. This research indicated that the constant ingestion of polypropylene microplastics is detrimental to freshwater environments and leads to ecological threats. [ABSTRACT FROM AUTHOR]

Here, we report on the synthesis of zinc oxide nanoparticles (ZnO NPs) and selenium nanowires (Se NWs) using microbial exopolysaccharides (EPS) as a mediator and then examine their antibacterial and ecotoxicity effects in vitro and in vivo, respectively. At 100 µg/mL, EPS, EPS-ZnO NPs, and EPS-Se NWs all exhibited potent in vitro antibacterial properties, drastically inhibiting the development of aquatic Gram(-) pathogens. In addition, antibiofilm studies using a microscope revealed that EPS, EPS-ZnO NPs, and EPS-Se NWs at 75 µg/mL prevented biofilm development. Furthermore, the in vivo toxicity was carried out via Danio rerio embryos and Ceriodaphnia cornuta. Danio rerio embryos were determined at different time intervals (6 hpf, 12 hpf, 24 hpf and 48 hpf). The maximum survival rate (100%) was obtained in a control group. Correspondingly, EPS, EPS-ZnO NPs and EPS-Se NWs treated embryos showed a considerable survival rate with 93.3%, 86.7% and 77.2%, respectively, at 100 µg/mL for 48 hpf. The total mortality of C. cornuta was seen at 100 µg/mL, with 56.7% in EPS, 60.0% in EPS-ZnO NPs, and 70.0% in EPS-Se NWs. For C. cornuta, the LC50 values for EPS, EPS-ZnO NPs, and EPS-Se NWs were 90.32, 81.99, and 62.99 µg/mL, respectively. Under a microscope, morphological alterations in C. cornuta were analyzed. After 24 h, an amount of dark substance was seen in the guts of C. cornuta exposed to 100 µg/mL, but in the control group, all of the living C. cornuta were swimming as usual. Our results show that EPS and EPS-ZnO NPs were less harmful than EPS-Se NWs, and that they were successfully employed to shield freshwater crustaceans from the toxins in aquatic environments. [ABSTRACT FROM AUTHOR]