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“Copper-loaded microplastics unleash endoplasmic reticulum stress-driven liver apoptosis in fish Channa punctatus”
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Researchers found that PVC microplastics loaded with copper caused severe liver damage in fish through a process called endoplasmic reticulum stress, which triggers cell death. The combined exposure to microplastics and copper was more harmful than either pollutant alone. This study demonstrates how microplastics can act as carriers for toxic metals, amplifying their harmful effects on organ health.
The extensive use of plastics has led to significant microplastic pollution, posing threats to environmental and human health. Concerns are growing about the toxicity of microplastics (MPs) and their ability to adsorb contaminants like Copper (Cu 2+ ). Therefore, this study investigated the effects of environmentally realistic concentrations of Polyvinyl Chloride (PVC)-MPs and Copper, both individually and together, with a particular focus on triggering Endoplasmic reticulum (ER) stress-driven apoptosis in the liver of Channa punctatus. Well-habituated fish were organized into four groups: Group I (Control), Group II (0.5 mg/L PVC-MPs), Group III (0.85 mg/L Copper), and Group IV (0.5 mg/L PVC-MPs + 0.85 mg/L Copper). The treatment period was 15, 30, 45 and 60 days. Various liver parameters were assessed according to standard protocols to understand the repercussions of intoxication. A significant ( p <0.05) increment in Reactive Oxygen Species (ROS) pointed to a substantial rise in oxidative stress. Enzymatic antioxidants like superoxide dismutase (SOD) and catalase (CAT) showed significantly ( p <0.05) elevated extents while reduced glutathione (GSH) levels significantly ( p <0.05) dropped in a duration-dependent pattern. Additionally, lipid peroxidation (LPO) activities surged significantly ( p <0.05), and notable hepato-structural disruptions were observed. The evidence of liver damage was further verified by a significant ( p <0.05) rise in concentrations of hepatic biomarkers viz. Serum Glutamic Oxaloacetic Transaminase (SGOT), Serum Glutamic Pyruvic Transaminase (SGPT), and Alkaline phosphatase (ALP). Moreover, ER-stress was validated through the increased intracellular calcium levels along with the heightened expression of grp78, chop, atf4, perk, eIF2α, and gadd34 in exposed groups. This intricate cascade subsequently elicited the activation of bax, caspase-3, caspase-9 , and apaf-1 , while modulation of bcl-2 , thereby driving hepatocyte-apoptosis via ER-stress response in C. punctatus , a widely consumed food-fish. Our findings underscore the toxic threats of Copper-laden PVC-MPs to aquatic life and potentially the broader ecosystem. • PVC-MPs and Copper disrupted ROS - antioxidant balance in fish liver • Raised oxidative stress led to build-up of misfolded proteins, provoking ER stress • PERK/eIF2α/ATF4/CHOP pathway is activated as part of the UPR response • Prolonged UPR accelerated hepatocyte apoptosis through shifts in apoptotic markers • The combined effect of PVC-MPs and Copper is far more damaging than either alone
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