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Dietary exposure to polyvinyl chloride microparticles induced oxidative stress and hepatic damage in Clarias gariepinus (Burchell, 1822)
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Catfish (Clarias gariepinus) fed PVC microparticle-spiked diets at three inclusion levels for 45 days showed dose-dependent liver damage, elevated antioxidant enzyme activity, and altered serum biochemistry, indicating that dietary PVC microplastic ingestion causes measurable hepatotoxicity.
The present study investigated the effects of polyvinyl chloride (PVC) microparticles (MP) on hepatic antioxidant enzymes activities, serum biochemical and liver histology of juvenile Clarias gariepinus. A total of 180 (25.15 g average weight) C. gariepinus were fed PVC MP (95.41 ± 4.23 μm) spiked diets at 0.5, 1.5, 3.0 percentage inclusion levels and a control diet for 45 days of exposure, then followed by 30 days of depuration trials. Fish specimens (9) from each treatment were sampled every 15-day interval for serum biochemical, liver antioxidant enzymes and histopathological assay. Glucose and triglyceride levels increased significantly in PVC-treated groups when compared with the control. Protein levels of 0.5% and 3.0% PVC-treated groups reduced significantly on the 15th and 30th day exposure periods, while serum enzyme activities of all PVC-treated groups increased significantly in a time-dependent manner. Antioxidant enzymes (superoxide dismutase, glutathione peroxidase, catalase) activity in the liver of the treated groups also decreased progressively in a time-dependent manner. A time-dependent elevation in lipid peroxidation levels was observed in PVC MP-treated groups. Histopathological assessment of the fish liver showed mild to severe levels of glycogen depletion, fatty vacuolation and degeneration, hepatocellular necrosis in PVC-treated groups with reference to the control. The present study revealed that PVC microplastic induced oxidative damage and hepatic histopathological alterations in the exposed fish.
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