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Polyvinyl Chloride Exposure Induces Liver Injury: A Biochemical and Histological Evaluation
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This rat study evaluated liver toxicity from 42 days of daily oral polyvinyl chloride administration at doses of 0.1, 0.2, and 0.3 mg/kg. Liver enzymes (AST, ALT, ALP) were elevated disproportionately, oxidative stress markers were disrupted, and histological changes were observed, suggesting dose-dependent hepatotoxicity from PVC microplastics.
Objective: Microplastics are ubiquitous in our environment, with evidence of its presence in various body tissues, however the extent of its toxicity at low dose from chronic administration and bioaccumulation in humans remains unknown. This study aims at evaluating the toxicological impact of sub-chronic administration of polyvinyl chloride on the liver. Methods: 50 adults male wistar rats were orally administered 10 ml/kg of deionized water (control), and treatment groups received 0.1,0.2 and 0.3mg/kg of PVC daily for 42 days using an oro-gastric tube. Liver enzymes (AST, ALT, ALP), oxidative biomarkers (GSH, GPx, CAT, SOD and MDA) and the histoarchitecture were examined. Statistical analysis was performed using ANOVA with p value <.05 Results: There was a disproportionate elevation of liver enzymes with a dose dependent pattern, suggestive of hepatic damage, antioxidative stress biomarkers where decreased (GSH, GPx, CAT and SOD) with an increase in pro-oxidative biomarker (MDA) indicative of an overwhelmed liver oxidative stress defense mechanisms, additionally the histomorphology of the liver showed distorted with loss of radial symmetry, ballooning of hepatocytes and loss of parenchyma organization. Conclusion: This finding provides empirical data that PVC induces dose dependent hepatotoxicity in wistar rats, with biochemical and histological evidence. This further demonstrates that sub-chronic exposure to PVC poses grave health risk to the liver of exposed population and the need for human translational studies and policy to safeguard exposed individuals.
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