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Protection of Exogenous Antioxidant of Cinnamomum burmanii as a Hepatoprotective on the Toxicological Responses of Nanoplastics in Rats (Rattus norvegicus L.)
Summary
Researchers tested whether Cinnamomum burmanni leaf extract (CLE) protects rat liver function from polystyrene nanoplastic toxicity, administering NPs orally for 14 days with or without 100–400 mg/kg CLE for 28 days. NPs caused oxidative stress and liver damage, while CLE at 200–400 mg/kg significantly reduced hepatotoxicity markers and restored antioxidant enzyme activity, suggesting hepatoprotective potential against nanoplastic-induced toxicity.
Nanoplastics of polystyrene (NPs) are widely dispersed and pose a serious concern as non-biodegradable pollutants to human health. Given our unintentional exposure to toxic chemicals in everyday life, it is crucial to evaluate their toxicity and inhibition. This can be achieved by employing exogenous antioxidants sourced from natural substances. We investigated the toxicity of NPs and the protective impact of exogenous antioxidants on the liver in an animal model. Each experimental group received NPs alone (10µL/kg, for 14 days) as negative control. Three additional treatment groups were exposed to a combination of NPs (for 14 days) along with Cinnamomum burmanii leaf extract (CLE) at concentrations of 100, 200, and 400mg/kg for 28 days, and one control group was used as a reference. All treatments were administrated via oral gavage. The toxic effects and protection from NPs and CLE were investigated based on the levels of SGOT, SGPT, bilirubin, and ALP in the blood serum and specific changes in the liver cells of Wistar rats. The results indicated oxidative damage caused by NPs exposure accompanied by disruptions in enzymatic biochemical parameters, levels of SGPT, SGOT, and ALP, with no changes in bilirubin levels. Histological changes in the liver revealed inflammation, necrotic cells, and chromosomal condensation as signals of increased cell proliferation. The addition of CLE could mitigate the oxidative damage induced by NPs. In conclusion, overall, our comprehensive observations indicate adverse effects of NPs exposure on hepatocyte structure and function. Increased levels of SGPT, SGOT, and ALP indicate liver disturbances, although bilirubin level remains unchanged. The addition of CLE (400 mg/kg) is capable of restoring the disturbance caused by NPs.
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