This evaluation reveals significant hepatic impairment and oxidative stress caused by Hexaconazole in mice, indicating potential health risks.
Hexaconazole (HEX), a commonly used triazole fungicide in agriculture, is widely applied in developing countries like India. Despite its effectiveness against fungal pathogens, its potential hepatotoxic effects in mammals remain insufficiently studied. This study evaluated the subchronic effects of HEX on liver function and histology in Swiss albino mice. Adult male mice were orally administered HEX at doses of 30.6, 61.2, and 122.4 mg/kg body weight daily for 30 days; a control group received distilled water. The study assessed body and liver weight, liver function biomarkers (ALT, AST, ALP, bilirubin, total protein, albumin, globulin), oxidative stress markers (SOD, CAT, GPx, lipid peroxidation), and liver histopathology. Results showed dose‐dependent increases in serum liver enzymes and bilirubin, along with elevated protein levels, indicating impaired liver function. Oxidative stress was evident from increased lipid peroxidation and decreased antioxidant enzyme activities, suggesting liver tissue damage. Histopathological analysis confirmed progressive liver degeneration, sinusoidal dilation, vacuolization, and necrosis correlating with dose. These findings demonstrate that subchronic HEX exposure causes significant hepatotoxicity in mice, characterized by biochemical alterations, oxidative damage, and structural liver injury. This study underscores the need for cautious regulation of HEX use and further investigation into its long‐term hepatic effects.
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Sharma et al. (2025) studied this question.
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