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Biochemical and histopathological changes induced by different time intervals of methomyl treatment in mice liver
Fatma El-Demerdash1, Azza A Attia, Reda H Elmazoudy
1Department of Environmental Studies, Institute of Graduate Studies and Research, Alexandria University, Alexandria, Egypt. feldemerdash@yahoo.com
Abstract:
The present study was designed to evaluate the toxic effects induced by different time intervals of methomyl exposure on liver antioxidant defense system, oxidative stress, liver function biomarkers and histopathology in CD-1 mice. Ten male mice per group were assigned to one of four treatment groups. Group one served as control while group 2, 3 and 4 were orally treated with one mg methomyl/kg BW for 10, 20 and 30 days, respectively. Results obtained showed that methomyl significantly induced TBARS and decreased the activity of antioxidant enzymes, glutathione S-transferase, superoxide dismutase and catalase and the levels of reduced glutathione in mice liver. Aminotransferases and alkaline phosphatase activities were significantly decreased in liver due to methomyl administration, while the activities of these enzymes were significantly increased in serum. In addition, liver lactate dehydrogenase activity was significantly increased. On the contrary, methomyl treatment caused a significant decrease in liver acid phosphatase. The histology of mice liver treated with methomyl for 10, 20 and 30 days of duration showed dilation of central vein, sinusoids between hypertrophied hepatocytes and nuclear degeneration with mononuclear cell infiltration. In conclusion, exposure to methomyl induced toxicity and oxidative stress in mice liver via free radicals mechanism. Also, methomyl might have affected cell metabolism, cell membrane permeability and the detoxification system in liver.
Insights
Methomyl exposure causes liver damage in mice by inducing oxidative stress and altering key enzymes. This insecticide disrupts the liver
Area of Science:
- Toxicology
- Biochemistry
- Histopathology
Background:
- Pesticide exposure poses risks to organ health.
- Understanding methomyl's impact on the liver is crucial for risk assessment.
Purpose of the Study:
- To evaluate methomyl's toxic effects on the liver antioxidant defense system.
- To assess methomyl-induced oxidative stress, liver function, and histopathological changes.
- To investigate the impact of different exposure durations (10, 20, 30 days).
Main Methods:
- CD-1 mice were exposed to methomyl (1 mg/kg BW) for varying durations.
- Liver antioxidant enzymes (glutathione S-transferase, superoxide dismutase, catalase), reduced glutathione, and TBARS were measured.
- Liver function biomarkers (aminotransferases, alkaline phosphatase, lactate dehydrogenase, acid phosphatase) were analyzed.
- Liver histopathology was examined.
Main Results:
- Methomyl significantly increased TBARS and decreased antioxidant enzyme activities and reduced glutathione levels.
- Liver enzyme activities decreased, while serum enzyme activities increased, indicating liver damage.
- Histopathological analysis revealed liver tissue damage, including central vein dilation and hepatocyte degeneration.
Conclusions:
- Methomyl exposure induces significant liver toxicity and oxidative stress in mice through a free radical mechanism.
- Methomyl disrupts liver cell metabolism, membrane permeability, and detoxification processes.
- The findings highlight the potential hepatotoxicity of methomyl with prolonged exposure.
