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Ginger extract ameliorates phosphamidon induced hepatotoxicity
Indian Journal of Experimental Biology
|November 10, 2015
Summary
Ginger extract (GE) effectively mitigates liver damage caused by the organophosphate pesticide phosphamidon (PHO). This safe and economical natural remedy reduces oxidative stress and apoptosis in the liver, offering a protective effect against pesticide-induced hepatotoxicity.
Area of Science:
- Toxicology
- Natural Product Chemistry
- Hepatology
Background:
- Organophosphorus (OP) compounds, widely used as pesticides, pose significant health risks.
- Phosphamidon (PHO), an OP insecticide, is known to induce hepatotoxicity.
- Oxidative stress and apoptosis are key mechanisms in PHO-induced liver injury.
Purpose of the Study:
- To investigate the protective effects of ginger extract (GE) against phosphamidon (PHO)-induced hepatotoxicity in a rat model.
- To evaluate the impact of GE on oxidative stress markers and apoptotic pathways in the liver.
Main Methods:
- GE was prepared and characterized for its antioxidant properties.
- Rats were administered a sub-lethal dose of PHO for varying durations (5-20 days).
- Four groups received simultaneous treatment with GE (1 mg/kg body weight) alongside PHO, while control groups received PHO alone.
Main Results:
- PHO administration led to increased oxidative stress markers, reactive oxygen species (ROS) generation, and DNA fragmentation in liver cells.
- GE treatment significantly attenuated these markers, indicating a reduction in oxidative stress.
- GE administration also mitigated the upregulation of apoptotic markers and reduced the incidence of apoptotic nuclei in hepatocytes.
- GE demonstrated no observable toxicity or mortality at doses up to 100 mg/kg for 30 days.
Conclusions:
- Ginger extract (GE) effectively protects against phosphamidon (PHO)-induced hepatotoxicity.
- GE ameliorates PHO-induced liver injury by reducing oxidative stress and inhibiting apoptosis.
- GE is a safe, economical, and effective natural agent for managing OP pesticide-induced liver damage.
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