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• W2275896570 abstract "Oxidative stress and mitochondrial dysfunction are thought to be the main mechanism of T-2 toxin toxicity. T-2 toxin is the most potent trichothecene mycotoxin which is present in agricultural products. L-carnitine, besides its anti-oxidative properties, facilitates the transportation of long-chain fatty acids in to mitochondrial matrix.In this study we tested whether L-carnitine, an antioxidant and a facilitator for long-chain fatty acid transportation across mitochondrial membranes, could protect rat hepatocytes against toxicity induced by T-2 toxin.L-carnitine in low and high doses (50 and 500 mg/kg) was administered for five consecutive days to male Wistar rats. Hepatocytes were isolated and freshly exposed to appropriate concentration of T-2 toxin for 2 h followed by oxidative stress and cell death evaluations.Glutathione depletion, ROS overproduction and mitochondrial membrane potential collapse were determined under T-2 toxin exposure. Pretreatment with L-carnitine particularly at high-dose reduced toxicity and prevented the hepatocytes from abnormal caspase-3 activity and apoptosis.Low toxicity of L-carnitine and its mitochondrial protective effects promises an effective way to reduce or prevent the toxicity induced by certain environmental pollutants, including T-2 toxin." @default.
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• W2275896570 date "2016-02-18" @default.
• W2275896570 modified "2023-10-16" @default.
• W2275896570 title "<scp>l</scp>-carnitine protects rat hepatocytes from oxidative stress induced by T-2 toxin" @default.
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• W2275896570 doi "https://doi.org/10.3109/01480545.2016.1141423" @default.
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