Abstract
Fipronil (FPN) is an insecticide that is widely used agriculturally or in the veterinary for controlling a variety of pests. Little mechanistic information is available on the oxidative stress and mitochondrial damage caused by FPN in the heart. The aim of this research is to study the cardiotoxic effect of FPN by evaluating oxidative stress and mitochondrial damage in the heart tissue using the isolated mitochondria. Results showed that FPN induced oxidative stress and mitochondrial dysfunction via an increase in mitochondrial reactive oxygen species (ROS) generation, lipid peroxidation (LPO), mitochondrial membrane potential (MMP) collapse, mitochondrial swelling, and cytochrome c release. According to the result, we suggest that FPN is capable to induce cardiotoxicity through mitochondrial damage and increased mitochondrial ROS generation in cardiomyocyte.
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