Toxicity of Fipronil on Rat Brain Mitochondria
- سال انتشار: 1398
- محل انتشار: پانزدهمین همایش سراسری سم شناسی ایران
- کد COI اختصاصی: TOXICOLOGY15_093
- زبان مقاله: انگلیسی
- تعداد مشاهده: 393
نویسندگان
Department of Pharmacology and Toxicology, Faculty of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran
Department of Pharmacology and Toxicology, Faculty of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran
Department of Pharmacology and Toxicology, Faculty of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran
Department of Pharmacology and Toxicology, Faculty of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran
چکیده
Introduction: Fipronil is an insecticide that is widely used agriculturally or in the veterinary for controlling a variety of pests, such as cock-roaches, mosquitoes, grasshoppers, fleas, ticks and lice .It belongs to the new generation of insecticides that have been developed to reduce damage to the environment and mammals. The 2017 Fipronil eggs contamination is an incident in Europe and Asia involving the spread of Fipronil insecticide which contaminated human consumed chicken eggs and egg products. Little data on mechanisms involved in Fipronil induced toxicity are available especially on brain.Methods: Therefore, we decided to explore the mechanisms of Fipronil neurotoxicity by using mitochondria isolated from rat brain. The isolated brain mitochondria were incubated with different concentration of Fipronil (6,12, and 24 μM) . The activity of complexӀӀ through the MTT assay, mitochondrial swelling, mitochondrial membrane potential (MMP) collapse, reactive oxygen species (ROS) formation and cytochrome c release were assessed to investigate Fipronil neurotoxicity on isolated rat brain mitochondria.Results: Our results showed that IC50 of Fipronil was assigned approximately 12μM. Exposure to Fipronil showed a marked elevation in oxidative stress accompanied by disturbance in function in MTT test as compared to control group. Results showed that Fipronil induced mitochondrial dysfunction via an increase in mitochondrial ROS production and membrane potential collapse, which correlated to cytochrome c release. Also mitochondrial membrane collapse led to mitochondrial swelling.Conclusion: According to the results, we suggest that Fipronil induced neurotoxicity is the result of ROS-mediated apoptosis signaling in neuron.کلیدواژه ها
Fipronil; ROS; Brain Mitochondria, Neurotoxicity, Apoptosisمقالات مرتبط جدید
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