Document Type : Original Article
Authors
1
Pesticides Toxicity to Mammals and Aquatic Organisms, Central Agricultural Pesticide Lab., Agricultural Research Center, Alexandria, Egypt
2
Mammalian & Aquatic Toxicology Department, Central Agricultural Pesticide Laboratory, Agricultural Research Center, Alexandria, Egypt
3
Mammalian & Aquatic Toxicology Department, Central Agricultural Pesticide Laboratory, Agricultural Research Center, 21616 -El-Sabahia, Alexandria, Egypt
Abstract
Mitochondria sustain healthy brain function. Herein we aimed to evaluate the thiamethoxam (MX) effect on the rat brain mitochondria in addition to the protective role of N-acetylcysteine (NAC) against MX harmful effects. Thiamethoxam was administered orally with five doses each week for 28 days to male albino rats at 1/50 of the LD50 (31.26 mg/kg bw). The results demonstrated that the thiamethoxam neurotoxicity was confirmed by the significant rising in acetylcholinesterase, and lactate dehydrogenase activities of plasma. A significant increase in mitochondrial antioxidants as superoxide dismutase and reduced glutathione was found. Also, significant induction of the oxidative stress and DNA damage via rising the malondialdehyde, and 8-hydroxy-2'-deoxyguanosine biomarkers was recorded by 32.5% and 118.61% respectively. Substantial depression in mitochondrial NADH dehydrogenase, cytochrome c reductase, cytochrome c oxidase, and Mg2+ ATPase complexesas well as 23 % cerebral infarction was manifested by histological evaluation using the dehydrogenase activity indicator, 2, 3, 5-triphenyl tetrazolium chloride staining. In conclusion, MX can pose a hazard to the integrity and functioning of rats' brain mitochondria, perhaps leading to neurodegenerative disorders. Additionally, earlier treatment of the synthetic antioxidant N-acetylcysteine could prove beneficial in combating the harmful effects of thiamethoxam.
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