Abdel-Razik, R., Mosallam, E., Hamed, N. (2022). Deterioration of Cytochrome C Content and Mitochondrial Dysfunction in Brain of Male Rats after Sub-Chronic Exposure to Thiamethoxam and Protective Role of N- Acetylcysteine. EKB Journal Management System, 43(1), 91-106. doi: 10.21608/asejaiqjsae.2022.223119
Reda Khamis Abdel-Razik; Eman Mohamad Mosallam; Nadia A Hamed. "Deterioration of Cytochrome C Content and Mitochondrial Dysfunction in Brain of Male Rats after Sub-Chronic Exposure to Thiamethoxam and Protective Role of N- Acetylcysteine". EKB Journal Management System, 43, 1, 2022, 91-106. doi: 10.21608/asejaiqjsae.2022.223119
Abdel-Razik, R., Mosallam, E., Hamed, N. (2022). 'Deterioration of Cytochrome C Content and Mitochondrial Dysfunction in Brain of Male Rats after Sub-Chronic Exposure to Thiamethoxam and Protective Role of N- Acetylcysteine', EKB Journal Management System, 43(1), pp. 91-106. doi: 10.21608/asejaiqjsae.2022.223119
Abdel-Razik, R., Mosallam, E., Hamed, N. Deterioration of Cytochrome C Content and Mitochondrial Dysfunction in Brain of Male Rats after Sub-Chronic Exposure to Thiamethoxam and Protective Role of N- Acetylcysteine. EKB Journal Management System, 2022; 43(1): 91-106. doi: 10.21608/asejaiqjsae.2022.223119
Deterioration of Cytochrome C Content and Mitochondrial Dysfunction in Brain of Male Rats after Sub-Chronic Exposure to Thiamethoxam and Protective Role of N- Acetylcysteine
1Pesticides Toxicity to Mammals and Aquatic Organisms, Central Agricultural Pesticide Lab., Agricultural Research Center, Alexandria, Egypt
2Mammalian & Aquatic Toxicology Department, Central Agricultural Pesticide Laboratory, Agricultural Research Center, Alexandria, Egypt
3Mammalian & 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.