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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 Mg 2+ ATPase complexes as 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.

1,1-bis (p-chlorophenyl)-2, 2, 2-trichloroethane (DDT) has been used for control of malaria mosquitoes and other insect vectors of human diseases since 1945. Its use poses an environmental dilemma and efforts to replace it have been hampered by lack of information about its molecular target. This work identifies the 23 kDa band responsible for the DDT sensitivity in bees, as the OSCP and subunit "d" of the ATP synthase. The OSCP of the bee's ATP synthase contained 207 amino acids compared to 190 in bovine, which is insensitive to DDT, and the identities were only 47%. Subunit "d" of the bees had no counterpart in the bovine. Whether DDT is interacting only with OSCP, only with subunit "d", or with both subunits, remains to be assessed. Identification of the molecular target of DDT will lead the way to new target based insecticides aimed to protect plant, combat malaria and other insect transmitted diseases.

The biochemical, oxidative DNA damage, and the histological alterations associated with thiamethoxam (MX) exposure, a second-generation neonicotinoid broadly used in Egyptian agriculture, were assessed. Also, the role of N-acetylcysteine (NAC), (150 mg/kg/ day) on the adverse effect of MX was investigated. Rats were orally preserved with a sub-lethal dose (1/50 LD 50 ) of MX at 31.26 mg/kg/day, five doses/week for 28 days. The MX exposure resulted in a significant decrease in rats' body weight, protein concentration of both serum and urine, sera catalase (CAT), and glutathione peroxidase (GPx) activities compared to control. In addition increase in sera creatinine, urea, bilirubin, alkaline phosphatase (ALP), superoxide dismutase (SOD), and malondialdehyde (MDA) levels were observed. While the assessment of DNA damage revealed significant altitude in 8-hydroxy-2'-deoxyguanosine (8-OH-2DG) levels in both serum and urine samples. The present findings were supported by microscopic observation of liver and kidney tissues. Evidently, thiamethoxam can damage liver and kidney functions impaired the DNA, and cause histoarchitecture lesions in rats at the tested sublethal dose. In addition, NAC supplementation significantly attenuated of MX adverse effect which reflects its protective influence against MXinduced hepatic-nephrotoxicity.