Mitochondrial dysfunction and oxidative stress in liver of male albino rats after exposing to sub-chronic intoxication of chlorpyrifos, cypermethrin, and imidacloprid

Taha, Taha A.; Badawy, Mohamed E.I.; Abdel-Razik, Reda; Younis, Hassan M.; Abo-El-Saad, Mahmoud M.

doi:10.1016/j.pestbp.2021.104938

Cited by 29 publications

(15 citation statements)

References 79 publications

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“…Yan et al (2016) Also found that MX caused oxidative stress in zebrafish livers, as seen by increased SOD, CAT, and GPx activity. Moreover, Taha et al (2021) reported that chlorpyrifos, cypermethrin, and imidacloprid cause oxidative stress by forming free radicals, suggesting a dysfunction of the mitochondrial respiratory chain. In contrast, Akbel et al (2018) recorded decreased SOD activity in brain tissues of malathion exposed rats.…”

Section: Discussionmentioning

confidence: 99%

“…Imidacloprid interacts exclusively with FoF1-ATP synthase, resulting in functional inhibition of the enzyme and impaired the mitochondrial bioenergetics (Bizerra et al, 2018). In addition, chlorpyrifos, cypermethrin, and imidacloprid induced hepatomitochondrial dysfunction in male albino rats as a result of the treatments by the 1/50 of the LD50 of each insecticide (Taha et al, 2021).…”

Section: Introductionmentioning

confidence: 99%

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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

Abdel-Razik

Mosallam

Hamed

2022

Alexandria Science Exchange Journal

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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.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

Abdel-Razik

Mosallam

Hamed

2022

Alexandria Science Exchange Journal

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“…Moreover, the total adenylate energy charge AEC; a reliable ratio representing cellular energy status (Abd‐Allah, Nasr, et al, 2020; Abdel Jaleel et al, 2020), was decreased in both the cardiac and hepatic tissue. Besides, the level of 8‐OHdG indicating oxidative DNA damage (Harris et al, 2021; Saleh et al, 2017; Taha et al, 2021; Yamada et al, 2020) was increased in both the hepatic and cardiac tissues. Finally, oxidative and nitrosative stresses were evident, representing a general state of hepatic and cardiac injury.…”

Section: Discussionmentioning

confidence: 99%

Curcumin nanoemulsion counteracts hepatic and cardiac complications associated with high‐fat/high‐fructose diet in rats

Mohamed

Nasr

Ibrahim

et al. 2022

Journal of Food Biochemistry

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The relationship between the incidence of cardiovascular abnormalities and non‐alcoholic fatty liver disease (NAFLD) has long been postulated. Curcumin (CUR) is a potential anti‐atherosclerotic agent but its poor water solubility hinders its pharmacological use. Therefore, the present study aimed to investigate the effect of formulation of CUR nanoemulsion prepared using the spontaneous emulsification technique on high fat high fructose (HFHF)‐induced hepatic and cardiac complications. Fifty Wistar rats were divided into five groups. CUR nanoemulsion at doses of 5 and 10 mg/kg and conventional powdered CUR at a dose of 50 mg/kg were orally administered daily to rats for two weeks, and compared with normal control and HFHF control. Results revealed that the high dose level of CUR nanoemulsion was superior to conventional CUR in ameliorating the HFHF‐induced insulin resistance status and hyperlipidemia, with beneficial impact on rats' recorded electrocardiogram (ECG), serum aspartate aminotransferase (ALT) and alanine aminotransferase (AST) levels, leptin, adiponectin, creatine phosphokinase, lactate dehydrogenase and cardiac troponin‐I. In addition, hepatic and cardiac oxidative and nitrosative stresses, oxidative DNA damage and disrupted cellular energy statuses were counteracted. Results were also confirmed by histopathological examination. Practical applications The use of curcumin nanoemulsion could be beneficial in combating hepatic and cardiac complications resulting from HFHF diets.

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“…Flow cytometry was applied to detect the content of intracellular ROS in L02 cells, and it was found that GSLS significantly reduced the accumulation of intracellular ROS and delayed the apoptosis process. As the main site of intracellular reactive oxygen species, mitochondria exerts a key role in metabolism and energy regulation [ 36 ].…”

Section: Discussionmentioning

confidence: 99%

Ros-mediated mitochondrial oxidative stress is involved in the ameliorating effect of ginsenoside GSLS on chlorpyrifos-induced hepatotoxicity in mice

Pei

Liu

Zeng

et al. 2022

Aging

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Chlorpyrifos (CPF), as an extensively used organophosphorus pesticide, often remains on food surfaces or contaminates water sources. CPF can cause many toxic effects on human production and life. As an additional product of non-medicinal parts of ginseng, the pharmacological activity of ginseng stem and leaf total saponin (GSLS) has been verified and applied in recent years. This study aimed to evaluate the protective effect of GSLS on CPF-induced liver damage in mice. Experimental results in vivo demonstrate that GSLS can reduce the accumulation of oxidation product MDA by relieving CPF-induced liver function indicators in mice and enhancing the antioxidant enzyme SOD and CAT activities of mice. With the decrease in mRNA expression of BAX, NF-KB, and TIMP in liver tissues, the mRNA expression of Nrf-2, HO-1, and XIAP increased. GSLS can alleviate CPF-induced liver toxicity through anti-inflammatory, antioxidant, and anti-inflammatory. In vitro experiments have proved that GSLS can show the ability to scavenge DPPH free radicals and hydroxyl radicals. In addition, GSLS can alleviate chlorpyrifos-induced ROS accumulation in L02 cells, alleviating cytokinetic potential reduction. In summary, by fighting oxidative stress, GSLS can alleviate liver damage caused by CPF.

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Mitochondrial dysfunction and oxidative stress in liver of male albino rats after exposing to sub-chronic intoxication of chlorpyrifos, cypermethrin, and imidacloprid

Cited by 29 publications

References 79 publications

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

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

Curcumin nanoemulsion counteracts hepatic and cardiac complications associated with high‐fat/high‐fructose diet in rats

Ros-mediated mitochondrial oxidative stress is involved in the ameliorating effect of ginsenoside GSLS on chlorpyrifos-induced hepatotoxicity in mice

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