Subacute and subchronic methomyl exposure induced toxic effects on intestines via oxidative stress in male albino rats: biochemical and histopathological study

Chabane, K.; Khene, M'hammed Amine; Zaida, Faiza; Ainouz, Lynda; Gadrey, Jean; Mameri, Saâdia; Baz, Ahsene

doi:10.1080/01480545.2020.1727496

Cited by 8 publications

(7 citation statements)

References 46 publications

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“…Treating the mice with ME caused cardiac tissue damage as indicated by a significant rise in AST and LDH activities. These results are in agreement with Chabane et al [26]. These MEinduced elevations may be due to increased ROS production, leading to oxidative stress in tissues and thus chronic permanent damage [27].…”

Section: Discussionsupporting

confidence: 93%

Green Tea Attenuates methomyl-Induced Cardiac Toxicity Through Modulating Oxidative Stress and Nuclear Factor kappa B Up- Regulation in Mice

Manar

Omali

Rehab

et al. 2021

Egyptian Journal of Basic and Applied Sciences

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Methomyl (ME) is a carbamate insecticide that is causes a change in biochemical parameters and affects the oxidative state in the body through the production of free radicals. Herbal medicines derived from plant extracts are useful in treating many diseases, as they are considered natural antioxidants that have a protective role against toxins. This study aimed to evaluate the ability of green tea extract (GTE) to treat ME-induced cardiac toxicity in experimental animals. The experimental animals were divided into five groups. Blood and tissue were collected to estimate the biochemical parameters. ME caused significantly elevated levels of AST, LDH, NF-κB, and malondialdehyde. While a significant decrease was observed in levels of superoxide dismutase, a decrease in glutathione and glutathione-S-transferase was observed. Alterations in these biochemical markers were referred to oxidative stress-induced cardiac damage. The administration of GTE at a concentration (1.5%) to the ME treated group caused the tested biochemical parameters to appear close to those of the control group. GTE alleviates ME-induced oxidative stress in female albino mice. A higher concentration of GTE {1.5%} appears to have a better therapeutic effect than a lower concentration of extract {0.75%} in cardiac toxicity ME.

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Section: Discussionsupporting

confidence: 93%

Green Tea Attenuates methomyl-Induced Cardiac Toxicity Through Modulating Oxidative Stress and Nuclear Factor kappa B Up- Regulation in Mice

Manar

Omali

Rehab

et al. 2021

Egyptian Journal of Basic and Applied Sciences

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“…This is possibly owing to the depletion of the antioxidant molecules, due to their consumption in the process of protecting cells against reactive oxygen species generated by the lannate. These results are similar to those of [63,64]. On the other hand, TOS in orange juice-treatment groups were significantly decreased while TAC was significantly increased.…”

Section: Discussionsupporting

confidence: 91%

Therapeutic Potency of Sweet Orange Juice Over Liver Genotoxicity Induced by Pesticide Lannate in Rats

Badr

Mohamed

2020

Int J Pharm Pharm Sci

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Objective: The aim of the present investigation was to study the potential effect of sweet orange juice against liver genotoxicity induced by lannate. Methods: adult 36 female rats were divided into 6 groups: group C (control group), group L (lannate group) injected intraperitoneal (i. p.) with 1 mg/kg b. wt. lannate for one day, group J (orange juice group) orally administered a dose of 0.1 ml/10 g b. wt. of orange juice for 48 h, group J+L received the orange juice prior to lannate, group J with L received lannate in continuous with the orange juice and group L+J received lannate prior to the orange juice. Tested parameters were DNA fragmentation, micronucleus, histopathology examination and biochemical analysis. Results: it was found that, the intake of lannate caused high DNA fragmentation and significant increase (P<0.001) in the number of micronucleated polychromatic erythrocytes in the bone marrow. Furthermore, lannate exhibited some pathological changes in the liver tissues as well as a significant (P<0.001) decrease in the total antioxidative capacity (TAC) and a significant increase in the total oxidative capacity (TOC). On the other hand, orange juice administration of all treatments (pre-treatment, continuous and post-treatment) gave some amelioration against liver damage induced by lannate. While the best results were evidenced in the continuous treatment group where the juice could attenuate liver DNA fragmentation and significantly decreased (P<0.001) the number of micronucleated polychromatic erythrocytes. In addition, it improved the induced degenerative histopathological changes as well as ameliorated the changes occurred in TAC and TOC significantly (P<0.001). Conclusion: the antigenotoxic impact of orange juice against lannate was therapeutic and hence can counteract the poisonous effect of the pesticide in people who exposed to it.

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“…This is a potential limitation of our study because it allows time for exposure-associated oxidative stress to resolve and antioxidant levels to rebound through compensatory mechanisms such as Nrf2 activation. Indeed, other studies also point to a pro-oxidant role for methomyl in rats [ 13 ] and mice [ 25 ].…”

Section: Discussionmentioning

confidence: 99%

“…The methomyl stock solution was prepared in nanopure water and used daily for 18 consecutive days. The dose of methomyl was selected based on previous studies to elicit toxic effects while avoiding overt toxicity and lethality [ 11 , 12 , 13 , 14 ]. Rodent cages were divided into four groups: control (0 mg/kg methomyl), 1 mg/kg methomyl exposure, 2.5 mg/kg methomyl exposure, and 5 mg/kg methomyl exposure.…”

Section: Methodsmentioning

confidence: 99%

Investigating the Acute Metabolic Effects of the N-Methyl Carbamate Insecticide, Methomyl, on Mouse Liver

Groswald,

Gripshover,

Watson

et al. 2023

Metabolites

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Many pesticides have been identified as endocrine and metabolism-disrupting chemicals with hepatotoxic effects. However, data are limited for insecticides in the n-methyl carbamate class, including methomyl. Here, we investigate the liver and systemic metabolic effects of methomyl in a mouse model. We hypothesize that methomyl exposure will disrupt xenobiotic and intermediary metabolism and promote hepatic steatosis in mice. Male C57BL/6 mice were exposed daily to 0–5 mg/kg methomyl for 18 days. Mice were fed water and regular chow diet ad libitum. Metabolic phenotyping was performed, and tissue samples were collected. Effects were generally greatest at the highest methomyl dose, which induced Cyp1a2. Methomyl decreased whole body weight while the liver:body weight and testes:body weight ratios were increased. Hepatic steatosis increased while plasma LDL decreased. Fasting blood glucose and the glucose tolerance test area under the curve decreased along with hepatic glycogen stores. Methomyl, however, did not increase liver oxidative stress or injury. Collectively, these data demonstrate that methomyl disrupts hepatic xenobiotic and intermediary metabolism while increasing the testes:body weight ratio, suggesting that it may be an endocrine disrupting chemical. Besides methomyl’s known action in cholinesterase inhibition, it may be involved in aryl hydrocarbon receptor activation. The potential impact of n-methyl carbamate insecticides on metabolic health and diseases, including toxicant-associated steatotic liver disease (TASLD), warrants further investigation.

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Subacute and subchronic methomyl exposure induced toxic effects on intestines via oxidative stress in male albino rats: biochemical and histopathological study

Cited by 8 publications

References 46 publications

Green Tea Attenuates methomyl-Induced Cardiac Toxicity Through Modulating Oxidative Stress and Nuclear Factor kappa B Up- Regulation in Mice

Green Tea Attenuates methomyl-Induced Cardiac Toxicity Through Modulating Oxidative Stress and Nuclear Factor kappa B Up- Regulation in Mice

Therapeutic Potency of Sweet Orange Juice Over Liver Genotoxicity Induced by Pesticide Lannate in Rats

Investigating the Acute Metabolic Effects of the N-Methyl Carbamate Insecticide, Methomyl, on Mouse Liver

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