Abstract

Exposure to mixtures of toxicants (e.g., pesticides) is common in real life and a subject of current concern. The present investigation was undertaken to assess some toxicological effects in male rats following exposure to methomyl (MET), abamectin (ABM), and their combination (MET+ABM), and to evaluate the ameliorative effect of zinc co-administration. Three groups of rats were designated for MET, ABM, and the mixture treatments. Three other groups were designated for zinc in conjunction with the pesticides. Additionally, one group received water only (control), and the other represented a positive zinc treatment. The obtained results revealed that MET was acutely more toxic than ABM. The tested pesticides induced significant elevation in lipid peroxidation and catalase levels, while declined the levels of the other tested parameters e.g., Superoxide dismutase (SOD), Glutathione-S-transferase (GST), Glutathione peroxidase (GPx), Glutathione reductase (GR), Cytochrome P450 (CYP450), testosterone, and thyroxine). Biochemical alterations induced by the mixture were greater than those recorded for each of the individual insecticides. The joint action analysis, based on the obtained biochemical data, revealed the dominance of antagonistic action among MET and ABM. Zinc supplementation achieved noticeable ameliorative effects. It was concluded that zinc may act as a powerful antioxidant, especially in individuals who are occupationally exposed daily to low doses of such pesticides.

Highlights

  • Methomyl, S-methyl N-(methylcarbamoyloxy) thioacetimidate (C5 H10 N2 OS), is an oximecarbamate insecticide produced by DuPont since 1966

  • The estimated oral LD50 for methomyl (MET) and abamectin (ABM) against the used male rats indicated that MET was more toxic (17.0 mg/kg b.w.) than ABM (20.3 mg/kg b.w.)

  • The results of the present study revealed that MET was acutely more toxic than ABM to male rats

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Summary

Introduction

S-methyl N-(methylcarbamoyloxy) thioacetimidate (C5 H10 N2 OS), is an oximecarbamate insecticide produced by DuPont since 1966. It is used widely for controlling insect pests on fruits, vegetables, vines, grains, soybeans, and cotton all over the world [1]. The N-methyl carbamate insecticides, such as methomyl, inhibit acetylcholinesterase (ChE) activity, inducing cholinergic overstimulation, and autonomic and neuromuscular dysfunction. At high doses, it causes coma and death [2]. It has been reported that methomyl is capable of inducing oxidative damage and lipid peroxidation in vitro in rat erythrocytes [4]

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