Role of vitamin E in mitigating methomyl induced acute toxicity in blood of male Wistar rats.

The present study was designed to evaluate the protective potential of vitamin E, if any, in attenuating the toxic effects induced by acute methomyl treatment in rats. Male Wistar rats, weighing between 230 and 250 g, received either a single oral dose of 9 mg/kg of methomyl, vitamin E alone injected intraperitoneally on alternate days (4 injections) at 50 mg/kg body for 1 week prior to methomyl treatment, or both methomyl plus vitamin E given in a similar manner. The effects of different treatments were studied on lipid peroxidation (LPO), reduced glutathione (GSH) and antioxidant enzymes, which included superoxide dismutase (SOD), glutathione-s-transferase (GST), glutathione reductase (GR), glutathione peroxidase (GSHPx) and catalase and various hematological parameters, including total leucocytes count (TLC), differential leukocyte count (DLC), hemoglobin, platelets counts, red cell counts, and scanning electron microscopy (SEM). Acute 24-h treatment to rats resulted in a significant increase in the LPO. GSH levels and the activities of catalase, GST, and GSHPx were found to be significantly decreased following methomyl treatment. A significant elevation in the activity of SOD and in TLC was also observed after 24 h of methomyl treatment. Further, a significant increase in the neutrophils and eosinophil counts was also observed. However, lymphocytes showed a significant decrease following methomyl treatment. SEMs showed significant morphological changes following methomyl treatment. Vitamin E pretreatment to methomyl-treated rats effectively normalized the levels of LPO and GSH. Vitamin E could also significantly elevate the activity of catalase, increase platelets counts and TLC, and normalized the activities of SOD and GSHPx. Vitamin E pretreatment improved the morphology of the red blood cells. The study concludes that vitamin E affords protection in methomyl-induced toxicity in the rat.

Rate of degradation of lambda-cyhalothrin and methomyl in grapes (Vitis vinifera L.).

Rates of degradation of lambda-cyhalothrin and methomyl residues in grape are reported. The dissipation behavior of both insecticides followed first-order rate kinetics with similar patterns at standard and double-dose applications. Residues of lambda-cyhalothrin were lost with pre-harvest intervals (PHI) of 12.0-12.5 and 15.0-15.5 days, corresponding to the applications at 25 and 50 g a.i. ha-1, respectively. In the case of methomyl, residues were lost with PHI of 55.0 and 61.0 days, following applications at 1 and 2 kg a.i. ha-1, respectively. The PHI, recommended on the basis of the experimental results, was shown to be effective in minimizing residue load of these insecticides below their maximum residue limits (MRLs) in vineyard samples.

Role of selenium on antioxidant capacity in methomyl-treated mice.

Methomyl carbamate is a pesticide widely used in the control of insects. The present work aims at studying the effect of selenium on the antioxidant system of methomyl-treated mice. Swiss albino mice were intraperitoneally administered a single dose of methomyl (7 mg/Kg body weight). Mice of another group were injected with sodium selenite (5 pmole/Kg b.wt.) 7 days before methomyl intoxication. After 24 hours, methomyl exposure resulted in significant increase in lactic dehydrogenase activity (LDH). The antioxidant capacity of hepatic cells in terms of the activities of superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), glutathione-S-transferase (GST) and glutathione (GSH) content was diminished. It appears that methomyl exerts its toxic effect via peroxidative damage to hepatic, renal and splenic cell membranes. Also, methomyl induced DNA damage in these organs as detected by alkaline filter elution technique. The distribution of methomyl in different organs of mice was detected by HPLC. Selenium administration prior to methomyl injection produced pronounced protective action against methomyl effects. It is observed that selenium enhances the endogenous antioxidant capacity of the cells by increasing the activities of SOD, CAT, GR and GST as well as increasing GSH content. The activity of LDH was decreased in blood and the damage of DNA was suppressed comparable to controls. In conclusion, the adverse effects of methomyl in mice could be ameliorated by selenium.

Assessment of the ability of propoxur, methomyl, and aldicarb, three carbamate insecticides, to induce micronuclei in vitro in cultured Chinese hamster ovary cells and in vivo in BALB/c mice.

Three carbamate insecticides (propoxur, methomyl, and aldicarb) were evaluated for their ability to induce micronuclei (MN) in vitro using cultured Chinese hamster ovary (CHO) cells, and in vivo in mouse bone marrow erythrocytes. In vitro, all three insecticides induced a significant increase in micronucleated binucleate cells, which was generally both dose and sample time dependent. The in vivo studies involved treating male BALB/c mice by different routes, either once or on 3 consecutive days, followed by multiple or single sampling. Treatment by intraperitoneal injection or oral gavage induced a significant increase in micronucleated reticulocytes (MNRETs) in peripheral blood. For all three chemicals, the MN response depended on sample time and the number of treatments, while for aldicarb, the response depended also on the route of exposure. These positive results demonstrate that propoxur, methomyl, and aldicarb are capable of inducing structural and/or numerical chromosomal aberrations in mammalian cells either in vitro or in vivo. Furthermore, based on the results obtained, on optimal in vivo MN protocol for carbamate insecticides is a single treatment followed by blood sampling at 24 and 48 hr after treatment.

Genotoxic effects of the carbamate insecticide, methyomyl. II. In vivo studies with pure compound and the technical formulation, "Lannate 25".

The carbamate insecticide, methomyl, and the methomyl-containing technical formulation, "Lannate 25", were tested for the induction of DNA damage in vivo. Swiss CD1 mice were treated intraperitoneally with test substances and the following tests were performed: alkaline elution of liver and kidney DNA, 8-hydroxyguanosine detection in liver DNA, and 32P-postlabelling analysis of DNA adducts in liver DNA. The clastogenic activity of the two pesticide preparations was also evaluated as micronucleus frequency in bone marrow. No DNA adducts were detected in liver DNA of mice treated with pure methomyl, while a dose-related increase in DNA adducts was found in Lannate 25-treated animals. All other tests were positive with both methomyl and Lannate 25. A summary of genotoxic activity of methomyl is also presented. The hypothesis that the observed genotoxic effects of methomyl are induced indirectly, through formation of active oxygen species, is discussed.

Cardiac toxicity following short-term exposure to methomyl in spraymen and rabbits.

A health surveillance study in 22 healthy spraymen showed significant T-wave changes (including inversion) in most of the limb leads and chest leads following 5 d exposure to methomyl, a carbamate pesticide. Significant changes in plasma cholinesterase and lactic dehydrogenase activities were also noticed. The ECG changes could be reproduced in rabbits and were dose dependent. This type of ECG change following exposure to a carbamate compound is reported for the first time in occupationally-exposed subjects. The study results indicate that these changes are probably directly related to methomyl rather than its toxicity through cholinesterase inhibition. The significance of these changes remain to be investigated.

Cumulative toxicity potential of methomyl aerosol by repeated inhalation.

There are few investigations concerning the cumulative toxicity of agricultural chemicals by repeated inhalation. In this study, Wistar male rats were exposed to methomyl powder (mass median aerodynamic diameter, 4.4 microns) for a single 4-hr exposure, or for 4 hr/day, 5 days/week for 3 months. The average exposure concentrations were controlled at 9.9 mg/m3 for the single exposure and at 14.8 mg/m3 for repeated exposures by a dust generator consisting of a continuous fluidized bed with an overflow pipe and a screw feeder. After the repeated exposures, plasma and red cell cholinesterase activities, and lipid concentrations of the rat lungs were measured and histopathological examinations were performed. There was no evidence of cumulative effects on the red cell cholinesterase activity, histopathological changes and lipid concentration in 3-month repeated inhalation.