The influence of anilinopyrimidine and carbamate derivatives on the rat redox status

Author:

Rakitskii Valerii N.1ORCID,Masaltsev Gleb V.1ORCID,Veshchemova Tatiana E.1ORCID,Chhvirkija Elena G.1ORCID,Lokhin Konstantin B.1ORCID

Affiliation:

1. Federal scientific center of hygiene named after F.F. Erisman

Abstract

Introduction. Oxidative stress can occur as the response to the toxic effects of pesticides. A study of the effect of two generic pesticides on the enzymes of the antioxidant defense system of warm-blooded animals was carried out within the framework of chronic food exposure. Material and Methods. 90 conventional male rats were kept in the vivarium of the Federal scientific center of hygiene named after F.F. Erisman for a year. Test objects including fungicide of the anilinopyrimidines class (compound A) and insecticide from of the carbamates class (compound B) were introduced into animal feed at doses of 0; 2; 20; 120 and 240 mg/kg body weight and 0; 2.5; 5 and 20 mg/kg body weight, respectively. Doses corresponded to the ranges found in the reports by the Joint Meeting of the FAO/WHO Meeting on Pesticide Residues for the original compounds in chronic toxicity studies. The effect of the studied compounds on the general antioxidant status (the activity of enzymes: superoxide dismutase (SOD), glutathione peroxidase (GPO), glutathione reductase (GR) and catalase (CAT)) was assessed at 3, 6, 9, and 12 months. Results. The test objects caused statistically significant changes in enzyme activity as early as at 3 months of the treatment, compared with animals of the concurrent negative control. For the compound A: a statistically significant dose-dependent increase in the activity of GR (Rho = 0.381, p = 0.017) and GAP (Rho = 0.355, p = 0.024), but not SOD and CAT, was recorded at 12 months. The compound B caused a statistically significant dose-dependent increase in SOD activity at 9 and 12 months (Rho = 0.491, p = 0.006; Rho = 0.506, p = 0.003) Conclusion. These observations indicate that compounds A and B could promote lipid peroxidation. Oxidative burst was registered in response to the influence of the compound B, which may have been caused by apoptosis of T-lymphocytes.

Publisher

Federal Scientific Center for Hygiene F.F.Erisman

Subject

Health, Toxicology and Mutagenesis,Public Health, Environmental and Occupational Health,Pollution,General Medicine

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