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Role of selenium on antioxidant capacity in methomyl-treated mice

Papel del selenio sobre la capacidad antioxidante en ratones tratados con metomil

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Abstract

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 μmole/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.

Resumen

El carbamato metomil es un pesticida ampliamente utilizado en el control de insectos. Se estudia en el presente trabajo el efecto del selenio sobre los procesos antioxidantes en ratones tratados con metomil. A ratones albinos Swiss se les inyectó una dosis única por vía intraperitoneal de metomil (7 mg/Kg peso corporal) y a un grupo de ellos se les había inyectado 7 días antes selenito sódico (5 micromoles/Kg p.c.). La administración de metomil produce, tras 24 horas, aumento de la actividad láctico deshidrogenase (LDH) y disminución de la capacidad antioxidante en células hepáticas, estimada por las actividades superóxido dismutasa (SOD), catalasa (CAT), glutation reductasa (GR) y glutation-S-transferasa (GST) y por el contenido en glutation (GSH). Esto parece indicar que la toxicidad del metomil se relaciona con daño peroxidativo en las membranas de las células esplénicas, renales y hepáticas. Además, tambien se observan en esos órganos alteraciones en el DNA. La administración previa de selenio protege de los efectos del metomil. El selenio aumenta la capacidad antioxidativa endógena celular por incremento de las actividades SOD, CAT, GR y GST asi como del contenido en GSH. La actividad LDH en sangre disminuye, asi como el daño en el DNA, hasta valores comparables a los controles. En suma, el selenio protege de los efectos adversos del metomil en el ratón.

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References

  1. Abdollahi, M., Rahmat-Jirdeh, N. and Soltaninejad, K. (2001):Hum. and Exper. Toxicol.,20, 28–33.

    Article  CAS  Google Scholar 

  2. Abdollahi, M., Ranjbar, A., Shadnia, S. and Nikfar, S. (2004):Med. Sci. Monit. 10, RA141–147.

    CAS  PubMed  Google Scholar 

  3. Aebi, H. (1984): “Catalase. In: Methods in enzymatic analysis”, Vol. 3, Bergmeyer, HU. Eds. Academic Press, New York.

    Google Scholar 

  4. Aron, C. K. and Howland, M. A. (1998): “Insecticides: Organophosphates and carbamates In: Goldfank Toxicology Emergencies”, 6th ed, Appleton and Lange, New York, London, Sydney, Toronto, Tokyo, New Jersey.

    Google Scholar 

  5. Banerjee, B. D., Seth, V. and Bhattacharya, A. (1999):Toxicol. Lett.,107, 33.

    Article  CAS  PubMed  Google Scholar 

  6. Beckett, G. J. and Arthur, J. R. (2005):J. Endocrinol.,184, 455–465.

    Article  CAS  PubMed  Google Scholar 

  7. Beutler, E. (1982): “Red cell metabolism. A manual of biochemical methods” Grune and Stratton, New York.

    Google Scholar 

  8. Cesarone, C. F., Bolognesi, C. and Santi, L. (1979):Ann. Biochem.,100, 188–197.

    Article  CAS  Google Scholar 

  9. Habig, W. H., Pabst, M. J. and Jakoby W. B. (1974):J. Biol. Chem.,249, 7130–7139.

    CAS  PubMed  Google Scholar 

  10. Hazarika, A., Sarkar, S. N. and Kataria, M. (2001):Indian J Exp. Biol.,39, 1113.

    CAS  PubMed  Google Scholar 

  11. Horn, H. D. (1971): “Glutathione reductase. In: Methods of enzymatic analysis” Bergmeyer HU, ed., Academic Press, New York.

    Google Scholar 

  12. Hulla, J. E., Miller, M. S. and Taglor, J. A. (1999):Toxicol. Sci.,51, 317.

    Article  CAS  Google Scholar 

  13. Kahler, W., Kuklinski, B., Ruhlmann, C. and Plotz, C. (1993):Z. Cesamte. Inn. Med.,18, 223–232.

    Article  Google Scholar 

  14. Lohinay, O. and Sinhaseni, P. (1998):Arh. Hig. Rada. Toksikol.,49, 231–238.

    Google Scholar 

  15. Lowry, O., Rosebrough, N., Fare, A. and Randall, R. (1951):Int. J. Tiss. React. 4, 153–139.

    Google Scholar 

  16. Moss, D. W., Hendersen, A. R. and Kachmar, J. R. (1986): In: Textbook of clinical chemistry”. Tietz NW. ed. Philadelphia, PA: WB Saunders.

    Google Scholar 

  17. Nishikimi, M., Rao, N. and Yagi, K. (1972):Biochem. Biophys. Res. Commun.,46, 844–853.

    Article  Google Scholar 

  18. Pajoumand, A., Jalali, N., Abdollahi, M. and Shadnia, S. (2002):J. Pharm. Pract. Res.,32, 297–299.

    Google Scholar 

  19. Pree, D. J., Whitty, K. J., Bittner, L. A. and Pogoda, M. K. (2003):Pest. Manag. Sci.,59, 79–84.

    Article  CAS  PubMed  Google Scholar 

  20. Ranjbar, A., Pasalar, P. and Abdollahi, M. (2002):Hum. Exp. Toxico.,21, 179–82.

    Article  CAS  Google Scholar 

  21. Sargent, E. V., Sina, J. F. and Barnum, J. E. (1999):Drug Chem. Toxicol.,22: 583.

    Article  CAS  PubMed  Google Scholar 

  22. Shen, H. M., Shi, C. Y., Lee, H. P. and Ong, C. N. (1991):Toxicol. Appl. Pharmacol.,127, 145–150.

    Article  Google Scholar 

  23. Shou, J., Osman, A. F. and Multani, A. S. (2002):Oncogen.,21, 878.

    Article  CAS  Google Scholar 

  24. Suramana, T., Sindhuphak, R. and Dusitsin, N. (2001):Sci. Total Environ.,270, 103.

    Article  CAS  PubMed  Google Scholar 

  25. Thapar, A., Sandhir, R. and Kiran, R. (2002):Indian J Ezp Biol.,40, 963–966.

    CAS  Google Scholar 

  26. Tsai, M. J., Wu, S. N., Cheng, H. A., Wang, S. H. and Chiang, H. T. (2003):J. Toxicol. Clin. Toxicol.,41, 969–973.

    Article  CAS  PubMed  Google Scholar 

  27. Tsatsakis, A. M., Tutudaki, M. I. and Tzatzarakis, M. N. (1998):Vet. Hum. Toxicol.,40, 200.

    CAS  PubMed  Google Scholar 

  28. Whanger, P. D. (2001):Nutr Neurosci.,4: 81–97.

    CAS  PubMed  Google Scholar 

  29. WHO.Environmental Health Criteria, 1996:178, 29.

    Google Scholar 

  30. Zeljezic, D. and Garaj-Vrhovac, V. (2001):Mutag.,16, 359.

    Article  CAS  Google Scholar 

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Correspondence to Ali Y. El-Khawaga.

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El-Khawaga, A.Y. Role of selenium on antioxidant capacity in methomyl-treated mice. J. Physiol. Biochem. 61, 501 (2005). https://doi.org/10.1007/BF03168375

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