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Melatonin treatment prevents modulation of cell-mediated immune response induced by propoxur in rats.
Indian J Biochem Biophys ; 2008 Aug; 45(4): 278-81
Article en En | IMSEAR | ID: sea-28025
The effect of melatonin, a major secretory product of the pineal gland, in attenuation of propoxur (2-isopropoxy phenyl N-methyl carbamate)-induced modulation of cell-mediated immune (CMI) response was studied in rats. Male Wistar albino rats were exposed to propoxur (a widely used pesticide) orally (10 mg/kg) and/or melatonin (10 mg/kg) orally for 4 weeks. CMI was measured by delayed-type hypersensitivity (DTH), leucocyte and macrophage migration inhibition (LMI and MMI) responses and estimation of cytokines TNF-alpha and IFN-gamma levels. Rats exposed to propoxur for 4 weeks showed significant decrease in DTH, LMI and MMI responses. Propoxur also suppressed TNF-alpha and IFN-gamma production significantly. Administration of melatonin alone caused a significant increase in DTH response. Although there were no changes in the LMI and MMI response, the cytokine levels were significantly increased, as compared to control. Co-administration of melatonin along with propoxur significantly nullified the effect of the pesticide on the CMI response, except DTH and reversed levels of cytokines to near control/normal values. Thus, melatonin treatment considerably attenuated immunomodulation caused by sub-chronic treatment of propoxur in experimental animals.
Asunto(s)
Texto completo: 1 Índice: IMSEAR Asunto principal: Plaguicidas / Propoxur / Glándula Pineal / Ratas / Factores de Tiempo / Masculino / Administración Oral / Citocinas / Factor de Necrosis Tumoral alfa / Ratas Wistar Idioma: En Revista: Indian J Biochem Biophys Año: 2008 Tipo del documento: Article
Texto completo: 1 Índice: IMSEAR Asunto principal: Plaguicidas / Propoxur / Glándula Pineal / Ratas / Factores de Tiempo / Masculino / Administración Oral / Citocinas / Factor de Necrosis Tumoral alfa / Ratas Wistar Idioma: En Revista: Indian J Biochem Biophys Año: 2008 Tipo del documento: Article