Hoijman Kleinman, EstebanRocha Viegas, LucianaKeller Sarmiento, María InésRosenstein, Ruth E.Pecci, Adali2022-06-142022-06-142004-010013-7227https://hdl.handle.net/2445/186609The antiapoptotic effect of melatonin has been described in several systems. In this study, the antagonistic effect of the methoxyindole on dexamethasone-induced apoptosis in mouse thymocytes was examined. Melatonin decreased both DNA fragmentation, and the number of annexin V-positive cells incubated in the presence of dexamethasone. Analysis of the expression of the members of the Bcl-2 family indicated that the synthetic glucocorticoid increased Bax protein levels without affecting the levels of Bcl-2, Bcl-XL, Bcl-XS, or Bak. This effect correlated with an increase in thymocytes bax mRNA levels. Dexamethasone also increased the release of cytochrome C from mitochondria. All of these effects were reduced in the presence of melatonin, which was ineffective per se on these parameters. In addition, the involvement of cAMP on glucocorticoid/melatonin antagonism was examined. Both melatonin and dexamethasone decreased the levels of this nucleotide in mouse thymocytes, indicating that the antagonistic action between both hormones involves a cAMP-independent pathway. In summary, the present results suggest that the antiapoptotic effect of melatonin on glucocorticoid-treated thymocytes would be a consequence of an inhibition of the mitochondrial pathway, presumably through the regulation of Bax protein levels.8 p.application/pdfeng(c) Association for the Study of Internal Secretions, 2004ApoptosiMelatoninaGlucocorticoidesProteïnesApoptosisMelatoninGlucocorticoidsProteinsinfo:eu-repo/semantics/article7152462022-06-14info:eu-repo/semantics/openAccess14500572