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Testosterone exerts antiapoptotic effects against H2O2 in C2C12 skeletal muscle cells through the apoptotic intrinsic pathway.
Pronsato, Lucía; Boland, Ricardo; Milanesi, Lorena.
Afiliação
  • Pronsato L; Departamento de Biología, Bioquímica y Farmacia, Universidad Nacional del Sur, San Juan 670, Bahía Blanca 8000, Argentina.
J Endocrinol ; 212(3): 371-81, 2012 Mar.
Article em En | MEDLINE | ID: mdl-22219300
Experimental data indicate that apoptosis is activated in the aged skeletal muscle, contributing to sarcopenia. We have previously demonstrated that testosterone protects against hydrogen peroxide (H(2)O(2))-induced apoptosis in C2C12 muscle cells. Here we identified molecular events involved in the antiapoptotic effect of testosterone. At short times of exposure to H(2)O(2) cells exhibit a defense response but at longer treatment times cells undergo apoptosis. Incubation with testosterone prior to H(2)O(2) induces BAD inactivation, inhibition of poly(ADP-ribose) polymerase cleavage, and a decrease in BAX levels, and impedes the loss of mitochondrial membrane potential, suggesting that the hormone participates in the regulation of the apoptotic intrinsic pathway. Simultaneous treatment with testosterone, H(2)O(2), and the androgen receptor (AR) antagonist, flutamide, reduces the effects of the hormone, pointing to a possible participation of the AR in the antiapoptotic effect. The data presented allow us to begin to elucidate the mechanism by which the hormone prevents apoptosis in skeletal muscle.
Assuntos

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Testosterona / Apoptose / Músculo Esquelético / Peróxido de Hidrogênio Limite: Animals Idioma: En Revista: J Endocrinol Ano de publicação: 2012 Tipo de documento: Article País de afiliação: Argentina País de publicação: Reino Unido

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Testosterona / Apoptose / Músculo Esquelético / Peróxido de Hidrogênio Limite: Animals Idioma: En Revista: J Endocrinol Ano de publicação: 2012 Tipo de documento: Article País de afiliação: Argentina País de publicação: Reino Unido