EFFECTS OF CASTRATION ON CITOPROTECTIVE GENES AND APOPTOTIC MECHANISMS IN RAT LUNG

BIAGGIO V.S.; ALVAREZ OLMEDO D.G.; PIGUILLEM S.N.; PEREZ CHACA M.V.; GIMENEZ M.S.; GÓMEZ N.N.

San Luis

Congreso; XXX Reunión Científica Anual de la Sociedad de Biología de Cuyo; 2012

Sociedad de Biología de Cuyo

There is strong evidence that oxidative stress plays a key role in the pathophysiology of several lung diseases. The presence of specific androgens and estrogen receptors in the lung implies that sex hormones play a physiological role in pulmonary function. The present study was designed to determine whether castration and androgen replacement result in changes in the lung histoarchitecture. Wistar male rats (200± 20 g) were separated in three groups: controls (Co), castrated (Ca), and castrated replaced with testosterone (Ca+T) and sacrificed 30 days after castrations. For light microscopy, the tissues were fixed and each antibody was assayed in at least three sections of each lung. ANOVA was used for statistical analysis. The results indicate that Hsp 27 immunostaining decreased in Ca group (p<0.001), while Hsp 70i (p<0.01), PTEN (p< 0.05),PCNA and Bcl-2 (p<0.05) positive staining, were increased in the same group, compared to  control. In Ca + T group, the markers evaluated were increased significantly. Our results suggest gene association between androgens and variation in several citoprotective and pro and anti-apoptotic genes. Further studies are needed to confirm these associations in lung tissue and testosterone replacement after castration produces a partial recuperation.