Captopril prenatal treatment induce apoptotic response during development in rat lung.

CAPELARI DN; FUENTES LB; CIUFFO GM.

Mendoza - Argentina.

Congreso; XXVI Reunión Científica Anual Sociedad de Biología de Cuyo (SBC); 2008

The process of programmed cell death, or apoptosis, is characterized by distinct morphological characteristics and energy-dependent biochemical mechanisms. Apoptosis is considered a vital component of various processes including normal cell turnover, proper development and chemical-induced cell death.  Bcl-2 family members determine cell death and survival by controlling mitochondrial membrane ion permeability, cytochrome c release, and the subsequent activation of caspase. The aim of this study was to investigate the effect of prenatal ACE inhibition on mediators of apoptotic signalling in postnatal lung tissue development. Mini-osmotic pumps with captopril or saline solution were implanted in pregnant Wistar rats during the last week of pregnancy. Pup`s lungs at four different ages: PND0, PND8, PND15 and PND30 were evaluated. The expression of anti-apoptotic Bcl2 or pro-apoptotic BAX was analysed by RT-PCR and caspase-3 activity was confirmed by Western blot analysis. Semiquantitative assessment indicated significant up-regulation of Bcl2 expression (ANOVA, P<0.001) at PND15 and significant down-regulation (ANOVA, P<0.001) at PND30 in captopril treatment group, respect to controls. We found high BAX expression without significant differences during development. Caspase-3 activity in treated rats was present in all ages evaluated, especially at PND0 and PND30. These results suggest that prenatal captopril treatment interferes with normal process of apoptosis in postnatal lung development.