Figure 3.

Prenatal treatment of either shAR or BBR ameliorates prenatal DHT exposure-induced oxidative stress and mitochondrial dysfunction by AR suppression. The 2 month-old female rats received either CTL or DHT treatment, which involved either DHT with shAR lentivirus infusion in the amygdala (DHT/shAR) or DHT with BBR injection (DHT/BBR) during the 21-day pregnancy. The subsequent 2 month-old male offspring were sacrificed, and amygdala tissues and/or amygdala neurons were isolated for further analysis. (A) The mRNA levels for gene expression of AR, ERβ and SOD2, n = 4. (B) The representative pictures for western blotting. (C) The quantitation of protein levels, n = 5. (D) In vivo superoxide anion release, n = 5. (E) Quantitation of 3-nitrotyrosine formation, n = 5. (F,G) The amygdala neurons were isolated for immunostaining by 8-oxo-dG and DAPI. (F) Quantitation of 8-oxo-dG staining, n = 5. (G) Representative pictures for 8-oxo-dG staining (green) and DAPI staining for nuclei (blue). (H) Mitochondrial DNA copies, n = 4. (I) Intracellular ATP levels, n = 5. *P < 0.05, vs. CTL group; ^¶P < 0.05, vs. DHT group. Data were expressed as mean ± SEM.