摘要

Background/Aim: Gender-associated dimorphism in renal oxidative stress may be related to the protective effects of estrogens or the adverse effects of testosterone. Signal transducer and activator of transcription-3 (STAT3)-dependent transcription is vital in renal antioxidant responses, which may be differentially regulated by sex hormones. Materials and Methods: Renal proximal tubule cells were treated with 400 mu M H2O2 in the presence or absence of 100 nM dihydrotestosterone (DHT), 100 nM 17 beta-estradiol (E2) or dominant-negative STAT3 (dnSTAT3). Production of reactive oxygen species (ROS), phosphorylation/transcriptional activation of STAT3 and promoter activity of the STAT3-regulated antioxidant gene (MnSOD) were determined. Results: After treatment with H2O2, DHT decreased tyrosine phosphorylation/transcriptional activity of STAT3 and promoter activity of MnSOD while E2 increased them. Consequently, DHT augmented while E2 attenuated ROS production. Effects of dnSTAT3 were similar to DHT. Conclusion: Sex hormones may influence renal oxidative stress through differential regulation of STAT3-dependent antioxidant responses.

  • 出版日期2014-12