17β-estradiol suppresses ROS-induced apoptosis of CHO cells through inhibition of lipid peroxidation-coupled membrane permeability transition

Chosei Miyaguchi, Shikibu Muranaka, Tomoko Kanno, Hirofumi Fujita, Jitsuo Akiyama, Tamotsu Yoshioka, Tatsuji Yasuda

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Oxidative stress-induced apoptotic cell death has been implicated to play a critical role in the mechanism of corpus luteum regression and follicular atresia. Recent studies suggests that reactive oxygen species (ROS) might play important roles in the regulation of luteal function. The present work describes the inhibitory effect of 17β-estradiol (E2) on ROS-induced mitochondrial membrane permeability transition (MPT) and apoptosis of Chinese hamster ovary (CHO) cells. ROS generated by Fe2+ and H2O2 induced mitochondrial lipid peroxidation, depolarization, activation of caspase-3 and DNA fragmentation in CHO cells by some E2-inhibitable mechanism. E2 suppressed the Fe2+/H2O2-induced lipid peroxidation and MPT of isolated mitochondria that was characterized by cyclosporin A-inhibitable swelling, depolarization and cytochrome c release. Furthermore, E2 scavenged the xanthine oxidase generated ROS. These results suggests that Fe2+.H2O2 induced MPT and apoptosis of CHO cells by a mechanism that could be suppressed by antioxidant properties of E2.

Original languageEnglish
Pages (from-to)21-35
Number of pages15
JournalPhysiological chemistry and physics and medical NMR
Volume36
Issue number1
Publication statusPublished - 2004
Externally publishedYes

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Physiology
  • Spectroscopy

Fingerprint Dive into the research topics of '17β-estradiol suppresses ROS-induced apoptosis of CHO cells through inhibition of lipid peroxidation-coupled membrane permeability transition'. Together they form a unique fingerprint.

  • Cite this