Ovarian dysfunction after ischemia-reperfusion of the ovarian blood vessel in experimental rats

Koichi Nariai; Risa Fukumoto; Shin Onota; Ken Watanabe; Hiroshi Uchiyama; Kiichi Kanayama; Kahei Sato

doi:10.3192/jsirib.24.77

Koichi Nariai, Risa Fukumoto, Shin Onota, Ken Watanabe, Hiroshi Uchiyama, Kiichi Kanayama, Kahei Sato

Author information

Koichi Nariai
Institute of Clinical Medicine and Research (ICMR), Research Center for Medical Sciences, The Jikei University School of Medicine
Laboratory Animal Facilities (LAF), Research Center for Medical Sciences, The Jikei University School of Medicine
Risa Fukumoto
Institute of Clinical Medicine and Research (ICMR), Research Center for Medical Sciences, The Jikei University School of Medicine
Shin Onota
Institute of Clinical Medicine and Research (ICMR), Research Center for Medical Sciences, The Jikei University School of Medicine
Ken Watanabe
Institute of Clinical Medicine and Research (ICMR), Research Center for Medical Sciences, The Jikei University School of Medicine
Hiroshi Uchiyama
Department of Applied Biology, College of Bioresource Sciences, Nihon University
Kiichi Kanayama
Department of Veterinary Medicine, College of Bioresource Sciences, Nihon University
Kahei Sato
Department of Applied Biology, College of Bioresource Sciences, Nihon University

Keywords: reactive oxygen species (ROS), superoxide anion radical, oxidative stress, superoxide dismutase (SOD), ischemia-reperfusion, ovarian function

JOURNAL FREE ACCESS

2009 Volume 24 Issue 2 Pages 77-80

DOI https://doi.org/10.3192/jsirib.24.77

Details

Abstract

Excessive production of reactive oxygen species (ROS) lead to oxidative stress in tissue or organ dysfunction. To confirm ovarian dysfunction by ROS, ischemia-reperfusion (I/R) treatment of the ovarian blood vessels was performed using experimental rats in this study. Preventive effect of superoxide dismutase (SOD) as a radical scavenger against ovarian I/R injury was also examined. Hormonal sensitivities to equine chorionic gonadotropin (eCG) and human chorionic gonadotropin (hCG) in the ovary decreased after the I/R. Ovarian tissue and ovum destruction were also observed. These changes could be prevented by SOD administration. Our data suggest that I/R injury related to ROS production causes ovarian dysfunction. The dysfunction is prevented by administration of a radical scavenger.

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