Oxidative stress and the ovary

Citation
Hr. Behrman et al., Oxidative stress and the ovary, J SOC GYN I, 8(1), 2001, pp. S40-S42
Citations number
24
Categorie Soggetti
Reproductive Medicine
Journal title
JOURNAL OF THE SOCIETY FOR GYNECOLOGIC INVESTIGATION
ISSN journal
10715576 → ACNP
Volume
8
Issue
1
Year of publication
2001
Supplement
S
Pages
S40 - S42
Database
ISI
SICI code
1071-5576(200101/02)8:1<S40:OSATO>2.0.ZU;2-2
Abstract
Superoxide (O-2(-)), hydrogen peroxide (H2O2), and lipid peroxides are gene rated in luteal tissue during natural and prostaglandin-induced regression in the rat, and this response is associated with reversible depletion of as corbic acid. Reactive oxygen species immediately uncouple the lutenizing ho rmone receptor from adenylate cyclase and inhibit steroidogenesis by interr upting transmitochondrial cholesterol transport. The cellular origin of oxy gen radicals in regressing corpora lutea is predominately from resident and infiltrated leukocytes, notably neutrophils. Reactive oxygen species are a lso produced within the follicle at ovulation and, like the corpus luteum, leukocytes are the major source of those products. Antioxidants block the r esumption of meiosis, whereas the generation of reactive oxygen induces ooc yte maturation in the follicle. Although oxygen radicals may serve importan t physiologic roles within the ovary, the cyclic production of these damagi ng agents over years may lead to an increased cumulative risk of ovarian pa thology that would probably be exacerbated under conditions of reduced anti oxidant status. (J Soc Gynecol Investig 2001;8:S40-S42) Copyright (C) 2001 by the Society for Gynecologic Investigation.