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Role of oxidative stress in endometriosis.

Authors :
Gupta, Sajal
Agarwal, Ashok
Krajcir, Natalie
Alvarez, Juan G.
Source :
Reproductive BioMedicine Online (Reproductive Healthcare Limited). Jul2006, Vol. 13 Issue 1, p126-134. 9p.
Publication Year :
2006

Abstract

Endometriosis is a chronic pleomorphic disorder with pelvic or systemic manifestations, and is characterized by the presence of endometrial glands and stroma. In the United States, the prevalence of the disease is estimated to range from 2 to 50% in women of reproductive age. No single theory can explain the histogenesis and the pleomorphic manifestations of endometriosis. Endometriosis is being reported in younger age women and manifesting with increasing severity, hence the need to understand the role of oxidative stress (OS) in endometriosis. The presence of elevated concentrations of free radicals and lowered antioxidant potential leads to OS. The development of OS in the local peritoneal environment may be one of the links in the chain of events leading to endometriosis. Redox levels may modulate the severity and the dynamics of endometriosis and progression of the disease. OS has been implicated in infertility associated with endometriosis. Recent literature reviewed investigates the role of molecular mechanisms and genetic pathways that may modulate cellular response to OS. Antioxidant supplementation, immunomodulators, and selective progesterone receptor modulators with antioxidant effects have been investigated as possible treatments for endometriosis, but compelling evidence on the benefits of the various modalities is lacking. Results of the limited number of animal and human trials need to be corroborated by larger randomized controlled trials. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
14726483
Volume :
13
Issue :
1
Database :
Academic Search Index
Journal :
Reproductive BioMedicine Online (Reproductive Healthcare Limited)
Publication Type :
Academic Journal
Accession number :
21559793
Full Text :
https://doi.org/10.1016/S1472-6483(10)62026-3