Endometriosis: A Disease of Oxidative Stress?

A A Murphy, Ana A. Murphy, Nalini Santanam, N Santanam, Sampath Parthasarathy, S Parthasarathy
Seminars in reproductive endocrinology · 1998 · vol. 16(04) , pp. 263–273 · doi:10.1055/s-2007-1016286 · PMID:10101808 · W2007163438
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

This review hypothesizes that oxidatively damaged cells and tissue in endometriosis trigger peritoneal macrophages, which generate oxidative stress that promotes ectopic endometrial growth and inflammation, impairing reproduction.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 ⓘ

This paper is a hypothesis-driven review proposing that oxidative damage in endometriosis—arising from oxidatively damaged red blood cells, apoptotic endometrial cells, or undigested tissue—can recruit and activate mononuclear phagocytes and lead to impaired macrophage scavenger receptor–mediated secretion. It argues that activated peritoneal macrophages generate oxidative stress in the peritoneal cavity, producing lipid peroxides and related oxidation products, and that peritoneal-fluid lipoproteins with lower vitamin E levels are more readily oxidized than plasma, potentially contributing actively to disease. The paper further suggests that this pro-oxidant environment promotes sterile inflammatory reactions involving growth factors, cytokines, and chemokines, which can be deleterious for reproduction and promote ectopic endometrial growth. The paper is centrally about endometriosis — it frames endometriosis pathophysiology as a disease of oxidative stress involving macrophage activation and oxidized peritoneal-fluid components.

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Abstract

Our central hypothesis proposes that oxidatively damaged red blood cells (RBCs), apoptotic endometrial cells or undigested endometrial tissue may signal the recruitment and activation of mononuclear phagocytes. Women with endometriosis are prone to respond to this stimulus with an inadequate macrophage scavenger receptor response although the secretory response is not impaired. Activated macrophages in the peritoneal cavity generate an oxidative stress, which consists of lipid peroxides, their degradation products, and products formed from their interaction with low-density lipoprotein (LDL) apoprotein and other proteins. The lipoproteins of the peritoneal fluid (interstitial fluid) have been shown to have lower vitamin E levels and to be more readily oxidized than plasma, so peritoneal fluid may actually contribute to the disease process actively rather than as a passive carrier of mediators of inflammation and growth. As a result of such a stress, a sterile, inflammatory reaction with secretion of growth factors, cytokines, and chemokines is generated, which is deleterious especially to successful reproduction. We propose that such a pro-oxidant environment (peritoneal fluid as well as activated macrophages) promotes growth of ectopic endometrium. The data presented in this review are just the beginning of exploring the role of oxidative stress in mediating the pathophysiology of endometriosis. Only by understanding the mechanisms involved in the pathogenesis of endometriosis can we develop the basis for new diagnostic and therapeutic approaches.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Endometrium Erythrocytes Macrophages Oxidative Stress Apoptosis Ascitic Fluid Choristoma Choristoma Choristoma Endometriosis Endometriosis Endometrium Endometrium Erythrocytes Female Humans Lipoproteins Lipoproteins Macrophages

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