Research: MURPHY and colleagues,

Listed in Issue 43


MURPHY and colleagues, Department of Gynecology and Obstetrics, Emory University School of Medicine, Atlanta, Georgia 30322 USA review (81 References) the mechanisms of endometriosis.


The authors write 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 may 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, consisting of lipid peroxides, their degradation products and products formed from interaction with low-density lipoprotein (LDL) apoprotein and other proteins. Lipoproteins of the peritoneal fluid (interstitial fluid) have been shown to have lower vitamin E levels and to be more readily oxidised than plasma. Hence, peritoneal fluid may contribute to the disease process actively rather than passively as a carrier of mediators of inflammation and growth. In response to such stress, a sterile, inflammatory reaction with the secretion of growth factors, cytokines and chemokines is generated, which is detrimental, particularly to successful reproduction.



The authors note that the data presented in this review merely begin to explore the role of oxidative stress in mediating the pathophysiology of endometriosis. They note that only by understanding the mechanisms involved in the pathogenesis of endometriosis can the basis for new diagnostic and therapeutic approaches be developed.



Murpy AA et al. Endometriosis: a disease of oxidative stress? Seminars in Reproductive Endocrinology. 16(4): 263-73. 1998.

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