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 although the secretory
response is impaired. Activated macrophages in 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 carrier of mediators of inflammation and growth. As a result of such a stress,
a sterile, 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 role of oxidative stress in mediating the pathophysiology
of endometriosis. Only by understanding the mechanisms involved in the pathogenesis
of endometriosis can we develop basis for new diagnostic and therapeutic approaches.
Keywords:
Endometriosis - oxidation - lyso phosphatidylcholine - M-OxLDL (minimally oxidized
LDL) - vitamin E
