Oxidative Stress and Endometriosis: A Systematic Review of the Literature.

Gennaro Scutiero,Savino Spadaro,Piergiorgio Iannone,Luigi Nappi,Giulia Bernardi,Carlo Alberto Volta,Gloria Bonaccorsi,Pantaleo Greco

doi:10.1155/2017/7265238

Abstract

Endometriosis is one of the most common gynaecologic diseases in women of reproductive age. It is characterized by the presence of endometrial tissue outside the uterine cavity. The women affected suffer from pelvic pain and infertility. The complex etiology is still unclear and it is based on three main theories: retrograde menstruation, coelomic metaplasia, and induction theory. Genetics and epigenetics also play a role in the development of endometriosis. Recent studies have put the attention on the role of oxidative stress, defined as an imbalance between reactive oxygen species (ROS) and antioxidants, which may be implicated in the pathophysiology of endometriosis causing a general inflammatory response in the peritoneal cavity. Reactive oxygen species are intermediaries produced by normal oxygen metabolism and are inflammatory mediators known to modulate cell proliferation and to have deleterious effects. A systematic review was performed in order to clarify the different roles of oxidative stress and its role in the development of endometriosis. Several issues have been investigated: iron metabolism, oxidative stress markers (in the serum, peritoneal fluid, follicular fluid, peritoneal environment, ovarian cortex, and eutopic and ectopic endometrial tissue), genes involved in oxidative stress, endometriosis-associated infertility, and cancer development.

Highlights

Endometriosis is an estrogen-dependent pelvic inflammatory disease characterized by implantation and growth of endometrial tissue outside the uterine cavity [1]
Recent studies have put the attention on the role of oxidative stress, defined as an imbalance between reactive oxygen species (ROS) and antioxidants, which may be implicated in the pathophysiology of endometriosis causing a general inflammatory response in the peritoneal cavity
Macrophages, erythrocytes, and apoptotic endometrial tissue that transplant into the peritoneal cavity through retrograde menstruation are well known inducers of oxidative stress; peritoneal production of ROS may be involved in endometriosis

Summary

Introduction

Endometriosis is an estrogen-dependent pelvic inflammatory disease characterized by implantation and growth of endometrial tissue (glands and stroma) outside the uterine cavity [1]. It affects about 10–15% of women of reproductive age [2, 3]. It is widely accepted that oxidative stress, defined as an imbalance between reactive oxygen species (ROS) and antioxidants, may be implicated in the pathophysiology of endometriosis causing a general inflammatory response in the peritoneal cavity [10,11,12]. Macrophages, erythrocytes, and apoptotic endometrial tissue that transplant into the peritoneal cavity through retrograde menstruation are well known inducers of oxidative stress; peritoneal production of ROS may be involved in endometriosis. Activated macrophages play an important role in the degradation of erythrocytes that release prooxidant and proinflammatory factors such as heme and iron, implicated in the formation of deleterious ROS [15]

Methods

Results

Conclusion