Roles of Oxidative Stress in Polycystic Ovary Syndrome and Cancers

Tao Zuo,Wenming Xu,Minghui Zhu

doi:10.1155/2016/8589318

Abstract

Oxidative stress (OS) has received extensive attention in the last two decades, because of the discovery that abnormal oxidation status was related to patients with chronic diseases, such as diabetes, cardiovascular, polycystic ovary syndrome (PCOS), cancer, and neurological diseases. OS is considered as a potential inducing factor in the pathogenesis of PCOS, which is one of the most common complex endocrine disorders and a leading cause of female infertility, affecting 4%–12% of women in the world, as OS has close interactions with PCOS characteristics, just as insulin resistance (IR), hyperandrogenemia, and chronic inflammation. It has also been shown that DNA mutations and alterations induced by OS are involved in cancer pathogenesis, tumor cell survival, proliferation, invasion, angiogenesis, and so on. Furthermore, recent studies show that the females with PCOS are reported to have an increasing risk of cancers. As a result, the more serious OS in PCOS is regarded as an important potential incentive for the increasing risk of cancers, and this study aims to analyze the possibility and potential pathogenic mechanism of the above process, providing insightful thoughts and evidences for preventing cancer potentially caused by PCOS in clinic.

Highlights

Polycystic ovary syndrome (PCOS) is one of the most common endocrine disorders of women at reproductive age and the major cause of anovulatory infertility [1]. It was first described as the change of ovarian morphology by Chereau in 1844 [2], and the diagnostic criteria were established by the European Society for Human Reproduction and Embryology (ESHRE) and American Society for Reproductive Medicine (ASRM) in 2003 based on the extensive studies during the last decades, which is the so-called Rotterdam Consensus Criteria [3]
polycystic ovary syndrome (PCOS) has been regarded as a chronic systemic disease instead of the simple local disease, and it is frequently associated with insulin resistance (IR), hyperandrogenemia, chronic inflammation, and oxidative stress (OS), though the pathogenesis mechanism has not been well defined [4,5,6,7,8]
It is known that DNA damage and methylation induced by oxidative stress (OS) play key roles in the early stage of tumor pathogenesis and tumor conversion by activating protooncogene and silencing antioncogene

Summary

Introduction

Polycystic ovary syndrome (PCOS) is one of the most common endocrine disorders of women at reproductive age and the major cause of anovulatory infertility [1]. It was first described as the change of ovarian morphology by Chereau in 1844 [2], and the diagnostic criteria were established by the European Society for Human Reproduction and Embryology (ESHRE) and American Society for Reproductive Medicine (ASRM) in 2003 based on the extensive studies during the last decades, which is the so-called Rotterdam Consensus Criteria [3]. Several investigations indicated that PCOS perhaps could increase the risk of developing endometrial cancer, and abnormal hormone level, IR, hyperinsulinemia, and even obesity were suggested as the potential inducements of endometrial cancer pathogenesis in PCOS patients [15,16,17,18]. OS could be one of the major underlying inducements of the increasing risk of gynecological cancers in PCOS patients

Altered Oxidative Stress in Polycystic Ovary Syndrome

Polycystic Ovary Syndrome and Cancers

Conclusion

Findings

Conflict of Interests