Research Article Role of Oxidative Stress in Obese and Nonobese PCOS Patients Kazım Uçkan , 1 Halit Demir, 2 Kasım Turan, 3 Eren Sarıkaya, 3 and Canan Demir 4 1 Van Training and Research Hospital, Department of Obstetrics and Gynecology, Van, Turkey 2 Van Yuzuncu Yil University, Department of Biochemistry, Van, Turkey 3 Clinic of Obstetrics and Gynecology Dr. KasımTuran, Van, Turkey 4 Van Yuzuncu Yil University, Vocational School of Health Services, Van, Turkey Correspondence should be addressed to Kazım Uçkan; druckan65@hotmail.com Received 30 September 2021; Accepted 15 January 2022; Published 9 February 2022 Academic Editor: Alexander Berezin Copyright © 2022 Kazım Uçkan et al. is is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Objective. e aim of this study was to evaluate the relationship between the oxidant-antioxidant status, endothelial dysfunction, lipid metabolism, and metabolic syndrome risk in women with polycystic ovary syndrome (PCOS). Materials and Methods. Forty-five obese (BMI >30 kg/m2) woman diagnosed with PCOS in the study, forty-five nonobese (BMI <30kg/m 2 ) PCOS diagnosis working groups, and forty-nine healthy control groups were created with patients. Serum malondialdehyde (MDA) levels with antioxidant activities, such as SOD, GSH, GPx, and CATactivities, were measured by spectrophotometry. Results. ere was a statistically significant difference in the mean serum MDA level in the obese PCOS group compared to the nonobese group and the control group (p < 0.001). When the antioxidant parameters, such as SOD, GPx, GSH, and CAT, were compared with the healthy control group, nonobese, and obese PCOS groups, the difference between the groups was statistically significant (p < 0.001). A positive correlation was observed between MDA and BMI, triglyceride, LDL, SBP, DBP, and HOMA-IR in the PCOS patient group. Conclusion. Oxidative stress and decreased antioxidant parameters in PCOS patients were correlated with hyperinsulinemia, hypertension, and dyslipidemia findings, and we think that this oxidative stress condition may contribute to metabolic syndrome and cardiovascular diseases in PCOS patients. 1. Introduction Polycystic ovary syndrome (PCOS) is a common endocrine disorderthataffects6%to20%ofwomenatreproductiveage [1]. Usually, women with PCOS have hyperandrogenism and hirsutism, oligo or amenorrhea, and anovulation. Although there is a long history of study on PCOS, its etiology is still unknown. Today, the role of inflammatory mechanisms, endothelial damage, oxidative stress, and genetic mecha- nisms are explained [2, 3]. It has been reported that women with polycystic ovary syndrome have abnormalities in estrogen and androgen metabolism. In one study, it has been determined that PCOS may be caused by abnormal function of the hypo- thalamic-pituitary-ovarian (HPO axis). In mammalian ovaries, LH has been found to induce androgen biosyn- thesis by the theca interna cells. However, FSH has been found to stimulate aromatase activity by the granulosa cells. e coordinated action of these two cells and pituitary hormones has been found to form the basis of the bicel- lular, bigonadotropin hypothesis for estrogen biosynthesis [4]. e characteristic features of PCOS include LH hyper- secretion both basally and in response to GnRH. erefore, LH hypersecretion can produce androgen in excess. us, the primary abnormalities in classic PCOS occur. LH/GnRH pulses cause hyperandrogenemia and impaired follicular maturation in PCOS patients. is renders it insensitive to estrogen/progesterone inhibition of hypothalamic GnRH formation. As a result of this insensitivity, perimenarchal abnormalities in hyperandrogenemic PCOS women may be a potential mechanism [5]. Cells have an efficient antioxidant defence system, mainly composed of enzymes, such as superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). ey can reactivate oxygen species (ROS) produced by cellular metabolism and make ROS level stable under physiological conditions [6]. Hindawi International Journal of Clinical Practice Volume 2022, Article ID 4579831, 9 pages https://doi.org/10.1155/2022/4579831