Stress In Polycystic Ovary Syndrome Research Articles

Oxidative Stress in Polycystic Ovary Syndrome: Impact of Combined Oral Contraceptives.

Polycystic Ovary Syndrome (PCOS) is a complex hormonal disorder that is associated with heightened metabolic risks. While oxidative stress (OS) is known to play a role in PCOS, the precise nature of the relationship between PCOS and increased OS remains not entirely understood. Combined oral contraceptives (COCs) are the first-line treatment to regulate menstrual cycles and androgen levels, but their impact on oxidative stress requires further study. We conducted a transcriptomic analysis using RNAseq and assessed the levels of various oxidative stress (OS) markers in serum samples from women with PCOS and controls and whether they were using combined oral contraceptives (COCs), including enzymatic activities, FRAP, and 8-isoprostane (8-iso). A total of 359 genes were differentially expressed in women with PCOS compared to control women. Genes differentially expressed were enriched in functions related to inflammation and, interestingly, oxidative stress response. In controls, 8-iso levels were increased in women using COCs, whereas in women with PCOS, 8-iso levels were reduced in those using oral contraceptives (191.1 ± 97 vs. 26.4 ± 21 pg/mL, p: <0.0001). Correlation analyses showed a trend for a negative correlation between 8-iso and Ferriman score in women with PCOS consuming COCs (r = -0.86, p = 0.06) and a negative correlation between GSH and hyperandrogenism in women with PCOS (r = -0.89, p = 0.01). These results reveal the presence of lipid peroxidation in women with PCOS, which was modified by the use of COCs, providing new insights into the pathophysiology of PCOS in the Chilean population.

Granulosa cell insight: unraveling the potential of menstrual blood-derived stem cells and their exosomes on mitochondrial mechanisms in polycystic ovary syndrome (PCOS)

BackgroundPolycystic ovary syndrome (PCOS) presents a significant challenge in women’s reproductive health, characterized by disrupted folliculogenesis and ovulatory dysfunction. Central to PCOS pathogenesis are granulosa cells, whose dysfunction contributes to aberrant steroid hormone production and oxidative stress. Mitochondrial dysfunction emerges as a key player, influencing cellular energetics, oxidative stress, and steroidogenesis. This study investigates the therapeutic potential of menstrual blood-derived stem cells (MenSCs) and their exosomes in mitigating mitochondrial dysfunction and oxidative stress in PCOS granulosa cells.MethodsUsing a rat model of PCOS induced by letrozole, granulosa cells were harvested and cultured. MenSCs and their exosomes were employed to assess their effects on mitochondrial biogenesis, oxidative stress, and estrogen production in PCOS granulosa cells.ResultsResults showed diminished mitochondrial biogenesis and increased oxidative stress in PCOS granulosa cells, alongside reduced estrogen production. Treatment with MenSCs and their exosomes demonstrated significant improvements in mitochondrial biogenesis, oxidative stress levels, and estrogen production in PCOS granulosa cells. Further analysis showed MenSCs' superior efficacy over exosomes, attributed to their sustained secretion of bioactive factors. Mechanistically, MenSCs and exosomes activated pathways related to mitochondrial biogenesis and antioxidative defense, highlighting their therapeutic potential for PCOS.ConclusionsThis study offers insights into granulosa cells mitochondria’s role in PCOS pathogenesis and proposes MenSCs and exosomes as a potential strategy for mitigating mitochondrial dysfunction and oxidative stress in PCOS. Further research is needed to understand underlying mechanisms and validate clinical efficacy, presenting promising avenues for addressing PCOS complexity.

Ameliorating effects of adropin on letrozole-induced polycystic ovary syndrome via regulating steroidogenesis and the microbiota inflammatory axis in rats.

Growing evidence supports the role of gut microbiota in chronic inflammation, insulin resistance (IR) and sex hormone production in polycystic ovary syndrome (PCOS). Adropin plays a pivotal role in the regulation of glucose and lipid metabolism and is negatively correlated with IR, which affects intestinal microbiota and sex hormones. However, the effect of adropin administration in PCOS has yet to be investigated. The present study aimed to assess the effects of adropin on letrozole (LTZ)-induced PCOS in rats and the potential underlying mechanisms. The experimental groups were normal, adropin, letrozole and LTZ+adropin. At the end of the experiment, adropin significantly ameliorated PCOS, as evidenced by restoring the normal ovarian structure, decreasing the theca cell thickness in antral follicles, as well as serum testosterone and luteinizing hormone levels and luteinizing hormone/follicle-stimulating hormone ratios, at the same time as increasing granulosa cell thickness in antral follicles, oestradiol and follicle-stimulating hormone levels. The ameliorating effect could be attributed to its effect on sex hormone-binding globulin, key steroidogenic genes STAR and CYP11A1, IR, lipid profile, gut microbiota metabolites-brain-ovary axis components (short chain fatty acids, free fatty acid receptor 3 and peptide YY), intestinal permeability marker (zonulin and tight junction protein claudin-1), lipopolysaccharides/Toll-like receptor 4/nuclear factor kappa B inflammatory pathway and oxidative stress makers (malondialdehyde and total antioxidant capacity). In conclusion, adropin has a promising therapeutic effect on PCOS by regulating steroidogenesis, IR, lipid profile, the gut microbiota inflammatory axis and redox homeostasis. KEY POINTS: Adropin treatment reversed endocrine and ovarian morphology disorders in polycystic ovary syndrome (PCOS). Adropin regulated the ovarian steroidogenesis and sex hormone-binding globulin in PCOS. Adropin improved lipid profile and decreased insulin resistance in PCOS. Adropin modulated the components of the gut-brain-ovary axis (short chain fatty acids, free fatty acid receptor 3 and peptide YY) in PCOS. Adropin improved intestinal barrier integrity, suppressed of lipopolysaccharides/Toll-like receptor 4/nuclear factor kappa B signalling pathway and oxidative stress in PCOS.

Exploring the Therapeutic Potential of Sodium Hydrosulfide in Alleviating Oxidative Stress and Ovarian Dysfunction in a Rat Model of Polycystic Ovary Syndrome.

Oxidative stress is known to play a key role in the occurrence of polycystic ovary syndrome (PCOS) as the most common cause of anovulatory infertility. The purpose of the current study was to investigate whether diminished activity of ovarian enzymes responsible for hydrogen sulfide (H2S) production, cystathionine β-synthase (CBS), and cystathionine γ-lyase (CSE) contributes to oxidative stress in PCOS. The study also explored whether administration of sodium hydrosulfide (NaSH), an H2S donor, could ameliorate PCOS symptoms by reducing oxidative stress. The total eighteen rats were randomly assigned into three groups (n=6): control, PCOS, and PCOS+NaSH. PCOS was induced by intramuscular injection of estradiol valerate to induce PCOS in the PCOS and PCOS+NaSH groups. The PCOS+NaSH group received 30 μmol/L of NaSH in drinking water for 27 days after PCOS induction. Ovarian tissue samples were analyzed for oxidative stress indices including malondialdehyde (MDA) levels and superoxide dismutase (SOD) activity. Additional analyses measured H2S levels, CBS, and CSE activity. PCOS induction led to a significant decrease in SOD activity, H2S levels, and CBS and CSE activity, accompanied by a significant increase in MDA levels (p<0.0001). Furthermore, PCOS caused severe histological alterations in the ovaries. However, administration of NaSH effectively restored all measured parameters to pre-PCOS induction levels (p<0.0001). This study showed that the decrease in the activity of H2S-producing enzymes and H2S levels may contribute to oxidative stress in PCOS. Therefore, administration of NaSH as a H2S donor can be considered as a potential therapeutic strategy for PCOS patients.

Anti-Müllerian hormone a surrogate of follicular fluid oxidative stress in polycystic ovary syndrome?

Polycystic ovary syndrome (PCOS) is the most common endocrinopathy in women at childbearing age. Anti-Müllerian hormone (AMH) is a widely accepted sensitive marker of ovarian reserve, which has been suggested that could also act as biomarker of ovarian morphology for PCOS diagnosis. Oxidative stress (OS) is known to be associated and have a negative impact factor in several reproductive conditions, including PCOS. However, the relationship between circulating AMH and OS within the follicular fluid (FF), and its potential impact on in vitro fertilization (IVF) outcomes of women with PCOS, remains largely unexplored. A total of 84 women, with PCOS (n = 30) or ovulatory controls (n = 54), were enrolled in this study. Women underwent individualized controlled ovarian stimulation for oocyte retrieval. Blood and FF obtained from mature follicles were collected at the time of oocyte retrieval, for measuring total testosterone, ∆4-androstenedione, progesterone, sex hormone binding globulin (SHBG) and AMH. OS in the FF was assessed by measuring total antioxidant capacity (TAC) through the ferric reducing antioxidant power (FRAP) and lipid peroxidation (LPO) by quantification of malondialdehyde (MDA) levels. Our results demonstrated that women with PCOS had significantly higher plasma levels of AMH, ∆4-androstenedione, total testosterone and a free androgen index (FAI) than observed in non-PCOS controls. In women with PCOS, total testosterone and AMH levels in the FF were also higher, while TAC was lower compared to non-PCOS. Furthermore, circulating AMH levels were positively correlated with ∆4-androstenedione, albeit negatively correlated with TAC. In this study we demonstrated that the susceptibility to OS, as assessed by the total antioxidant capacity in the FF, is higher in women with PCOS and inversely related to AMH levels. This study results lead us to forge the reasonable hypothesis that the greater susceptibility to OS within the follicle microenvironment is potentially at the end of a roadway that starts with elevated ∆4-androstenedione and AMH within the FF, which in turn are mirrored by circulating AMH and androgen levels. Thus, suggesting that circulating AMH levels could act as a surrogate biomarker of follicular fluid oxidative stress in women with PCOS.

Oxidative stress in polycystic ovary syndrome: a case-control study.

To compare the serum levels of biochemical and oxidative stress markers i.e., malondialdehyde (MDA) and paraoxonase-1(PON1) in polycystic ovary syndrome (PCOS) patients and healthy female individuals of reproductive age group (18-40 years). This case-control study was conducted in Dow University of Health Sciences (DUHS), Karachi from June 2019 to October 2020. Seventy Subjects including 35 PCOS patients that have primary subfertility problem (cases) and 35 healthy and fertile females (controls) were recruited. Serum samples were collected for analysis of insulin, sex hormone-binding globulin, testosterone, fasting blood glucose and lipid profile. PON 1 and MDA levels were estimated by ELISA. Comparison between the two groups was done using independent t-test. The patients had significantly increased mean body mass index (28.5+4.6 kg/m2 vs 25.7+4.5 kg/m2, p=0.014), systolic (129.6±13.9 mm of Hg vs 113±7.7 mm of Hg, p<0.001) and diastolic (78.7±8.8 mm of Hg vs 74.6±6.7 mm of Hg, p=0.032) blood pressures compared to controls. The high-density lipoprotein cholesterol levels were significantly lower in PCOS (42.2±8.6mg/dl) than controls (48.8±11.8mg/dl, p=0.009, p=0.009). Serum insulin (14.3±5.8 uIU/mL) vs (10.0±5.2 uIU/mL), p=0.002 and testosterone levels (1.3±0.9 nmol/L) vs (0.82±0.3 nmol/L), p<0.001 were significantly higher whereas sex hormone binding globulin (SHBG) levels (35.2±19.7nmol/L vs 58.8±31.0 nmol/L) were significantly lower in patients than healthy controls (p<0.001). Both oxidative stress markers, paraoxonase 1 (7.7±2.4 vs 6.4±2.6 μg/mL, p=0.04) and malondialdehyde (2.5±1.0 vs 1.9+0.51μg/mL, p=0.034) levels were significantly elevated in PCOS patients than controls. No significant correlation was found between dietary habits and life style between cases and controls. The study reported significantly elevated levels of oxidative stress markers in PCOS patients.

Map4k4 is up-regulated and modulates granulosa cell injury and oxidative stress in polycystic ovary syndrome via activating JNK/c-JUN pathway: An experimental study

The regulatory mechanism on granulosa cells (GCs) oxidative injury is becoming increasingly important in polycystic ovary syndrome (PCOS) studies. Serine/threonine kinase mitogen-activated protein 4 kinase 4 (Map4k4) is linked with oxidative injury and possibly associated with premature ovarian failure and ovarian dysgenesis. Herein, we investigated the function and mechanism of Map4k4 in a PCOS rat model. A microarray from GEO database identified Map4k4 was up-regulated in the ovarian of PCOS rats, and functional enrichments suggested that oxidative stress-associated changes are involved. We verified the raised Map4k4 expression in an established PCOS rat model and also in the isolated PCOS-GCs, which were consistent with the microarray data. Map4k4 knockdown in vivo contributed to regular estrous cycle, restrained steroid concentrations and ovarian injury in PCOS rats. Both Map4k4 silencing in vivo and in vitro attenuated the PCOS-related GC oxidative stress and apoptosis. Mechanically, Map4k4 activated the JNK/c-JUN signaling pathway. Importantly, a JNK agonist restored the suppressive effects of Map4k4 silencing on PCOS-induced granulosa cell injury and oxidative stress. Besides, Map4k4 may be a target gene of miR-185-5p. In conclusion, Map4k4, a potential target of miR-185-5p, is up-regulated and induces ovarian GC oxidative injury by activating JNK/c-JUN pathway in PCOS. The Map4k4/JNK/c-JUN mechanism may provide a new idea on the treatment of PCOS.

A case-control study about markers of stress in normal-/overweight women with polycystic ovary syndrome and in controls.

Polycystic ovary syndrome (PCOS) is linked to an elevated risk of psychological disorders, decreased quality of life and emotional distress. Serum cortisol as a potential stress marker has been found to be increased in women with PCOS. The aim of this study was to evaluate both saliva stress markers and subjective psychological distress in women with PCOS. In a prospective case-control study, 31 PCOS women and 31 healthy controls were included. Salivary cortisol, and metanephrines were collected in the morning and in the evening. Emotional distress and quality of life were assessed by means of the Perceived Stress Scale (PSS-10) and the Short Form-36 (SF-36). Multivariable generalized linear models were applied to test the influence of various parameters on numerical outcome parameters. After correction for age and body mass index (BMI), there were no statistically significant differences of salivary biomarkers between PCOS women and healthy controls (p>0.05). PCOS patients revealed significantly higher increased PSS total scores and lower quality of life in all SF-36 modules apart from pain (p< 0.05). The PSS total score was positively correlated to prolactin in PCOS women (r= 0.450; p= 0.011). In overweight/obese PCOS patients, a higher BMI, a higher Ferriman Gallwey score and higher age significantly predicted the PSS total score (p< 0.05). Stress measured by salivary biomarkers did not differ between PCOS women and healthy controls, whereas stress scores evaluated by questionnaires were significantly greater in women with PCOS. A higher BMI, hirsutism and a higher age seem to be the main modulators of subjective stress in PCOS. Prolactin might serve as a biomarker for chronic stress in PCOS women.

Total antioxidant capacity and oxidative stress in Polycystic ovary syndrome, a case-control study

Total antioxidant capacity and oxidative stress in Polycystic ovary syndrome, a case-control study

The Key Role of Inflammation and Oxidative Stress in Polycystic Ovary Syndrome and Testicular Torsion: A Review of Their Induction in Rat Model

The Key Role of Inflammation and Oxidative Stress in Polycystic Ovary Syndrome and Testicular Torsion: A Review of Their Induction in Rat Model

Could sestrin protein in serum be a new marker of oxidative stress in patients with polycystic ovary syndrome?

Objective PCOS (polycystic ovary syndrome) is one of the most common endocrinological disorders and it is the threshold of many systemic disorders. There are many studies in the literature on the mechanisms that cause increased oxidation in PCOS. Sestrin protein is known to regulate the oxidation. In this study, it is aimed to examine the changes in the level of sestrin protein in women with PCOS. Methods A total of 60 women participated the study, 30 of whom were diagnosed with PCOS according to the Rotterdam criteria. Also, 30 women were included in the study as the control group. Demographic information, biochemical analysis results, and sestrin levels of the patients in each group were compared. Results The median sestrin level was 6.2 ± 0.8 in the PCOS group and 3.38 ± 0.4 in the control group (p < 0.001). As a result of the evaluation made with ROC analysis, it is observed that serum sestrin levels may be meaningful in the diagnosis of polycystic ovary syndrome. The area under the curve (AUC) value for the 4.69 level was 99.4% (p < 0.001, 95% CI: 96.7% vs. 100%, sensitivity: 100%, specificity: 96.7%). Conclusions Sestrin protein is associated with oxidative stress. Sestrin protein can be used as an indicator of increased oxidative stress in PCOS.

Abnormal Endometrial Receptivity and Oxidative Stress in Polycystic Ovary Syndrome.

Polycystic ovary syndrome (PCOS) is a common endocrine and metabolic disorder in women of childbearing age. Individual heterogeneity is evident, and the prevalence rate ranges between 6 and 15% globally. The prevalence rate of PCOS in Chinese women of childbearing age is 5.6%. The main manifestations are infertility, sparse menstruation, irregular vaginal bleeding, long-term endometrial hyperplasia, and endometrial cancer. PCOS is often associated with hyperandrogenemia, insulin resistance, hyperinsulinemia, obesity, metabolic syndrome, and intestinal flora disorder. Although there have been many studies in the past, the underlying pathophysiological mechanism of the disease is still unclear. Studies have shown that PCOS diseases and related complications are closely related to local oxidative stress imbalance in the endometrium, leading to poor endometrial receptivity and effects on pregnancy. Previous reviews have mainly focused on the abnormal mechanism of ovarian oxidative stress in women with PCOS, while reviews on endometrial receptivity and oxidative stress are relatively insufficient. This study reviews the abnormal cellular and molecular mechanisms of oxidative stress due to comorbidities in women with PCOS, leading to a downregulation of endometrial receptivity.

Psikoneuroimunologi Depresi pada Polycystic Ovary Syndrome (PCOS)

&lt;p&gt;&lt;strong&gt;&lt;em&gt;Introduction&lt;/em&gt;&lt;/strong&gt;&lt;em&gt;: Polycystic ovary syndrome (PCOS) is heterogeneous, complex endocrine disorder with unknown etiology, affecting 4%−18% of reproductive age women and associated with reproductive, metabolic and psychological dysfunction. Along with physical disorders, many mental disorders are also associated with PCOS, about 40% of women with PCOS have depression. This literature review aims to explore how PCOS can lead to depression in term of psychoneuroimmunology aspects.&lt;/em&gt;&lt;/p&gt;&lt;p&gt;&lt;strong&gt;&lt;em&gt;Method&lt;/em&gt;&lt;/strong&gt;&lt;em&gt;: Literature review was conducted through search engine from Google Scholar and Clinical Key with keywords “Polycystic ovary syndrome”, “depression”, “psychoneuroimmunology”, “distress”, and “inflammation” from 2015-2020.&lt;/em&gt;&lt;/p&gt;&lt;p&gt;&lt;strong&gt;&lt;em&gt;Result&lt;/em&gt;&lt;/strong&gt;&lt;em&gt;: The important role of the HPG axis in the pathophysiology of mood disorder has concluded that high comorbidity between depression and PCOS are caused by hyperandrogenism and insulin resistance mediated by low grade chronic inflammation. The activation of HPA by stress exerts an inhibitory effect on the female reproductive system. CRH can inhibit GnRH secretion from the hypothalamus. The anti-reproductive action of CRH in the ovaries of women with high psychosocial stress lead to early ovarian failure. In addition, the pathophysiology of depression and mental stress in PCOS is associated with various changes including high activity of pro-inflammation markers and the body's immune system during stress, it has also been linked to increased cortisol levels, increased sympathetic activity and decreased serotonin levels in the central nervous system.&lt;/em&gt;&lt;/p&gt;&lt;p&gt;&lt;strong&gt;&lt;em&gt;Result&lt;/em&gt;&lt;/strong&gt;&lt;em&gt;: There’s close relationship between PCOS and depression in terms of psychoneuroimmunology aspects, by HPG axis role. Comprehensive management of depression is improving outcome strategy in women with PCOS by involving CLP.&lt;/em&gt;&lt;/p&gt;&lt;p&gt;&lt;strong&gt;&lt;em&gt;Keywords&lt;/em&gt;&lt;/strong&gt;&lt;em&gt;: &lt;strong&gt;Polycystic ovary syndrome (PCOS), Depression, Psychoneuroimmunology, HPG axis&lt;/strong&gt;&lt;/em&gt;&lt;/p&gt;

Inter relationship of sympathetic reflex response and oxidative stress in polycystic ovary syndrome

Background: Polycystic ovary syndrome (PCOS) is a very common reproductive endocrine disorder. Altered cardiovascular autonomic modulation and oxidative stress may predispose PCOS patients to cardiac events in the long term. Objective: To assess the relationship between sympathetic autonomic reactivity and oxidative stress in patients with polycystic ovary syndrome. Methods: This cross-sectional study was conducted in the Department of Physiology, Bangabandhu Sheikh Mujib Medical University (BSMMU), Shahbag, Dhaka from September 2018 to August 2019 on 35 newly diagnosed obese (BMI ≥25kg/m2) PCOS patients aged 20-35 years. Age and BMI matched 35 apparently healthy subjects were also enrolled. Two noninvasive conventional autonomic function tests, such as systolic blood pressure (SBP) fall during active standing and diastolic blood pressure (DBP) rise during sustained handgrip were conducted on all subjects for evaluation of sympathetic reactivity. For assessment of oxidative stress, plasma malondialdehyde level as oxidant and plasma catalase level as antioxidant were measured in all subjects by spectrophotometry. For statistical analysis Independent sample “t” test, Pearson’s correlation test and multiple regression analysis were done. Results: In this study PCOS patients had significantly higher resting heart rate, SBP and DBP than healthy control (p&lt;0.01). Fall of SBP during standing was significantly lower (p&lt;0.05) while rise of DBP during sustained handgrip was significantly higher (p&lt;0.05) in PCOS compared to healthy control. Plasma catalase level was significantly lower (p&lt;0.01) and plasma malondialdehyde level significantly higher (p&lt;0.001) in PCOS in comparison to healthy control. On correlation analysis, rise of DBP showed significant negative correlation (p&lt;0.05) with plasma catalase level in PCOS. On multiple regression analysis rise of DBP showed significant negative (p&lt;0.01) association with plasma catalase and significant positive (p&lt;0.01) association plasma malondialdehyde in PCOS. Conclusion: Based on these results it is concluded that measures of sympathetic reactivity were related to oxidative stress in PCOS. J Bngladesh Soc Physiol 2021;16(1): 61-69

Effects of salubrinal on ER stress in an experimental model of polycystic ovary syndrome

ABSTRACT This study aimed to investigate the role of endoplasmic reticulum (ER) stress in polycystic ovary syndrome (PCOS) and the effect of salubrinal (SAL) on this role. Animals were divided into four groups as control, PCOS, PCOS+SAL and SAL. Weights and serum testosterone levels were increased in the PCOS group while serum LH and ATF4 expressions were decreased. Morphometrically, number of follicles with a diameter between 150 and 300 µm were declined and number of follicles larger than 300 µm as well as the percentage of cystic follicles (CFs) were increased. Immunoreactivities of GRP78 and p-eIF2α were decreased, whereas oxidative stress (OS) dependent PAR expression was increased. Ultrastructurally, the PCOS group had no ER enlargement which was observed in the control group, while there were mitochondrial damage in granulosa cells (GCs). Elevated OS levels did not induce but rather decreased ER stress in GCs, and SAL injection in the PCOS model was ineffective on searched parameters. Since ER stress plays roles in certain physiological processes, we suggest that inhibitors of ER stress may not be always useful for reproductive tissues.

Role of Oxidative Stress in Polycystic Ovary Syndrome

Introduction: Polycystic ovary syndrome is one of the most common causes of infertility. 6 to 8 percent of women of childbearing age have this endocrine disorder. Biochemical abnormalities in these patients lead to imbalance of female hormones and increased androgens, which can have consequences such as menstrual cycle disorder, hirsutism, acne vulgaris and androgenic alopecia. Despite the long history of studies on polycystic ovary syndrome, the cause is still unknown. Oxidative stress is an imbalance between the production of reactive oxygen species and the amount of antioxidant. When this balance is disturbed, the result is an increase in the level of oxidative stress. Oxidative stress is currently recognized as one of the major pathophysiologies of many disorders and diseases, including polycystic ovary syndrome. Understanding the mechanisms of oxidative stress is crucial for developing strategies for the prevention and treatment of this disease. In this article, we reviewed the data on the mechanism of oxidative stress in polycystic ovary syndrome.

Indicator of early kidney injury in adolescents with polycystic ovary syndrome: Can urine NGAL level be?

Introduction and Purpose The Urinary Neutrophil-gelatinase associated lipocalin (NGAL) levels which are a biomarker for early diagnosis of kidney damage that may develop in patients with Polycystic Ovary Syndrome (PCOS) were investigated in the study. Material and Methods The 30 patients diagnosed with Polycystic Ovarian Syndrome between the ages of 13 and 18 who applied to the Yuzuncu Yil University General Children's Outpatient Clinic were included in the PCOS group and 30 healthy adolescents without any known acute or chronic illness and drug use were included in the control group. Findings Urine NGAL value was 842.204 ± 21.561 in PCOS group and 775.379 ± 23.98 in control group. NGAL level in PCOS group was statistically significantly higher than control group (p: .045). When we examine the relationship between dyslipidemia and PCOS; While dyslipidemia was positive in 10 (33.7%) patients in the PCOS group, it was negative in 20 (66.7%) patients. While 1 patient had dyslipidemia, 29 patients did not have dyslipidemia in the control group. A significant relationship was found between dyslipidemia and PCOS (p: .005). Conclusion We found that subclinical kidney dysfunction started in early stage patients in PCOS in our study. The urine NGAL level was thought to increase in response to increased oxidative stress in PCOS. We found no relationship between, insulin resistance and urea, BUN, creatinine and NGAL levels. However, we found a negative correlation between NGAL level and LDL. In addition, dyslipidemia, insulin resistance and ALT elevation were detected in the PCOS group.

Relationship between parasympathetic reactivity and oxidative stress in Polycystic ovary syndrome

Background: Polycystic ovary syndrome (PCOS) is a very common reproductive hormone disorder. Altered cardiovagal autonomic modulation and oxidative stress may predispose PCOS patients to increased cardiovascular morbidity.&#x0D; Objective: To assess the relationship between parasympathetic reactivity and oxidative stress in patients with PCOS.&#x0D; Methods: This crosssectional study was conducted in the Department of Physiology, Bangabandhu Sheikh Mujib Medical University (BSMMU), Shahbagh, Dhaka from September 2018 to August 2019 on 35 newly diagnosed obese (BMI ≥25kg/m2) PCOS patients aged 20-35 years. Age and BMI matched 35 apparently healthy women were also enrolled as control. Three noninvasive conventional autonomic function tests, such as heart rate response to deep breathing, standing and the Valsalva maneuver, were used for evaluation of parasympathetic reactivity. For assessment of oxidative stress, plasma malondialdehyde level (oxidant) and plasma catalase level(antioxidant) were measured in all subjects by spectrophotometry. Data were expressed as mean± SD. For statistical analysis Independent sample “t” test, Pearson’s correlation test and multiple regression analysis were done as applicable.&#x0D; Results: In this study PCOS patients had significantly higher (p&lt;0.01)resting heart rate, systolic and diastolic blood pressure than that of healthy control. But Expiration: Inspiration ratio, Expiration:Inspiration difference and 30:15 ratio during standing were significantly lower (p&lt;0.001, p&lt;0.01 and p&lt;0.05 respectively) in PCOS compared to control. In addition, plasma catalase level was significantly lower (p&lt;0.01)and plasma malondialdehyde level significantly higher (p&lt;0.001) in PCOS in comparison to healthy control. Multiple regression analysis showed plasma catalase as a significant positive predictor (p&lt;0.05) of the Valsalva ratio in PCOS. Also, Valsalva ratio showed significant negative association (p&lt;0.05) with plasma malondialdehyde (p&lt;0.01)in PCOS.&#x0D; Conclusion: Based on these results it is concluded that impaired parasympathetic reactivity showed inverse relationship with oxidative stress in PCOS.&#x0D; J Bangladesh Soc Physiol. 2019, December; 14(2): 48-55

Association between miRNAs Expression and Signaling Pathways of Oxidative Stress in Polycystic Ovary Syndrome.

Association between miRNAs Expression and Signaling Pathways of Oxidative Stress in Polycystic Ovary Syndrome.

Oxidative Stress and Polycystic Ovary Syndrome: A Brief Review.

Polycystic ovary syndrome (PCOS) is one of the most common hormonal disorders, occurring in 5–10% women in reproductive ages. Despite a long history of studies on PCOS, its etiology is still unknown. Oxidative stress is now recognized to play a central role in the pathophysiology of many different disorders, including PCOS. Although intracellular reactive oxygen species (ROS) production and propagation are controlled by highly complex antioxidant enzymatic and non-enzymatic systems, understanding of mechanisms that oxidative stress is important to develop strategies for prevention and therapy of PCOS. This article reviews the literature data related to the mechanisms of oxidative stress in PCOS.