N-acetyl cysteine reduces oxidative toxicity, apoptosis, and calcium entry through TRPV1 channels in the neutrophils of patients with polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS) is a common inflammatory and oxidant disease with an uncertain pathogenesis. N-acetyl cysteine (NAC) decreases oxidative stress, intracellular free calcium ion [Ca(2+)]i, and apoptosis levels in human neutrophil. We aimed to investigate the effects of NAC on apoptosis, oxidative stress, and Ca(2+) entry through transient receptor potential vanilloid 1 (TRPV1) and TRP melastatin 2 (TRPM2) channels in neutrophils from patients with PCOS. Neutrophils isolated from PCOS group were investigated in three settings: (1) after incubation with TRPV1 channel blocker capsazepine or TRPM2 channel blocker 2-aminoethyl diphenylborinate (2-APB), (2) after supplementation with NAC (for 6 weeks), and (3) with combination (capsazepine + 2-APB + NAC) exposure. The neutrophils in TRPM2 and TRPV1 experiments were stimulated by N-formyl-L-methionyl-L-leucyl-L-phenylalanine (fMLP; 1 µM) and capsaicin (10 µM) as concentration agonists, respectively. Neutrophil lipid peroxidation and capsaicin-induced increase in [Ca(2+)]i concentrations were reduced by capsazepine and NAC treatments. However, the [Ca(2+)]i concentration did not change by fMLP stimulation. Neutrophil lipid peroxidation, apoptosis, caspase-3, caspase-9, cytosolic reactive oxygen species production, and mitochondrial membrane depolarization values were decreased by NAC treatment although neutrophil glutathione peroxidase and reduced glutathione levels were increased by the NAC treatment. Serum lipid peroxidation, luteinizing hormone, testosterone, insulin, interleukin-1 beta, and homocysteine levels were decreased by NAC treatment although serum vitamin A, beta-carotene, vitamin E, and total antioxidant status were increased by the NAC treatment. In conclusion, NAC reduced oxidative stress, apoptosis, cytokine levels, and Ca(2+) entry through TRPV1 channel, which provide supportive evidence that oxidative stress and TRPV1 channel plays a key role in etiology of PCOS.

The evaluation of carotid intima-media thickness and visceral obesity as an atherosclerosis predictor in newly-diagnosed polycystic ovary syndrome.

PURPOSE: Polycystic ovary syndrome (PCOS) is a common endocrine disorder which is associated with multiple risk factors for atherosclerosis. The aim of this study was to investigate the CIMT which is used in the early diagnosis of atherosclerosis and visceral obesity by ultrasound in newly diagnosed polycystic ovary syndrome with normal body mass index. MATERIALS AND METHODS: A case-control study was conducted on 25 PCOS women (18-30 years of age) and 25 controls. BMI was matched volunteer controls. Carotid intima media thickness (CIMT) and fat distribution as visceral fat thickness (VFT) with subcutaneous fat thickness (SFT) were measured by ultrasound. After, visceral fat ratio (VFR) fat ratio (VFR) was calculated using VFT divided by SFT. The variables were compared using the χ(2)-test and Student's t test. RESULTS: Comparing women with PCOS to the control group showed that CIMT was similar in both groups (p=0.84). The VFT in the PCOS group was higher than the control group (p=0.048). Whereas, the SFT was higher in the control group when compared to women with PCOS (p=0.007). The VFR was significantly higher in women with PCOS when compared to the control group (1.12 ± 0.38 vs. 0.81 ± 0.34; p=0.005). CONCLUSIONS: CIMT which used as early atherosclerosis predictors have not increased in newly diagnosed PCOS women. Body fat distribution was observed in visceral area in the newly diagnosed PCOS women. VFR follow up may provide benefit as a quantitative method for the assessment and follow up of visceral obesity in women with PCOS.