OBJECTIVE: To determine whether polycystic ovary syndrome (PCOS) independently influences oxidative stress and inflammation or if the culprit is the comorbidities of obesity and/or insulin resistance common to this condition. STUDY DESIGN: Thirty women with PCOS were matched for age, body mass index and insulin resistance with 30 control subjects. Oxidative stress was examined by measuring the total oxidant status (TOS) and total antioxidant capacity (TAC) by spectrophotometric assay. The inflammatory biomarkers, C-reactive protein, plasminogen activator inhibitor-1, myeloperoxidase, neopterin, and serum amyloid A were measured by ELISA methodologies. RESULTS: Oxidative status was increased in the PCOS subjects relative to their weight-matched controls (TOS: obese PCOS patients vs. obese controls, 42.42 +/- 4.49 vs. 32.57 +/- 1.97, p<0.05; lean PCOS patients vs. lean controls, 33.69 +/- 1.59 vs. 28.69 +/- 1.18 micromol H2O2 Equiv/L, p < 0.05). Furthermore, antioxidant capacity was lower in the lean PCOS group relative to their weight-matched controls (TAC: lean PCOS patients vs. lean controls, 1.10 +/- 0.09 vs. 1.49 +/- 0.03 nmol Trolox Equiv/L, p < 0.05). CONCLUSION: These results suggest that PCOS independently influenced oxidative stress. Overall, the presence of PCOS may increase cardiovascular risk.
OBJECTIVE: To determine whether polycystic ovary syndrome (PCOS) independently influences oxidative stress and inflammation or if the culprit is the comorbidities of obesity and/or insulin resistance common to this condition. STUDY DESIGN: Thirty women with PCOS were matched for age, body mass index and insulin resistance with 30 control subjects. Oxidative stress was examined by measuring the total oxidant status (TOS) and total antioxidant capacity (TAC) by spectrophotometric assay. The inflammatory biomarkers, C-reactive protein, plasminogen activator inhibitor-1, myeloperoxidase, neopterin, and serum amyloid A were measured by ELISA methodologies. RESULTS: Oxidative status was increased in the PCOS subjects relative to their weight-matched controls (TOS: obese PCOSpatients vs. obese controls, 42.42 +/- 4.49 vs. 32.57 +/- 1.97, p<0.05; lean PCOSpatients vs. lean controls, 33.69 +/- 1.59 vs. 28.69 +/- 1.18 micromol H2O2 Equiv/L, p < 0.05). Furthermore, antioxidant capacity was lower in the lean PCOS group relative to their weight-matched controls (TAC: lean PCOSpatients vs. lean controls, 1.10 +/- 0.09 vs. 1.49 +/- 0.03 nmol Trolox Equiv/L, p < 0.05). CONCLUSION: These results suggest that PCOS independently influenced oxidative stress. Overall, the presence of PCOS may increase cardiovascular risk.
Authors: Sana N Khan; Faten Shaeib; Tohid Najafi; Mahendra Kavdia; Bernard Gonik; Ghassan M Saed; Pravin T Goud; Husam M Abu-Soud Journal: PLoS One Date: 2015-07-21 Impact factor: 3.240
Authors: Sara Samino; Maria Vinaixa; Marta Díaz; Antoni Beltran; Miguel A Rodríguez; Roger Mallol; Mercedes Heras; Anna Cabre; Lorena Garcia; Nuria Canela; Francis de Zegher; Xavier Correig; Lourdes Ibáñez; Oscar Yanes Journal: Sci Rep Date: 2015-06-23 Impact factor: 4.379