Macut D, Simic T, Lissounov A, Pljesa-Ercegovac M, Bozic I, Djukic T, Bjekic-Macut J, Matic M, Petakov M, Suvakov S, Damjanovic S, Savic-Radojevic A
Institute of Endocrinology, Diabetes and Metabolic Diseases, Clinical Center of Serbia, University of Belgrade, Serbia.
Exp Clin Endocrinol Diabetes. 2011 Jul;119(7):451-5. doi: 10.1055/s-0031-1279740. Epub 2011 Jun 10.
To get more insight into molecular mechanisms underlying oxidative stress and its link with insulin resistance, oxidative stress parameters, as well as, antioxidant enzyme activities were studied in young, non-obese women with polycystic ovary syndrome (PCOS). Study was performed in 34 PCOS women and 23 age and body mass index (BMI)-matched healthy controls. Plasma nitrotyrosine and malondialdehyde (MDA), representative byproducts of protein and lipid oxidative damage, were determined by enzyme immunoassay. Antioxidant enzyme activities, superoxide dismutase (SOD) and glutathione peroxidase (GPX) were studied spectrophotometrically. Insulin resistance was calculated using homeostasis assessment model (HOMA-IR). Plasma nitrotyrosine and MDA were increased, but only nitrotyrosine was significantly higher (p < 0.05) in PCOS women compared to controls. Uric acid (surrogate marker of × antine oxidase) was also significantly elevated in PCOS (p < 0.05). Both plasma SOD and GPX activity showed no statistically significant difference between PCOS and controls. Indices of insulin resistance (insulin and HOMAIR) were significantly higher in PCOS group and positively correlated with level of MDA (r = 0.397 and r = 0.523, respectively; p < 0.05) as well as GPX activity (r = 0.531 and r = 0.358, respectively; p < 0.05). Our results indicate that insulin resistance could be responsible for the existence of subtle form of oxidative stress in young, nonobese PCOS women. Hence, presence of insulin resistance, hyperinsulinemia and oxidative damage are likely to accelerate slow development of cardiovascular disease in PCOS.
为了更深入了解氧化应激的分子机制及其与胰岛素抵抗的联系，我们对患有多囊卵巢综合征（PCOS）的年轻非肥胖女性的氧化应激参数以及抗氧化酶活性进行了研究。研究对象为34名PCOS女性和23名年龄及体重指数（BMI）匹配的健康对照者。采用酶免疫分析法测定血浆硝基酪氨酸和丙二醛（MDA），它们分别是蛋白质和脂质氧化损伤的代表性副产物。通过分光光度法研究抗氧化酶超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GPX）的活性。使用稳态评估模型（HOMA-IR）计算胰岛素抵抗。与对照组相比，PCOS女性的血浆硝基酪氨酸和MDA升高，但只有硝基酪氨酸显著更高（p<0.05）。尿酸（X抗氧化酶的替代标志物）在PCOS中也显著升高（p<0.05）。PCOS组和对照组之间血浆SOD和GPX活性均无统计学显著差异。PCOS组的胰岛素抵抗指标（胰岛素和HOMA-IR）显著更高，且与MDA水平呈正相关（分别为r=0.397和r=0.523；p<0.05）以及GPX活性呈正相关（分别为r=0.531和r=0.358；p<0.05）。我们的结果表明，胰岛素抵抗可能是年轻非肥胖PCOS女性中存在轻微氧化应激形式的原因。因此，胰岛素抵抗、高胰岛素血症和氧化损伤的存在可能会加速PCOS患者心血管疾病的缓慢发展。
