Savić-Radojević Ana, Mažibrada Ilijana, Djukić Tatjana, Stanković Zoran B, Plješa-Ercegovac Marija, Sedlecky Katarina, Bjekić-Macut Jelica, Simić Tatjana, Mastorakos George, Macut Djuro
Clinic for Endocrinology, Diabetes and Metabolic Diseases, Clinical Centre of Serbia, Belgrade, Serbia, Serbia and Montenegro.
Endokrynol Pol. 2018;69(4):366-374. doi: 10.5603/EP.a2018.0034. Epub 2018 Jun 28.
It has been supposed that endocrine disturbances might be responsible for polycystic ovary syndrome (PCOS)-associated oxida-tive stress, with special emphasis on hyperandrogenism. Considering the potential relationship between hyperandrogenism and increased free radical production, parameters of oxidative stress were determined in non-obese normoinsulinemic adolescent girls newly diagnosed with PCOS.
Nitrotyrosine, thiol group concentrations, glutathione peroxidase, and superoxide dismutase activities were determined under fasting conditions and during oral glucose tolerance test (OGTT) in 35 PCOS patients and 17 controls. Insulin resistance was assessed by the homeostasis model (HOMA-IR), HOMA β, insulinogenic index (IGI), Matsuda insulin sensitivity index (ISI), and AUC for glucose. Glutathione S-transferases (GSTs) polymorphisms were determined by PCR.
Under fasting conditions, no significant difference of oxidative stress parameters was found between PCOS and controls. Acute hyperglycaemia during OGTT induced significant alteration in parameters of oxidative protein damage in PCOS patients. Alteration in nitrotyrosine concentrations correlated with testosterone, DHEAS, androstenediones, FAI, and LH, while changes in thiol groups cor-related with DHEAS. Significant inverse association was found between LH and ISI, as well as AUC glucose and thiol groups. PCOS girls, carriers of GSTM1-null genotype, had significantly lower testosterone in comparison to ones with GSTM1-active genotype.
PCOS girls exhibited high free radical production together with unchanged antioxidant enzymatic capacity, independently from obesity and insulin resistance. Based on associations between oxidative stress parameters and testosterone, DHEAS, and androsten-edione, it can be suggested that increased free radical production, probably as a consequence of hyperandrogenaemia, is an early event in the development of PCOS.
人们认为内分泌紊乱可能是多囊卵巢综合征（PCOS）相关氧化应激的原因，其中特别强调高雄激素血症。考虑到高雄激素血症与自由基产生增加之间的潜在关系，我们对新诊断为PCOS的非肥胖正常胰岛素血症青春期女孩的氧化应激参数进行了测定。
在空腹条件下以及口服葡萄糖耐量试验（OGTT）期间，测定了35例PCOS患者和17例对照者的硝基酪氨酸、巯基浓度、谷胱甘肽过氧化物酶和超氧化物歧化酶活性。通过稳态模型（HOMA-IR）、HOMA β、胰岛素生成指数（IGI）、松田胰岛素敏感性指数（ISI）和葡萄糖曲线下面积（AUC）评估胰岛素抵抗。通过聚合酶链反应（PCR）测定谷胱甘肽S-转移酶（GSTs）基因多态性。
在空腹条件下，PCOS患者与对照组之间的氧化应激参数无显著差异。OGTT期间的急性高血糖导致PCOS患者氧化蛋白损伤参数发生显著变化。硝基酪氨酸浓度的变化与睾酮、硫酸脱氢表雄酮（DHEAS）、雄烯二酮、游离雄激素指数（FAI）和促黄体生成素（LH）相关，而巯基的变化与DHEAS相关。LH与ISI以及AUC葡萄糖与巯基之间存在显著负相关。GSTM1基因缺失型的PCOS女孩与GSTM1基因活性型的女孩相比，睾酮水平显著降低。
PCOS女孩表现出高自由基产生，同时抗氧化酶能力未改变，且与肥胖和胰岛素抵抗无关。基于氧化应激参数与睾酮、DHEAS和雄烯二酮之间的关联，可以认为自由基产生增加可能是高雄激素血症的结果，是PCOS发生发展的早期事件。
