Redox status assessment in infertile patients with non-obstructive azoospermia undergoing testicular sperm extraction: A prospective study
Redox status assessment in infertile patients with non-obstructive azoospermia undergoing testicular sperm extraction: A prospective study
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DOI：
10.1111/andr.12721
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发表时间：
2019-11-13
期刊：
影响因子：
4.5
通讯作者：
Coccia, Maria E.
中科院分区：
文献类型：
--
作者：
Cito, Gianmartin;Becatti, Matteo;Coccia, Maria E.
氧化应激（OS）是精子损伤最常见的原因之一，通过内源性产生过氧化氢、超氧阴离子和羟基自由基的毒性作用。外周白细胞是研究os介导的内稳态病理生理学的可行模型，它可能负责细胞功能障碍和细胞损伤。目的评价非阻塞性无精子症（NOA）患者的氧化还原状态，探讨活性氧（ROS）在睾丸分泌性损伤发生中的潜在作用。材料与方法2018年5月至2019年3月，39例患者入组本前瞻性单中心队列研究，分为两组。组1纳入NOA患者19例，组2纳入有输卵管因素的不孕女性伴侣无精子男性20例。所有患者都进行了血清血液检查。NOA接受睾丸精子提取（TeSE）。通过荧光活化细胞分选（FACS）分析评估ROS生成（淋巴细胞、单核细胞和粒细胞）。采用脂质过氧化标志物（MDA）和总抗氧化能力（TAC）评估血浆氧化应激，两者均采用荧光技术评估。结果平均淋巴细胞ROS生成为967.0 +/- 224.5 vs 728.0 +/- 98.0 (NOA vs对照组，P < 0.001)，单核细胞ROS生成为2102.5 +/- 517.5 vs 1253 +/- 171 (P < 0.001)，粒细胞ROS生成为2366.5 +/- 595.4 vs 1751.0 +/- 213.0 （P < 0.001）。与对照组相比，NOA患者血浆脂质过氧化标志物显著增加（2.7 +/- 0.8 vs 0.37 +/- 0.2 nmol/mL, P < 0.001）。与对照组相比，NOA组TAC显著降低（13.4 +/- 3.9 vs 3.0 +/- 0.2 μ mol/mL Trolox当量，P < 0.001）。在血液白细胞亚群ROS生成、血浆脂质过氧化和TAC方面，各组无显著差异（精子回收阳性与阴性，P < 0.05）。结论ROS的产生与精子发生障碍直接相关，导致男性不育的严重情况，包括无精子症。
Background Oxidative stress (OS) is one of the most prevalent causes of sperm damage, through the toxic effects of endogenously generated hydrogen peroxide, superoxide anion, and hydroxyl radicals. Peripheral leukocytes represent a feasible model for studying the pathophysiology of OS-mediated homeostasis, which can be responsible for cell dysfunction and cell injury. Objective To evaluate the redox status in patients with non-obstructive azoospermia (NOA), establishing the potential role exerted by reactive oxygen species (ROS) in the genesis of testicular secretory injury. Material and methods From May 2018 to March 2019, 39 patients were enrolled in this prospective single-center cohort study and divided into two groups. Group 1 included 19 patients with NOA, and Group 2 included 20 normozoospermic men, partners of women with infertility tubal factor. All patients underwent serum blood tests. NOA underwent testicular sperm extraction (TeSE). ROS production (in lymphocytes, monocytes, and granulocytes) was assessed by fluorescence-activated cell sorting (FACS) analysis. Plasma oxidative stress was evaluated by lipid peroxidation markers (MDA) and total antioxidant capacity (TAC) both assessed by fluorometric techniques. Results Mean lymphocyte ROS production resulted 967.0 +/- 224.5 vs 728.0 +/- 98.0 (NOA vs Controls, P < .001), monocyte ROS resulted 2102.5 +/- 517.5 vs 1253 +/- 171 (P < .001), and granulocyte ROS were 2366.5 +/- 595.4 vs 1751.0 +/- 213.0 (P < .001). Significant increases plasma lipid peroxidation markers were found in NOA patients compared with controls (2.7 +/- 0.8 vs 0.37 +/- 0.2 nmol/mL, P < .001). Significant decreased TAC was evident in NOA compared with controls (13.4 +/- 3.9 vs 3.0 +/- 0.2 mu mol/mL Trolox equivalents, P < .001). No significant differences were found in blood leukocyte subpopulations ROS production, plasma lipid peroxidation, and TAC comparing groups (positive vs negative sperm retrieval, P > .05). Conclusion ROS production can be directly related to disorders of spermatogenesis, leading to severe conditions of male infertility, including azoospermia.