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Seminal Malondialdehyde Concentration And Superoxide Dismutase, Catalase Activity In Male Infertility

机译:男性不育症患者精液丙二醛浓度和超氧化物歧化酶,过氧化氢酶活性

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Aims & objectives- Reactive oxygen species (ROS) induced lipid peroxidation is associated with sperm function. Malondialdehyde (MDA) concentration, Superoxide dismutase and Catalase (CAT) activity represent the lipid peroxidation and spermicidal antioxidant status respectively. The present study aimed to evaluate the relationship of MDA, Superoxide dismutase and Catalase levels with sperm parameters. Materials & methods-Specimens were divided into two groups: Group I - Normospermia (n=30); Group II - Oligoasthenozoospermia (n=30). Seminal MDA concentration was measured by thiobarbituric acid reaction method. Seminal SOD activity was measured by Marklund and Marklund method. Seminal Catalase activity was measured by potassium dichromate colorimetric assay. Seminal MDA levels, SOD and Catalase activities in both groups were compared. Significance of the data is analyzed using unpaired t-test. Results - MDA concentrations in both groups were significantly different (12.65 ± 1.68 nmole/m vs 21.58 ± 1.54 nmole/ml). SOD & Catalase activities in both groups were also significantly different. SOD levels in oligoasthenozoosperia were 27.99 ± 4.36 Units/ml and in normospermia 12.96 ± 3.35 U/ml whereas levels of catalase in oligiasthenozoosperia were 1.36 ± 0.44 Units/mg of protein and normospermia were 5.12 ± 1.03 Units/mg of protein. SOD & Catalase activities were positively and significantly correlated with the sperm concentration and sperm motility. Conclusion : Measurement of seminal MDA concentrations, antioxidant enzymes SOD & CAT can be used as a additional, simple and useful tool in predicting quality of sperm parameters. Introduction Infertility has been a major medical problem as well as social stigma. Despite of enormous progress in research, most of the blame for infertility is placed on the female. Advances in understanding of gonadal/sperm physiology have increased our knowledge of male infertility. Defective sperm function is the most prevalent cause of male infertility. [1]. Many environmental, physiological, and genetic factors have been implicated in infertility. Hence, it is very important to identify factors, which affect normal sperm function. Free radical-induced oxidative damage to spermatozoa is a condition, which is gaining considerable attention for its role in inducing poor sperm function [2]. Understanding of such conditions will help in designing new and effective treatment strategies.Until recently, Reactive oxygen species (ROS), were considered toxic to the human spermatozoa. However a strong evidence suggests that small amounts of ROS are necessary for spermatozoa to acquire fertilizing capabilities [3], [4],[5]. Theoretically, cellular damage in the semen is due to improper balance between ROS generation and scavenging activities which causes ‘Oxidative stress’.The increased ROS formation leads to lipid peroxidation. This is correlated with reduced sperm motility [6], [7], due to decrease in axonemal protein phosphorylation and sperm immobilization, both of which are associated with a reduction in membrane fluidity [8]. Another hypothesis is that H2O2 can diffuse across the cell membranes and inhibit the activity of enzyme, glucose-6-phosphate dehydrogenase (G6PD). Inhibition of G6PD decreases the availability of NADPH and results in accumulation of oxidized glutathione, which reduces the antioxidant defense of the spermatozoa [9].The seminal plasma is well endowed with an array of antioxidants such as Superoxide dismutase (SOD), Catalase. These antioxidants protect spermatozoa against oxidative stress [10],[11],[12]. SOD scavenges superoxide anion and converts it into less potent hydrogen peroxide. Catalase detoxifies H2O2 to water and oxygen [13] This study was undertaken to correlate detrimental effect of free radicals on sperm physiology in infertile males. The prime aim of the study was to estimate the lipid peroxidation product; MDA & some antioxidants in men with oligoasthenozoospermia compared to
机译:目的与目标-活性氧(ROS)诱导的脂质过氧化与精子功能有关。丙二醛(MDA)浓度,超氧化物歧化酶和过氧化氢酶(CAT)活性分别代表脂质过氧化和杀精子抗氧化剂状态。本研究旨在评估MDA,超氧化物歧化酶和过氧化氢酶水平与精子参数的关系。材料和方法-标本分为两组:第一组-正常精子症(n = 30);第二组-正常精子症(n = 30)。第二组-少精子症(n = 30)。通过硫代巴比妥酸反应法测定精氨酸的MDA浓度。通过Marklund和Marklund方法测量精液SOD活性。通过重铬酸钾比色法测量精液过氧化氢酶活性。比较两组的精液MDA水平,SOD和过氧化氢酶活性。使用不成对的t检验分析数据的重要性。结果-两组中的MDA浓度显着不同(12.65±1.68 nmole / m对21.58±1.54 nmole / ml)。两组中的SOD和过氧化氢酶活性也显着不同。少突舌癣菌中的SOD含量为27.99±4.36单位/毫升,正常精子中的SOD含量为12.96±3.35 U / ml,而少儿精子症精子中的过氧化氢酶含量为1.36±0.44单位/ mg蛋白质,正常精子中的SOD含量为5.12±1.03单位/ mg蛋白质。 SOD和过氧化氢酶活性与精子浓度和精子活力呈显着正相关。结论:精子MDA浓度,抗氧化酶SOD和CAT的测量可作为预测精子参数质量的附加,简单且有用的工具。引言不育一直是主要的医学问题,也是社会的污名。尽管研究取得了巨大进展,但不孕症的大部分归咎于女性。对性腺/精子生理的了解的进步增加了我们对男性不育的了解。精子功能缺陷是男性不育的最普遍原因。 [1]。许多环境,生理和遗传因素都与不育有关。因此,确定影响正常精子功能的因素非常重要。自由基引起的对精子的氧化损伤是一个条件,由于其在诱导精子功能不良中的作用而受到了广泛的关注[2]。了解这些情况将有助于设计新的有效治疗策略。直到最近,活性氧(ROS)仍被认为对人类精子有毒。然而,有力的证据表明,少量的ROS对于精子获得受精能力是必需的[3],[4],[5]。从理论上讲,精液中的细胞损伤是由于ROS产生和清除活性之间的不适当平衡所致,从而导致“氧化应激”。ROS形成的增加导致脂质过氧化。这与降低的精子活力[6] [7]有关,这是由于轴突蛋白磷酸化和精子固定化的降低,两者均与膜流动性的降低有关[8]。另一个假设是H2O2可以扩散到整个细胞膜上并抑制酶,即6磷酸葡萄糖脱氢酶(G6PD)的活性。抑制G6PD会降低NADPH的利用率并导致氧化型谷胱甘肽的积累,从而降低精子的抗氧化防御能力[9]。精浆中具有多种抗氧化剂,如超氧化物歧化酶(SOD),过氧化氢酶。这些抗氧化剂保护精子免受氧化应激[10],[11],[12]。 SOD清除超氧阴离子并将其转化为效力较低的过氧化氢。过氧化氢酶将H2O2解毒为水和氧气[13]进行这项研究,以研究自由基对不育男性精子生理的有害影响。该研究的主要目的是估计脂质过氧化产物。与男性少精症男性精子症相比MDA和某些抗氧化剂

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