D. Vorobets, O. Оnufrovych, R. Fafula, U. Yefremova, Z. Vorobets
{"title":"不同形式病态精子症男性不育精子中l -精氨酸转化的no合成酶途径","authors":"D. Vorobets, O. Оnufrovych, R. Fafula, U. Yefremova, Z. Vorobets","doi":"10.25040/ECPB2016.03.047","DOIUrl":null,"url":null,"abstract":"Elucidation patterns of male germ cells functioning is of particular relevance in the present conditions due to increasing trends in male reproductive disorders [1]. Men infertility is caused by the effect of different pathological processes in genital organs and glands, resulting in pathospermia, which reduces fertilizing ability of sperm cells. Common methods for diagnosis of infertility including clinical and morphological, cytological, bacteriological methods do not always indicate the cause of the decrease in viability of spermatozoa and do not reveal mechanisms of the changes [13]. Over the past two decades a large amount of researches devoted to studying the role of nitric oxide and NO-synthase in the regu lation of physiological functions and pathological processes appeared. However, the role of NO-synthase in sperm cells in different forms of male infertility remains poorly understood [9, 11]. The NO formation in the human body is carried out as a result of oxidation of nitrogen atom that is part of the amino acid L-arginine by enzyme – Nitric Oxide Synthase (NOS) [4, 10, 11, 20]. There are three of its isoforms: neuronal – NOS (nNOS), inducible (macrophage) – NOS II (iNOS) and endothelial – NOS III (eNOS). Constitutive isoforms of NO-synthase (nNOS, eNOS) provide a synthesis of NO in physiological conditions. iNOS is inactive in physiological conditions and is activated in response to pathogenic stimuli [3–6, 12, 20, 26]. Therefore, the functional and regulatory features of inducible isoform of NOS depend on the nature of pathological process and the affected organ [12]. Both constitutive and inducible isoforms of NOS are related to NO production in the early phase of inflammation and their pro-inflammatory effect is manifested. Late phase of inflammation is associated with local leukocyte activity and infiltration. Its development is contributed only by NO, produced by iNOS, localized in leukocytes [12]. The elucidation of changes in NOS isoforms activity in men with impaired fertility determines actuality of present work. The aim of the research is to detect changes in the activity of NOS isoforms of sperm cells in patients with different forms of infertility. Materials and methods. Spermatozoa preparation. Semen samples of men aged 21–44 years were used in the research. Relatively healthy donors with no reproductive disorders and infertile men were among the men under study. The control group consisted of 20 healthy men with somatic fertility, normozoospermia and confirmed parenthood (married for 3–10 years and have 1–3 healthy children). Before turning to the study, all men had familiarized themselves with patient information leaflets and gave informed consent to participate in the research.","PeriodicalId":10397,"journal":{"name":"Clinical physiology and biochemistry","volume":"68 Supplement 1","pages":"47-53"},"PeriodicalIF":0.0000,"publicationDate":"2016-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":"{\"title\":\"NO-Synthase Pathway of L-Arginine Transformation in Spermatozoa of Infertile Men with Different Forms of Pathospermia\",\"authors\":\"D. Vorobets, O. Оnufrovych, R. Fafula, U. Yefremova, Z. Vorobets\",\"doi\":\"10.25040/ECPB2016.03.047\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Elucidation patterns of male germ cells functioning is of particular relevance in the present conditions due to increasing trends in male reproductive disorders [1]. Men infertility is caused by the effect of different pathological processes in genital organs and glands, resulting in pathospermia, which reduces fertilizing ability of sperm cells. Common methods for diagnosis of infertility including clinical and morphological, cytological, bacteriological methods do not always indicate the cause of the decrease in viability of spermatozoa and do not reveal mechanisms of the changes [13]. Over the past two decades a large amount of researches devoted to studying the role of nitric oxide and NO-synthase in the regu lation of physiological functions and pathological processes appeared. However, the role of NO-synthase in sperm cells in different forms of male infertility remains poorly understood [9, 11]. The NO formation in the human body is carried out as a result of oxidation of nitrogen atom that is part of the amino acid L-arginine by enzyme – Nitric Oxide Synthase (NOS) [4, 10, 11, 20]. There are three of its isoforms: neuronal – NOS (nNOS), inducible (macrophage) – NOS II (iNOS) and endothelial – NOS III (eNOS). Constitutive isoforms of NO-synthase (nNOS, eNOS) provide a synthesis of NO in physiological conditions. iNOS is inactive in physiological conditions and is activated in response to pathogenic stimuli [3–6, 12, 20, 26]. Therefore, the functional and regulatory features of inducible isoform of NOS depend on the nature of pathological process and the affected organ [12]. Both constitutive and inducible isoforms of NOS are related to NO production in the early phase of inflammation and their pro-inflammatory effect is manifested. Late phase of inflammation is associated with local leukocyte activity and infiltration. Its development is contributed only by NO, produced by iNOS, localized in leukocytes [12]. The elucidation of changes in NOS isoforms activity in men with impaired fertility determines actuality of present work. The aim of the research is to detect changes in the activity of NOS isoforms of sperm cells in patients with different forms of infertility. Materials and methods. Spermatozoa preparation. Semen samples of men aged 21–44 years were used in the research. Relatively healthy donors with no reproductive disorders and infertile men were among the men under study. The control group consisted of 20 healthy men with somatic fertility, normozoospermia and confirmed parenthood (married for 3–10 years and have 1–3 healthy children). Before turning to the study, all men had familiarized themselves with patient information leaflets and gave informed consent to participate in the research.\",\"PeriodicalId\":10397,\"journal\":{\"name\":\"Clinical physiology and biochemistry\",\"volume\":\"68 Supplement 1\",\"pages\":\"47-53\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2016-09-29\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"1\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Clinical physiology and biochemistry\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.25040/ECPB2016.03.047\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Clinical physiology and biochemistry","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.25040/ECPB2016.03.047","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 1
摘要
由于男性生殖障碍的增加趋势,阐明男性生殖细胞功能模式在当前情况下具有特别的相关性[1]。男性不育症是由于生殖器官和腺体的不同病理过程的影响,导致精子不足,使精子细胞的受精能力降低。常用的不孕症诊断方法,包括临床和形态学、细胞学、细菌学方法,并不总能指出精子活力下降的原因,也不能揭示这种变化的机制[13]。近二十年来,出现了大量研究一氧化氮和no合酶在调节生理功能和病理过程中的作用的研究。然而,no合酶在不同形式男性不育的精子细胞中的作用仍然知之甚少[9,11]。一氧化氮合酶(NO)在人体内形成一氧化氮是由氨基酸l -精氨酸组成的氮原子被一氧化氮合酶(NOS)氧化而形成的[4,10,11,20]。它有三种亚型:神经元型- NOS (nNOS)、诱导型(巨噬细胞)- NOS II (iNOS)和内皮型- NOS III (eNOS)。NO合成酶的组成型同工型(nNOS, eNOS)在生理条件下提供NO的合成。iNOS在生理状态下不活跃,在对病原刺激的反应中被激活[3 - 6,12,20,26]。因此,NOS诱导异构体的功能和调控特征取决于病理过程的性质和受影响的器官[12]。NOS的组成型和诱导型亚型均与炎症早期NO的产生有关,并表现出促炎作用。炎症晚期与局部白细胞活动和浸润有关。它的发展仅由NO促成,由白细胞中的iNOS产生[12]。不育男性NOS同工异构体活性变化的阐明决定了目前工作的现状。该研究的目的是检测不同形式不孕症患者精子细胞NOS同种异构体活性的变化。材料和方法。精子的准备。研究中使用了21-44岁男性的精液样本。研究对象中包括相对健康的捐赠者,没有生殖障碍和不育男性。对照组为20名身体生育、无精子症、已确认为人父母(结婚3-10年,育有1-3名健康子女)的健康男性。在参加这项研究之前,所有男性都熟悉了患者信息传单,并知情同意参加这项研究。
NO-Synthase Pathway of L-Arginine Transformation in Spermatozoa of Infertile Men with Different Forms of Pathospermia
Elucidation patterns of male germ cells functioning is of particular relevance in the present conditions due to increasing trends in male reproductive disorders [1]. Men infertility is caused by the effect of different pathological processes in genital organs and glands, resulting in pathospermia, which reduces fertilizing ability of sperm cells. Common methods for diagnosis of infertility including clinical and morphological, cytological, bacteriological methods do not always indicate the cause of the decrease in viability of spermatozoa and do not reveal mechanisms of the changes [13]. Over the past two decades a large amount of researches devoted to studying the role of nitric oxide and NO-synthase in the regu lation of physiological functions and pathological processes appeared. However, the role of NO-synthase in sperm cells in different forms of male infertility remains poorly understood [9, 11]. The NO formation in the human body is carried out as a result of oxidation of nitrogen atom that is part of the amino acid L-arginine by enzyme – Nitric Oxide Synthase (NOS) [4, 10, 11, 20]. There are three of its isoforms: neuronal – NOS (nNOS), inducible (macrophage) – NOS II (iNOS) and endothelial – NOS III (eNOS). Constitutive isoforms of NO-synthase (nNOS, eNOS) provide a synthesis of NO in physiological conditions. iNOS is inactive in physiological conditions and is activated in response to pathogenic stimuli [3–6, 12, 20, 26]. Therefore, the functional and regulatory features of inducible isoform of NOS depend on the nature of pathological process and the affected organ [12]. Both constitutive and inducible isoforms of NOS are related to NO production in the early phase of inflammation and their pro-inflammatory effect is manifested. Late phase of inflammation is associated with local leukocyte activity and infiltration. Its development is contributed only by NO, produced by iNOS, localized in leukocytes [12]. The elucidation of changes in NOS isoforms activity in men with impaired fertility determines actuality of present work. The aim of the research is to detect changes in the activity of NOS isoforms of sperm cells in patients with different forms of infertility. Materials and methods. Spermatozoa preparation. Semen samples of men aged 21–44 years were used in the research. Relatively healthy donors with no reproductive disorders and infertile men were among the men under study. The control group consisted of 20 healthy men with somatic fertility, normozoospermia and confirmed parenthood (married for 3–10 years and have 1–3 healthy children). Before turning to the study, all men had familiarized themselves with patient information leaflets and gave informed consent to participate in the research.