精浆中的氧自由基对精子活动的影响

氧自由基（OFR或ROS）是一种具有多种生物学功能且有双重作用的介质。生理量的氧自由基可以维持正常的精子活动功能，超过生理量就会对精子产生毒性作用，降低其活动力和活动率，导致男性生育能力低下甚至不育。     

精浆中的氧自由基对精子活动的影响

氧自由基 (OFR或ROS)是一种具有多种生物学功能且有双重作用的介质。生理量的氧自由基可以维持正常的精子活动功能 ,超过生理量就会对精子产生毒性作用 ,降低其活动力和活动率 ,导致男性生育能力低下甚至不育。     

精子低温保存与精子功能

自５０年代美国和日本相继用低温保存的精液复温后作人工受精,并获得成功以来［１～３］,目前精液低温保存在不育症的治疗、生殖保险、计划生育和优生等领域得到广泛开展。精子功能是影响人工受精成功率的关键因素之一,而低温冻存及复温过程中均会对精子的功能造成一定...     

一氧化氮对精子功能的影响

一氧化氮 (NO)是一种具有广泛生物学活性的信使分子和细胞毒性因子。近年研究表明 ,NO对哺乳动物的生殖活动具有重要的调节作用。NO参与精子发生、获能并影响精子质量。低浓度NO具有保护精子活力 ,促进精子获能的作用 ;而高浓度NO则损害生精功能 ,抑制精子活动度及降低顶体反应率。NO与氧自由基相互作用 ,共同参与精子功能的调节。     

钙调素与精子功能

钙调素集中分布于精子头和尾部的多个区域，钙调素通过激活精子的多种功能酶活性调节精子内的Ｃａ＾＋＋浓度，ＣＡＭＰ水平及至精子的鞭毛运动，影响精子的获能与顶体反应，钙调素与在受精过程中起重要作用的Ａｃｔｉｎ ＰＬＡ２等相互作用从而参与精卵融合的调节。     

钙离子与精子功能

钙离子是生物体内重要的阳离子,虽然钙离子在精子中的调控作用还不清楚,但近些年来有关钙离子在精子中的功能不断有新的报道,如钙离子参与精子的发生,是精子运动的调控者,精子获能的参与者,还是顶体反应的第二信使。现对钙离子与精子功能间的关系进行综述。     

精子功能的检测与评估

临床上已广泛采用ＷＨＯ标准精液分析,项目包括精子密度、活力和形态学检查等,作为评估男性生育力的重要指标。但它们仅仅是关于精液中活动的结构上正常的精子数量上的浅表的分析,对精子功能和受精潜能,则所提供的信息是有限的,不能对男性生育力提供精确的诊断及预后估计。对精子受精能力的判断,传统的人精子穿透去透明带仓鼠卵试验,虽能在某种程度上反映受精能力的本质,但是方法繁琐、费用昂贵、重复性差等问题,难以作为不育的常规检查,而且穿卵率的临床意义尚有争论。常规工作中低渗肿胀试验、顶体状态的测定、精子活力与运动…     

环核苷酸门控通道与精子功能

环核苷酸门控通道(CNG)是非选择性阳离子通道,直接由环核苷酸活化,是Ca2+进入细胞内的主要通道之一。CNG通道蛋白由6个不同基因编码,4个A亚单位和2个B亚单位。CNG通道受Ca2+/钙调蛋白和磷酸化/去磷酸化作用所调控。近年来,CNG通道在生殖系统方面的研究受到了广泛关注。大量研究表明,CNG通道在精子运动、获能和顶体反应中起着重要的作用。本文对CNG通道与精子功能的关系进行综述。     

冷冻复温后低温保护剂和精子激活剂对精子功能影响的研究

本文对冷冻复温后精子的功能进行了研究观察，发现精液保护剂对冷冻复温后精子的存活有明显的保护作用，而单纯应用卵黄或甘油溶液却对精子功能存在不利的影响。体外处理精子时应用ＡＴＰ，肌苷对精子的功能无任何的改善。     

Infection and reactive oxygen species

Summary. In previous years the physiologic and pathophysiologic significance of reactive oxygen species (ROS) on sperm function has been recognized. The impact of ROS during the invasion, adhesion and multiplication of microorganisms in the male genital tract are largely unknown. However, it is known that the resulting activation of leukocytes leads to an increased generation of ROS. There is growing evidence that spermatozoa are protected from detrimental ROS effects by the powerful antioxidants in seminal plasma since disturbances of sperm function by ROS were demonstrated in the absence of seminal plasma, i.e., during epididymitis or after semen preparation. If seminal plasma is present, ROS generated by physiologic numbers of granulocytes (< 1 times 10⁶ ml⁻¹) apparently do not damage spermatozoa. Interestingly, ROS generated by leukocytes during male genital tract infections are critical for the techniques of semen preparation for assisted reproduction. These ROS impair sperm function if the protective effects of seminal plasma are not present. The relevance of ROS production by higher leukocyte numbers in human semen is presently unknown as is the relevance of ROS generated in the female reproductive tract.
In previous years the ambiguous role of reactive oxygen species (ROS) generation in human semen has been recognized. On one hand, ROS appear to be involved in physiologic reactions such as capacitation (De Lamirande & Gagnon, 1995; Griveau et al. , 1995a), while on the other hand, there is ample evidence that an increased ROS production impairs sperm functions and the fertilizing capacity of spermatozoa (Ochsendorf & Fuchs, 1993; Aitken, 1994; Griveau et al. , 1995b). The objective of this review is to summarize the relevance of reactive oxygen species during infections of the male genital tract.     

Targeting reactive oxygen species in hypertension

PURPOSE OF REVIEW: Hypertension is a major risk factor for vascular diseases such as stroke, myocardial infarction, and renal microvascular disease. The mechanism by which vascular disease develops is complex, and growing evidence suggests that an increase in reactive oxygen species during hypertension is a major contributing factor. NADPH oxidase, the primary source of reactive oxygen species in the cardiovascular system, is a strong candidate for the development of therapeutic agents to ameliorate hypertension and end-organ damage. RECENT FINDINGS: Various scavengers and inhibitors of reactive oxygen species have been proposed for use in animal as well as human studies. While many of these agents are effective at lowering tissue reactive oxygen species levels, their specificity is a serious concern. Our laboratory has developed cell-permeant peptidic inhibitors targeting key interactions among the different NAD(P)H oxidase homologues. One of these inhibitors targeting nox2 and p47-phox interaction has proven useful in attenuating target neoplasia and hypertrophy. SUMMARY: Strategies aimed at specifically inhibiting NAD(P)H oxidase have proven effective in attenuating cardiovascular oxidative stress. The development of new inhibitors targeting novel oxidase homologues appears to hold significant promise for clarifying the physiologic role of these homologues as well as for the development of new antioxidant therapies.     

Glucocorticoids: Dose-related effects on osteoclast formation and function via reactive oxygen species and autophagy

Whether glucocorticoids directly enhance or interrupt osteoclastogenesis is still a controversial subject. In this study, we ascertained the dose-dependent positive effects of glucocorticoids on osteoclastogenesis in vivo and in vitro as well as investigated the mechanism in vitro. As the dose of glucocorticoids increased, osteoclastogenesis was stimulated at 0.1 μM, a peak was achieved at 1 μM and a corresponding decrease occurred at 10 μM. Reactive oxygen species (ROS), which play a crucial role in osteoclastogenesis, and autophagy flux activity, a cellular recycling process, were consistently up-regulated along with the dose-dependent effects of the glucocorticoids on osteoclast formation and function. N-acetyl-cysteine (NAC), a ROS scavenger, abrogated the effects of the glucocorticoids on autophagy and osteoclastogenesis. Moreover, 3-methyladenine (3-MA), an autophagy inhibitor, interrupted osteoclastogenesis stimulation by the glucocorticoids. These results implied that with glucocorticoid administration, ROS and autophagy, as a downstream factor of ROS, played vital roles in osteoclast formation and function. 3-MA administration did not enhance ROS accumulation, so that autophagy had no effect on ROS induced by glucocorticoids. Our investigation demonstrated that glucocorticoids had dose-dependent positive effects on osteoclast formation and function via ROS and autophagy. These results provide support for ROS and autophagy as therapeutic targets in glucocorticoid-related bone loss diseases such as glucocorticoid-induced osteoporosis.     

Protection of melatonin against damage of sperm mito-chondrial function induced by reactive oxygen species

Aim: To study the mitochondrial function damage of sperm in-duced by reactive oxygen species (ROS) and the protection of melatonin (MLT) against the damage. Methods: Normal function spermatozoa were selected from semen samples by Percoll gradi-ent centrifugation technique. The ROS generated by the hypoxan-thine xanthine oxidase system was incubated with the normal sper-matozoa in the presence or absence of MLT (6 retool/L) for 30 and 60 minutes.     

Rosacea, reactive oxygen species, and azelaic Acid

Rosacea is a common skin condition thought to be primarily an inflammatory disorder. Neutrophils, in particular, have been implicated in the inflammation associated with rosacea and mediate many of their effects through the release of reactive oxygen species. Recently, the role of reactive oxygen species in the pathophysiology of rosacea has been recognized. Many effective agents for rosacea, including topical azelaic acid and topical metronidazole, have anti-inflammatory properties. in-vitro models have demonstrated the potent antioxidant effects of azelaic acid, providing a potential mechanistic explanation for its efficacy in the treatment of rosacea.     

Free reactive oxygen species and nephrotoxicity of contrast agents

BACKGROUND: The nephrotoxicity induced by contrast media remains a serious clinical problem, and the underlying mechanism has not been completely understood. Experimental and clinical investigations suggest that reactive oxygen species (ROS) are critical determinants of radiocontrast nephropathy (RCN), and that antioxidants can prevent this damage. METHODS: Cultured human proximal renal tubule cells (HK-2) were exposed to hydrogen peroxide (H2O2) at different concentrations. H2O2-induced tubular DNA damage was examined in the presence of the antioxidant MESNA (sodium-2-mercaptoethane sulphonate). The induction of DNA damage was measured with the alkaline comet assay (single cell gel electrophoresis). We also studied 12 patients with stable renal impairment (median baseline creatinine 296 micromol/l; range: 203-495 micromol/l) undergoing cardiac catheterization/intervention prospectively. Patients received 800 mg MESNA intravenously 30 min before exposure to the contrast agent in addition to 0.9% saline hydration. RESULTS: In the cell cultures, oxidative stress on HK-2 cells induced increased DNA migration in the comet assay. Treatment of tubular cells with the antioxidant MESNA prior to the addition of H2O2 significantly reduced DNA migration in the comet assay. In the clinical study, treatment of the patients with MESNA prevented the adverse renal effect of contrast media (median serum creatinine 293; range: 187-433 micromol/l) 48 h after coronary angiography/intervention. CONCLUSION: Both the in vivo and the in vitro studies suggest that the ROS-mediated renal injury could be inhibited by a potent antioxidant such as MESNA.     

皮肤光老化、活性氧簇与抗氧化剂

皮肤长期反复暴露于日光紫外线（UV）下可导致皮肤光老化.近年来研究表明活性氧簇（ROS）在UV致皮肤光老化过程中起重要作用.UV可在皮肤中诱生高浓度ROS,这些具有一个或多个未配对电子的原子或分子如不能被皮肤抗氧化系统及时清除则会和皮肤中的核酸、脂质、蛋白质等生物大分子发生化学反应,并影响相关细胞信号转导途径和基因表达,导致皮肤光老化发生,使用抗氧化剂清除ROS可能成为一种重要的光老化防治策略.