睾酮对大鼠睾丸形态学的影响

本文研究了丙酸睾酮对大鼠睾丸形态超微结构的影响,结果发现：大剂量外源性丙酸睾酮可使睾丸出现抑制性超微结构的形态学改变。     

两种睾丸活检术前后血清睾酮水平的检测及临床意义

目的探讨两种睾丸活检方法：切开活检和穿刺活检对血清睾酮影响的差别。方法 56例男性不育患者分为两组,分别行传统切开睾丸活检和穿刺活检。在术前和术后3、6、12个月采静脉血测定血清睾酮水平。结果两组患者睾丸活检术后血清睾酮均下降,术后6个月达到最低水平,术后12个月逐渐恢复,但未达到正常水平。切开活检组术后睾酮水平显著低于穿刺活检组。结论睾丸穿刺活检对血清睾酮水平影响小,优于切开活检,但睾丸活检术后均需常规补充外源性的雄激素。     

杜仲水提液对幼鼠睾丸间质细胞睾酮合成和caspase9的影响

目的:探讨杜仲水提液对幼鼠睾丸间质(Leydig)细胞睾酮合成功能和caspase9的影响。方法:原代分离、鉴定幼鼠的Leydig细胞,进行细胞培养。在加入不同剂量杜仲水提液培养24 h后,用化学发光法测定睾酮的浓度;分别在加药24 h、36 h和48 h后,用MTT法检测各组的吸光度;在加药24 h后,用流式细胞仪分析细胞凋亡率、存活率和死亡率;用实时定量反转录聚合酶链反应测定caspase9 mRNA的表达。结果:在Leydig细胞中加入杜仲水提液24 h后,上清液的睾酮浓度明显增加,与空白组比较差异有统计学意义(P<0.01);药物刺激24 h、36 h和48 h后,其吸光度与空白组比较差异均有统计学意义(P<0.01);药物刺激24 h后,细胞凋亡率和死细胞率明显降低,活细胞率明显提高,与空白组比较差异有统计学意义(P<0.01);药物刺激24 h后,caspase9 mRNA的表达量明显降低,与空白组比较差异有统计学意义(P<0.05)。结论:杜仲水提液能通过下调caspase9的表达,降低Leydig细胞的凋亡,促进其增殖,而提高其合成睾酮的能力。     

男性糖尿病患者血清睾酮浓度变化与糖尿病微血管的关系

目的 了解糖尿病患者血清睾酮浓度与微血管病变的关系。方法 测定３０例男性糖尿病患者及３４例正常男性血清睾酮、黄体生成素、狼泡刺激素、泌乳素、雌二醇,比较观察糖尿病患者垂体一性腺轴变化。结果 糖尿病血清睾酮水平明显低于对照组,糖尿病患者中睾酮水平减低组的微血管病变的发生率明显高于睾酮水平正常组,蓁因清黄体生成素水平明显高于血清睾酮水平正确组,提示微血管病变在糖尿病患者垂体一性腺轴变化中有一定影响。     

男性急性胰腺炎患者血清睾酮、雌二醇、黄体生成激素和促卵泡生成素水平的观察

急性胰腺炎是临床上较常见的急腹症之一。为探讨急性胰腺炎对男性患者的垂体—性腺轴的影响 ,我们对男性急性胰腺炎患者的血清Ｔ、Ｅ2 、ＬＨ、ＦＳＨ进行测定 ,现将结果报告如下。1　资料与方法1 1　病例选择　实验组 32例 ,为 1999年 9月至2 0 0 0年 5月我院收治入院的男性急性胰腺炎患者 ,所有病例均符合中华医学会外科学会胰腺学组 1996年贵阳制定的临床诊断及分级标准。年龄 15～ 77岁 ,平均 4 5 8岁 ,其中轻型急性胰腺炎 2 2例 ,重症急性胰腺炎 10例。所有病例无可引起生殖腺机能减退的疾病、长期酗酒史 ,未使用可能影响性激素分泌或…     

D-半乳糖对雄性大鼠腰椎骨密度和血清睾酮含量的影响

目的:观察D半乳糖对雄性大鼠腰椎骨密度的影响及其产生的原因。方法:12只6月龄雄性大鼠随机分成2组,对照组和D半乳糖组,每组6只。对照组每天皮下注射生理盐水,D半乳糖组皮下注射5%的D半乳糖,剂量为100mg·kg-1,连续给药3个月后,心脏取血处死大鼠,取出第4腰椎,放入福尔马林中固定;同时取出睾丸,放入固定液中固定。取出的血液静置一段时间后,离心获取血清,放入-70℃冰箱中冷冻保存备用。第4腰椎经梯度脱水后,塑料包埋、切片,用图象分析仪上进行骨量分析。睾丸制作普通石蜡切片,光镜下观察。冷冻血清,解冻后用放射免疫法测定血清睾酮促、黄体生成素(LH)含量。结果:D半乳糖组大鼠腰椎骨出现骨质疏松。与对照组相比,D半乳糖组血清睾酮含量明显降低,而黄体生成素无明显变化,睾丸切片呈现老化表现,但黄体生成素无明显变化。结论:D半乳糖会导致雄性大鼠骨质疏松,其原因可能是影响了下丘脑垂体性腺轴的功能,导致血清睾酮含量降低,最终引起骨质疏松。     

糖尿病前期男性患者血清睾酮和雌二醇变化初探

目的初步探讨糖尿病前期男性患者血清睾酮和雌二醇的变化。方法 168例男性,根据血糖状况分为正常血糖组(85例)和糖尿病前期组(83例),分析两组人群血清睾酮和雌二醇的变化。结果与正常血糖组比较,糖尿病前期组患者血清睾酮水平显著降低和雌二醇水平显著增高(均为P<0.01)。结论糖尿病前期男性患者存在低睾酮血症和高雌二醇血症。     

男性糖尿病患者血清睾酮浓度变化与糖尿病微血管病的关系

目的　了解糖尿病患者血清睾酮浓度与微血管病变的关系。方法　测定 30例男性糖尿病患者及 34例正常男性血清睾酮、黄体生成素、卵泡刺激素、泌乳素、雌二醇 ,比较观察糖尿病患者垂体—性腺轴变化。结果糖尿病血清睾酮水平明显低于对照组 ,糖尿病患者中睾酮水平减低组的微血管病变的发生率明显高于睾酮水平正常组 ,其血清黄体生成素水平明显高于血清睾酮水平正常组 ,提示微血管病变在糖尿病患者垂体—性腺轴变化中有一定影响     

运动与下丘脑-垂体-睾丸轴

睾酮作为雄激素的代表,与运动的关系非常密切。关于运动对下丘脑-垂体-睾丸轴的影响,长期以来存在争议。生理状态下,睾酮的相对稳定主要取决于下丘脑和垂体的调控。那么运动后血清睾酮水平的变化主要是下丘脑及垂体调节,还是存在于外周机制,目前尚不明确,有待进一步深入研究。本文就睾酮的生理特性、作用、运动对睾酮代谢的影响及运动影响睾酮代谢的因素做一综述,以供读者参考。     

Alterations in gene expression and testosterone synthesis in the testes of male rats exposed to perfluorododecanoic acid.

Perfluorododecanoic acid (PFDoA, C12), a synthetic perfluorinated chemical containing 12 carbons, has broad industrial applications and has been detected in sera from humans and other animals; however, few reports have addressed the effects of PFDoA exposure on male reproduction. In the present study, the effects of PFDoA exposure on testes ultrastructure, testosterone levels, and steroidogenic gene expression were investigated. Male rats were orally dosed for 14 days with 1, 5, or 10 mg PFDoA/kg/day or with vehicle. Absolute testis weight was diminished at the highest dose while relative testes weight was markedly increased at doses of 5 and 10 mg/kg/day. Total serum cholesterol levels were significantly increased at the highest dose. While luteinizing hormone was significantly decreased at the highest dose, testosterone was markedly decreased at doses of 5 and 10 mg PFDoA/kg/day. Serum levels of follicle-stimulating hormone were not significantly affected by PFDoA, and estradiol levels were markedly decreased only at 5 mg/kg/day. Leydig cells, Sertoli cells, and spermatogenic cells from rats that received 5 or 10 mg PFDoA/kg/day, exhibited apoptotic features including dense irregular nuclei, condensed chromatin, ill-defined nuclear membranes, and abnormal mitochondria. PFDoA exposure resulted in significant declines in mRNA expression of several genes involved in cholesterol transport and steroid biosynthesis at doses of 5 and 10 mg PFDoA/kg/day, while the gene expression of luteinizing hormone receptor and aromatase was not significantly changed. Our results demonstrate that PFDoA affects the reproduction function of male rats via alterations in steroidogenesis genes, testosterone levels, and testes ultrastructure.     

Pubertal and early adult exposure to fenvalerate disrupts steroidogenesis and spermatogenesis in mice at adulthood

Fenvalerate, a pyrethroid insecticide used worldwide, has been shown to have a potentially adverse effect on male reproduction. Our earlier study showed that maternal fenvalerate exposure during lactation impaired testicular development in male offspring. In this study, we investigated the effects of pubertal and early adult exposure to fenvalerate on steroidogenesis and spermatogenesis in mice. Male mice were administered fenvalerate (60 mg/kg) by gavage daily from postnatal day 35 (PND35) to PND63. Results showed that sperm count was significantly decreased in fenvalerate‐treated mice. In addition, fenvalerate markedly decreased the layers of spermatogenic cells, disturbed the array of spermatogenic cells and increased the number of apoptotic cells in testes. The adverse effects of fenvalerate on male reproduction seemed to be associated with a decrease in serum and testicular testosterone (T). Although pubertal and early adult exposure to fenvalerate had little effect on the number of Leydig cells in testes, mRNA and protein levels of testicular T biosynthetic enzymes including P450_17α and P450scc were significantly downregulated in fenvalerate‐treated mice. In conclusion, pubertal and early adult fenvalerate exposure induces a deleterious effect on steroidogenesis and spermatogenesis in adulthood. The decreased testicular T synthesis partially contributes to fenvalerate‐induced impairment on spermatogenesis. Copyright © 2010 John Wiley & Sons, Ltd.     

Effect of gestational exposure to perfluorononanoic acid on neonatal mice testes

Perfluoroalkyl acids (PFAAs) are widely used in commercial products and are found in many goods of daily use. Perfluorononanoic acid (PFNA) is one of the PFAAs that possesses endocrine disrupting properties and we have recently shown that PFNA affects testicular functions in Parkes mice. Exposure to environmental endocrine disruptors during fetal life is believed to affect gonadal development and they might produce reproductive abnormalities in males. Therefore, the present study examined the effect of gestational exposure to PFNA on the testes of neonatal mice offspring. Pregnant Parkes mice were orally administered PFNA (2 and 5 mg/kg body weight) or distilled water from gestational day 12 until parturition. Male pups were killed on postnatal day 3. PFNA treatment decreased testosterone biosynthesis by inhibiting expression of steroidogenic acute regulatory protein, cytochrome P450scc, and 3β‐ and 17β‐hydroxysteroid dehydrogenase; proliferation of testicular cells was also affected in treated mice. Furthermore, a marked decrease in expression of Wilms tumor 1, steroidogenic factor 1 and insulin‐like factor 3 was noted in neonatal mice testes, indicating that the PFNA treatment may affect the development of the testis. Moreover, observation of the dose‐related expression of anti‐müllerian hormone and c‐Kit in neonatal mice testes is also suggestive of an interference with gonadal development by PFNA exposure. In conclusion, the results suggest that the gestational exposure to PFNA decreased testosterone biosynthesis and altered the expression of critical factors involved in the development of the testis, thereby advocating a potential risk of PFNA to male reproductive health.     

Ejaculatory dysfunction in streptozotocin-induced diabetic rats: the role of testosterone

Hyperglycemic and hypoinsulinemic states caused by diabetes mellitus are usually related to some type of sexual dysfunction, resulting in infertility in humans and experimental models, mostly due to their effects on ejaculatory function. This study aimed to evaluate the possible role of testosterone in the restoration of normal ejaculatory function in diabetic rats. Male Wistar rats were randomly allocated into 3 experimental groups: control, diabetic (streptozotocin), and diabetic with testosterone supplementation (streptozotocin plus testosterone). The following parameters were assessed at the end of the experiment: body weight, circulating testosterone levels, number of spermatozoa ejaculated in the uterus through natural mating, and weight and in vitro isometric contractions of the vas deferens. Diabetic rats showed reduced plasma testosterone levels and ejaculatory dysfunction as observed by a lack in the spermatozoa ejaculated into the uterus of receptive females. In these diabetic rats, no difference was observed in the sensitivity of the vas deferens to norepinephrine, with or without the presence of the cocktail (cocaine plus propranolol). In spite of this, an increased sensitivity to methoxamine through the α1-adrenoceptor was observed. Testosterone supplementation did not restore these parameters to control values.We conclude that, in this experimental model, the lack of testosterone was not directly related to the diabetes-induced ejaculatory dysfunction.     

In utero and lactational exposure to TCDD; steroidogenic outcomes differ in male and female rat pups.

TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin) has a potency to induce decreased fertility and structural reproductive anomalies in male and female mammals. While the activity profile of sex steroid hormone production distinctly differs in developing males and females, we wanted to analyze sex-specific effects of TCDD introduced in utero and via lactation on gonadal steroidogenesis and gonadotropin levels in male and female rat infant pups. One oral dose of TCDD (0, 0.04, 0.2, or 1.0 microg/kg) was given to dams on gestational day (GD) 13. Plasma testosterone, estradiol, progesterone, follicle stimulating hormone (FSH), luteinizing hormone (LH), and gonadal mRNA levels for steroid acute regulatory protein (StAR), cytochrome P-450 cholesterol side-chain cleavage (P450scc), 3beta-hydroxy-steroid-dehydrogenase/Delta(5)-Delta(4) isomerase type I (3beta-HSD1), P-450 17alpha-hydroxylase/17,20-lyase (P450-17alpha), and cytochrome P-450 aromatase (P450arom) were determined on postnatal days (PND) 10-16. TCDD 1.0 mug/kg reduced body weights but did not affect relative testis weight or alter testicular and ovarian histology. Plasma estradiol levels in dams and female pups were reduced on PND 14 and 16. Progesterone levels remained unaltered, and FSH levels were increased in female pups. In males, testosterone levels were elevated on PND 10. Gonadal mRNA levels for StAR and steroidogenic enzymes increased during the postnatal growth. TCDD caused no changes in relatively low testicular mRNA levels. However, significant reductions in StAR and P450arom mRNA levels were seen in PND 14 ovaries, and P450arom activity was decreased in isolated ovarian follicles. We conclude that developing testis and male gonadotropin secretion are resistant to TCDD-induced toxicity. In female pups, reduced estradiol, ovarian P450arom expression and enzyme activity levels, and elevated FSH levels may have a role in the development of ovarian dysfunction reported in TCDD-exposed females.     

伐地那非、十一酸睾酮合用与单用伐地那非治疗糖尿病患者勃起功能障碍的疗效比较

目的比较联合应用伐地那非和十一酸睾酮与单用伐地那非治疗糖尿病患者勃起功能障碍的疗效及不良反应。方法该院男科门诊患有糖尿病的勃起功能障碍患者58例,随机分成A、B组,每组29例,A组口服伐地那非20mg,性生活前30min服用;B组除了同样服用伐地那非外,每日早晚饭后服用十一酸睾酮40mg,共观察12周。比较两组治疗前后的国际勃起功能指数-5(IIEF-5)问卷中的评分、每周性交频率以及治疗期间的不良反应,并评估在疗程结束时,患者及其配偶对性生活的满意程度。结果 A、B两组患者IIEF-5评分在治疗后均显著增加,而B组较A组增加更显著(P<0.05);治疗后每周性交频率两组均显著增多,两组之间比较B组增加更明显(P<0.05)。治疗结束时,A组患者对性生活感到满意的有15例(51.7%),B组有21例(72.4%),B组满意比例较A组更高(P<0.05)。在不良反应方面,B组患者共有6例(20.7%)发生不良反应,较A组的5例(17.2%)无统计学意义(P>0.05)。结论在对糖尿病患者勃起功能障碍的治疗上,联合应用伐地那非和十一酸睾酮比单用伐地那非治疗糖尿病患者勃起功能障碍疗效要好,同时引起的不良反应却无明显增加。     

中老年男性体内睾酮与生长激素关系探讨

目的观察中老年睾酮(testosterone,T)与生长激素(growth hormone,GH)水平之间的关系。方法 80例体检发现T水平低下的中老年男性随机分两组,治疗组38例予以T补充治疗,对照组42例无特殊处理,观察1年,检测治疗前后T及胰岛素样生长因子(IGF)-1浓度的变化。结果实验前两组T及IGF-1无明显差异,1年后,治疗组T、IGF-1浓度较治疗前增加,差异有统计学意义(P0.001);相关性分析显示T与IGF-1成正相关(r=0.330,P=0.003)。结论中老年男性血清T水平与GH水平密切相关。     

The role of cyclic AMP production,calcium channel activation and enzyme activities in the inhibition of testosterone secretion by amphetamine

1. The aim of this study was to investigate the mechanism by which amphetamine exerts its inhibitory effect on testicular interstitial cells of male rats.
2. Administration of amphetamine (10⁻¹²–10⁻⁶ M) in vitro resulted in a dose-dependent inhibition of both basal and human chorionic gonadotropin (hCG, 0.05 iu ml⁻¹)-stimulated release of testosterone.
3. Amphetamine (10⁻⁹ M) enhanced the basal and hCG-increased levels of adenosine 3′:5′-cyclic monophosphate (cyclic AMP) accumulation in vitro (P<0.05) in rat testicular interstitial cells.
4. Administration of SQ22536, an adenylyl cyclase inhibitor, decreased the basal release (P<0.05) of testosterone in vitro and abolished the inhibitory effect of amphetamine.
5. Nifedipine (10⁻⁶ M) alone decreased the secretion of testosterone (P<0.01) but it failed to modify the inhibitory action of amphetamine (10⁻¹⁰–10⁻⁶ M).
6. Amphetamine (10⁻¹⁰–10⁻⁶ M) significantly (P<0.05 or P<0.01) decreased the activities of 3β-hydroxysteroid dehydrogenase (3β-HSD), P450c17, and 17-ketosteroid reductase (17-KSR) as indicated by thin-layer chromatography (t.l.c.).
7. These results suggest that increased cyclic AMP production, decreased Ca²⁺ channel activity and decreased activities of 3β-HSD, P450c17, and 17-KSR are involved in the inhibition of testosterone production induced by the administration of amphetamine.