血清抑制素B在鉴别梗阻性与非梗阻性无精子症中的意义

目的通过测定血清抑制素B（INHB）并与卵泡刺激素（FSH）和精浆中性α-葡糖苷酶（α-Glu）等经典指标比较,评价INHB在鉴别诊断梗阻性（OA）和非梗阻性无精子症（NOA）中的应用价值,并对睾丸精子发生障碍作出预判。方法实验采集健康生育男性组（n=60）,以睾丸活检为金标准确定OA组（n=39）和NOA组（n=77）,留取血液和精液标本,进行精液常规分析,检测血清INHB、FSH和精浆中性α—Glu的水平;采用受试者工作特征（ROC）曲线法,通过计算ROC曲线下面积,确定切点值并分析评价检测指标的敏感性和特异性。结果本实验室健康育龄男性血清INHB的95％参考值范围为：20．37-206．21pg／ml。血清INHB、FSH、精浆中性α—Glu、血清INHB／FSH比值以及INHB＋FSH联合在OA组与NOA组之间均差别显著,具有统计学意义（P〈0．01）。其中血清INHB的曲线下面积最大,为0．985,诊断价值最高,敏感性为97．4％,特异性为92．2％,切点值为49．89pg／ml。结论血清INHB比血清FSH、精浆中性α—Glu、血清INHB／FSH比值或INHB＋FSH联合指标在鉴别OA与NOA方面具有更好的敏感性与特异性。     

不育病人精浆胆固醇酯转运蛋白的检测

目的 :检测不育病人精浆胆固醇酯转运蛋白 (cholesterolestertransferprotein ,CETP)的含量 ,并探讨其与不育的关系。　方法 :随机选择 163例不育病人及 15例生育男性 ,行精液常规分析及精浆CETP浓度测定 ,其中5 5例不育病人同时测定了血清CETP含量。　结果 :不育病人及生育男性精浆CETP含量分别为 ( 2 .2 1± 1.2 3 )μg/L和 ( 1.40± 0 .45 ) μg/L ,两组间差异无显著性 (P >0 .0 5 ) ;在不育病人中 ,无精子症组 (n =2 9)、少弱精子症组(n =5 8)、少精子症组 (n =15 )、弱精子症组 (n =44 )及正常精子症组 (n =17)间CETP含量差异也无显著性 (P >0 .0 5 )。精浆平均CETP含量仅占血清的 1/ 10 0 0 ,不育病人精浆及其血清CETP含量间并无相关性 (r =0 .0 0 9,P>0 .0 5 )。　结论 :精浆CETP含量极低 ,与精子密度、活率的改变无关 ,可能保证了精子在未进入女性生殖道前膜结构与功能的完整性     

少精子症患者血清、精浆中游离睾酮水平的测定及意义

目的 :通过测定少精子症患者血清、精浆中游离睾酮 (FT)水平 ,分析血清、精浆FT与少精子症的关系。　方法 :正常对照组 (n =4 4 )、少精子症组 (n =4 4 )男性于上午 8:0 0～ 10 :0 0留取血标本 ;正常对照组 (n =30 )、少精子症组 (n =37)同时留取精液。男性精液常规分析判断精子密度 ,放射免疫分析法测定血清、精浆中FT水平。　结果 :少精子症患者血清中FT浓度为 [(94 .88± 4 2 .0 4 )pmol/L],与正常对照组 [(97.5 0± 4 6 .96 )pmol/L]相比差异无显著性 (P >0 .0 5 ) ,但少精子症患者精浆中FT浓度 [(0 .5 2± 0 .4 4 ) pmol/L]显著低于正常对照组 [(2 .0 1±0 .32 )pmol/L],P <0 .0 1。　结论 :精浆中FT的测定较早反映睾丸的功能 ,有利于少精子症患者的早期诊断和治疗。     

血清抑制素B对非阻塞性无精子症睾丸精子存在的预测价值

目的:探讨血清抑制素B(INHB)对非阻塞性无精子症(NOA)患者睾丸精子存在与否的预测价值。方法:分别对40例NOA、20例阻塞性无精子症(OA)及10例正常生育男性以双抗体夹心ELISA法测定其血清INHB水平。并用化学发光法检测了上述研究对象的卵泡刺激素(FSH)水平。结果:NOA患者的血清FSH[(21.34±12.15)IU/L]明显高于OA组和正常生育男性组[(3.94±1.52)IU/L和(4.27±2.84 IU/L],而血清INHB水平[(53.15±58.74)ng/L]明显低于后两者[(162.49±78.38)ng/L和(228.49±110.68)ng/L]。正常生育男性与OA组患者的血清INHB水平差异无显著性(P>0.05)。NOA患者血清INHB水平与其睾丸精子抽吸(TESE)的结果有相关性(r=0.528,P<0.01)。TESE获得精子者血清INHB水平[(90.31±72.18)ng/L]显著高于TESE无精子者[(19.54±20.38)ng/L,P<0.01];而两者的血清FSH差异无显著性(P>0.05)。结论:血清INHB可作为预测TESE的参考指标。血清INHB的测定有望替代睾丸活检确定睾丸精子的存在与否。     

生育与不育男性精浆总抗氧化能力分析

目的:分析生育与不育男性精浆中总抗氧化能力(TAC)及其在男性生育中意义。方法:225例男性不育患者分为6组,分别为:梗阻性无精子症组(n=10),非梗阻性无精子症组(n=42),少精子症组(n=20),弱精子症组(n=78),少弱精子症组(n=57),以及正常精子症组(n=18)。28例正常生育男性作为对照(生育组)。分别采用计算机辅助精液分析(CASA)系统进行精液参数分析,采用比色法检测精浆TAC水平。结果:生育组男性精浆TAC为(19.82±6.33)U,梗阻性无精子症组(1.71±1.33)U,非梗阻性无精子症组(12.73±9.44)U,少精子症组(10.85±6.64)U,弱精子症组(13.88±8.24)U,少弱精子症组(11.20±7.02)U,正常精子症组(18.07±8.73)U;与生育组精浆TAC[(19.82±6.33)U]相比,在各不育症组中,除正常精子症组精浆TAC与生育组差异无显著性外,其余各组均显著低于生育组(P<0.01)。精浆TAC与精子密度(r=0.182,P<0.05)和a级精子(r=0.150,P<0.05)呈显著正相关。结论:精浆中TAC水平与男性不育密切相关,精浆中过低的TAC水平可能是引起男性不育的病因之一。     

血清抑制素B检测在无精子症患者经睾丸抽吸术结局预评估中的应用

目的:探讨血清抑制素B(INHB)检测在无精子症患者经睾丸抽吸术(TESE)结局预评估中的意义。方法:根据研究需要将受试者分为3组:梗阻性无精子症(OA)组(n=191),非梗阻性无精子症(NOA)组(n=360),精液参数正常对照组(n=100)。NOA组根据TESE结局分为TESE无精子组(TESE-,n=127)和TESE有精子组(TESE+,n=233)。血液标本均于上午8:00~10:00收集,测定其INHB值。采用受试者工作特征曲线(ROC)分析评价血清INHB预测TESE结局的敏感性和特异性。结果:TESE-组的血清INHB水平[(19.7±34.8)pg/ml]显著低于OA组[(106.8±66.2)pg/ml]、TESE+组[(98.2±62.4)pg/ml]及精液参数正常对照组[(108.3±65.0)pg/ml](P0.01),TESE+组的血清INHB水平与OA组、精液参数正常对照组无显著性差异(P0.05)。ROC曲线分析显示,血清INHB最佳分割点为19.1 pg/ml,此时ROC曲线下面积(AUCROC)为0.88,敏感性为90.1%,特异性为84.2%,诊断准确性达88.1%。结论:血清INHB是一种良好的非侵入性的精子生成预测指标,无精子症患者TESE前应该常规行血清INHB检测以评估其TESE结局。     

男性不育病人精浆血管紧张素Ⅱ测定及临床意义

目的 :探讨人精浆血管紧张素Ⅱ(AngⅡ)对精液常规指标的影响及其与男性不育症的关系。　方法 :通过固相提取 高效液相分离 放免法 (SPE HPLC RIA)测定 4 3例不育男性 (无精子症 13例 ,少弱精子症 8例 ,弱精子症17例 ,精液常规正常 5例 )和 10例正常生育男性对照组的血浆和精浆AngⅡ 。　结果 :精浆AngⅡ 水平明显高于血浆AngⅡ 水平 ,为血浆值的 3倍多 (P <0 .0 1) ;无精子症组精浆AngⅡ 浓度明显高于其他生育与不育男性 (P <0 .0 5 ) ;血浆、精浆AngⅡ与精子密度、活力、存活率、畸形率和精子顶体反应率等均无相关性。　结论 :精浆AngⅡ很可能由男性生殖道局部产生 ,除睾丸、附睾外 ,前列腺和 (或 )精囊也可能是其来源 ;无精子症病人精浆高AngⅡ 水平的原因及精浆AngⅡ在男性生育调节中可能发挥的具体作用 ,还需要进一步研究。     

精浆AMH、INHB、血清INHB对常规IVF受精结局的预测价值

目的:分析精浆AMH、INHB及血清INHB与少弱精子症患者精液参数之间的相关性,同时探讨对其常规体外受精(IVF)结局的预测价值及影响。方法:收集2016年8月至2017年2月因男方少弱精子症或女方输卵管因素就诊于宁夏医科大学总医院生殖中心行IVF助孕的88例不孕夫妇的临床资料,检测精浆AMH、INHB、血清INHB及精液参数(精子活动率、浓度、总数、前向运动精子百分率及正常形态精子百分率),采用受试者工作特征曲线(ROC)分析精浆AMH、INHB、血清INHB及精液参数对其受精率的预测能力;Pearson相关分析检验精浆AMH、INHB及血清INHB与精液参数之间的关系,均设定P0.05为有统计学差异。结果:精浆AMH:AUC=0.807(敏感度84.6%,特异度76.0%,截断点3.529,P=0.000),精浆INHB:AUC=0.768(敏感度84.6%,特异度88.7%,截断点31.117,P=0.002);血清INHB与精子浓度(r=0.346,P=0.001)、精子总数(r=0.378,P=0.000)、精子活动率(r=0.521,P=0.000)、前向运动(r=0.343,P=0.001)。结论:精浆AMH、INHB可作为预测少弱精子症患者受精率的实验室指标;血清INHB与少弱精子症精液参数(精子浓度、精子总数、活动率及前向运动精子百分率)呈显著正相关。     

不育男性血清和精浆抑制素B水平与生精功能的关系

目的探讨血清和精浆抑制素B(INH-B)与睾丸生精功能的关系。方法回顾性分析2015年1~6月来深圳中山泌尿外科医院生殖医学中心就诊的141例男性不育症患者资料。根据精液参数分为5组:精子浓度正常组(A组,43例)、轻中度少精子症组(B组,40例)、重度少精子症组(C组,27例)、梗阻性无精子症组(OA组,9例)和非梗阻性无精子症组(NOA组,22例);NOA组中有17例患者接受睾丸细针精子抽吸术(TESA)取精,根据TESA结果分为成功组(13例)和失败组(4例)。比较各组的精液参数(精子总数、浓度及活动力),测定其血清和精浆INH-B水平及血清FSH、LH、T、E_2、泌乳素(PRL)、孕酮(P)的水平,分析血清性激素、INH-B与精液质量之间的关系。结果 A、B组的睾丸总体积显著高于OA和NOA组(P0.05)。C组和NOA组的血清INH-B显著低于A组和OA组,A组的精浆INH-B浓度显著高于C组、OA组和NOA组(P均0.05)。不同生精功能男性的血清INH-B与血清FSH、LH及PRL呈负相关,与血清T和精浆INH-B呈正相关(P均0.05);精浆INH-B与血清FSH和LH呈负相关(P0.05)。A、B、C组中血清和精浆INH-B与总精子数呈低度正相关(P0.01)。NOA组中血清INH-B与睾丸总体积呈高度正相关,与血清FSH和LH呈负相关(P均0.01);精浆INH-B与血清FSH呈极弱负相关(P0.05)。TESA取精成功组的睾丸总体积和血清INH-B显著高于TESA失败组,血清FSH和LH则显著低于TESA失败组(P均0.01)。结论血清和精浆INH-B与血清性激素、总精子数具有一定相关性,可作为评估男性生精功能的参考。无精子症中尤其是NOA患者,血清INH-B可以评估睾丸生精状态、鉴别诊断无精子症、预测取精结局。     

无精子症患者瘦素水平及其临床应用价值初探

目的:检测无精子症患者的精浆及血清瘦素(leptin,Lep)水平,探索精浆、血清Lep单独以及联合血清卵泡刺激素(FSH)鉴别梗阻性无精子症(OA)和非梗阻性无精子症(NOA)的方法及意义。方法:选取OA患者45例、原因不明的NOA患者41例,精液参数正常对照30例。无精子症患者行附睾/睾丸细针穿刺精子抽吸术及睾丸活检,所有研究对象均检测血清FSH、精浆及血清Lep。用Fisher判别分析结合ROC曲线法,对单个或多个联合指标进行分析评价。结果:在体重指数无差别的情况下,与精液参数正常对照者相比,OA患者精浆Lep水平显著增高,有统计学意义(P=0.048);NOA患者血清FSH(P=0.000)、血清Lep(P=0.000)及精浆Lep(P=0.000)都显著增高。与OA患者相比,NOA患者血清FSH(P=0.000)、血清Lep(P=0.006)及精浆Lep(P=0.033)都显著增高。在区别OA及NOA方面,精浆Lep及血清Lep的ROC曲线下面积(AUCROC)分别为0.658、0.702,均显著大于0.5,P值分别为0.014、0.002;精浆Lep、血清Lep及FSH三者联合,AUCROC最大(0.953),且以0.026×精浆Lep+0.05×血清Lep+0.106×FSH-2.197为联合指标值,以-0.289为临界值(≥临界值,判定为NOA),其敏感度及特异度均达到最高,分别为0.878及0.902。结论:在鉴别OA和NOA方面,精浆及血清Lep水平有一定价值,联合精浆Lep、血清Lep及FSH,可能优于单个指标。     

Seminal plasma anti-Müllerian hormone level correlates with semen parameters but does not predict success of testicular sperm extraction (TESE)

AIM: To assess seminal plasma anti-Müllerian hormone (AMH) level relationships in fertile and infertile males. METHODS: Eighty-four male cases were studied and divided into four groups: fertile normozoospermia (n = 16), oligoasthenoteratozoospermia (n = 15), obstructive azoospermia (OA) (n = 13) and non-obstructive azoospermia (NOA) (n = 40). Conventional semen analysis was done for all cases. Testicular biopsy was done with histopathology and fresh tissue examination for testicular sperm extraction (TESE) in NOA cases. NOA group was subdivided according to TESE results into unsuccessful TESE (n = 19) and successful TESE (n = 21). Seminal plasma AMH was estimated by enzyme linked immunosorbent assay (ELISA) and serum follicular stimulating hormone (FSH) was estimated in NOA cases only by radioimmunoassay (RIA). RESULTS: Mean seminal AMH was significantly higher in fertile group than in oligoasthenoteratozoospermia with significance (41.5 +/- 10.9 pmol/L vs. 30.5 +/- 10.3 pmol/L, P < 0.05). Seminal AMH was not detected in any OA patients. Seminal AMH was correlated positively with testicular volume (r = 0.329, P = 0.005), sperm count (r = 0.483, P = 0.007), sperm motility percent (r = 0.419, P = 0.021) and negatively with sperm abnormal forms percent (r = -0.413, P = 0.023). Nonsignificant correlation was evident with age (r = -0.155, P = 0.414) and plasma FSH (r = -0.014, P = 0.943). In NOA cases, seminal AMH was detectable in 23/40 cases, 14 of them were successful TESE (57.5%) and was undetectable in 17/40 cases, 10 of them were unsuccessful TESE (58.2%). CONCLUSION: Seminal plasma AMH is an absolute testicular marker being absent in all OA cases. However, seminal AMH has a poor predictability for successful testicular sperm retrieval in NOA cases.     

Possible relationship between seminal plasma inhibin B and spermatogenesis in patients with azoospermia

Inhibin B is bidirectionally secreted by Sertoli cells, basal secretion into the circulation exerts negative feedback on follicle-stimulating hormone secretion, and serum inhibin B is considered a marker of spermatogenesis. The precise role of apical secretion is unknown. The objective of our work was to study the relationship between seminal inhibin B and spermatogenesis. Dimeric inhibin B was measured by immunoassay in seminal plasma of volunteers with normozoospermia (n = 10, group 1), in men after vasectomy (n = 10, group 2), and in men with azoospermia (n = 50, group 3). Testicular biopsy and testicular sperm extraction were performed in men with azoospermia. Seminal inhibin B levels were higher in men in group 1 than in men in groups 2 and 3 (P <.0001). In seminal plasma, inhibin B presents a positive correlation with alpha glucosidase activity (r =.37, P =.002). Seminal inhibin B is inversely related with serum FSH (r = -.58, P <.001), and presents a weak positive correlation with serum testosterone concentration (r =.29, P =.03). No difference was found between inhibin B levels in seminal plasma of patients with nonobstructive or obstructive azoospermia, and between positive or negative outcome of TESE. We conclude that inhibin B secretion by Sertoli cells is differentially regulated. The contribution of accessory sex glands limits the use of seminal plasma inhibin B as a marker of spermatogenesis.     

Effect of smoking on seminal plasma ascorbic acid in infertile and fertile males

This work aimed to assess the relationship of seminal ascorbic acid levels with smoking in infertile males. One hundred and seventy men were divided into four groups: nonobstructive azoospermia [NOA: smokers (n = 20), nonsmokers (n = 20)]; oligoasthenozoospermia [smokers (n = 30), nonsmokers (n = 20)]; asthenozoospermia [smokers (n = 20), nonsmokers (n = 20)] and normozoospermic fertile men [smokers (n = 20), nonsmokers (n = 20)]. The patients underwent medical history, clinical examination, conventional semen analysis and estimation of ascorbic acid in the seminal plasma calorimetrically. There was a significant decrease in the mean seminal plasma ascorbic acid levels in smokers versus nonsmokers in all groups (mean +/- SD; 6.03 +/- 2.18 versus 6.62 +/- 1.29, 7.81 +/- 1.98 versus 9.44 +/- 2.15, 8.09 +/- 1.98 versus 9.95 +/- 2.03, 11.32 +/- 2.15 versus 12.98 +/- 12.19 mg dl(-1) respectively). Fertile subjects, smokers or not, demonstrated significant higher seminal ascorbic acid levels than any infertile group. Seminal plasma ascorbic acid in smokers and nonsmokers was correlated significantly with sperm concentration (r = 0.59, 0.60, P < 0.001), sperm motility (r = 0.65, 0.55, P < 0.001) and negatively with sperm abnormal forms per cent (r = -0.53, -0.50, P < 0.001). Nonsignificant correlations were elicited with semen volume (r = 0.2, 0.09) or liquefaction time (r = 0.03, 0.06). It is concluded that seminal plasma ascorbic acid decreased significantly in smokers and infertile men versus nonsmokers and fertile men, and is significantly correlated with the main sperm parameters: count, motility and normal morphology. Also, cigarette smoking is associated with reduced semen main parameters that could worsen the male fertilizing potential, especially in borderline cases.     

精浆游离L-肉毒碱水平及其与精子密度、活动率及活力的相关性研究

目的:研究正常生育及不育男性精浆中游离L-肉毒碱水平差异及其与精子密度、活动率(a+b+c级精子百分率)及活力(a+b级精子百分率)之间的相关性,探讨精浆中游离L-肉毒碱水平对男性生育力的影响及其在不育症检查和治疗中的作用。方法:分别采用高效液相色谱法和计算机辅助精液分析系统,测定了230例不育症患者(精子密度正常117例,少精子症81例,无精子症32例)和30例正常生育男性精浆中游离L-肉毒碱水平及精子密度、活动率、活力等参数。根据检查结果对不育症患者分组后,以SPSS12.0软件包进行统计学分析,比较各组间游离L-肉毒碱水平的差异以及游离L-肉毒碱水平与精子密度、活动率、活力之间的相关性。结果:正常生育组精浆游离L-肉毒碱水平明显高于不育组(P<0.01)。精液中精子密度越低、活力越弱,这种差异性越显著。相关性分析结果显示,精浆游离L-肉毒碱水平与精子密度呈显著正相关关系(r=0.521,P<0.01),与精子活动率和活力之间也具有正相关关系(r=0.319,P<0.01;r=0.251,P<0.01)。结论:精浆L-肉毒碱水平与精子密度、活动率和活力之间密切相关,其含量测定作为一项有用的生化指标,可为男性不育症检查及临床诊治和进行有关男性生殖功能机制研究提供参考。     

血清和精浆抑制素B在无精子症诊断中的应用研究

目的:评价血清和精浆抑制素B浓度在诊断梗阻性和非梗阻性无精子症中的应用价值。方法:测定25例正常生育者(正常对照组),37例梗阻性无精子症以及33例非梗阻性无精子症者的血清卵泡刺激素(FSH)、血清和精浆抑制素B浓度,对无精子症者行睾丸病理Johnsen评分。结果:精浆和血清抑制素B浓度比值在正常对照组和非梗阻性无精子组分别为2.17和3.63,差异无显著性(P=0.29);在梗阻性无精子症组两者比值为0.18,与正常对照组和非梗阻性无精子症组比较显著降低(P<0.01)。结论:精浆和血清抑制素B浓度比值可用于临床诊断梗阻性和非梗阻性无精子症。     

Assessment of seminal plasma laminin in fertile and infertile men

Aim： To assess laminin levels in the seminal plasma of infertile and fertile men, and to analyze the correlation of laminin levels with sperm count, age, sperm motility and semen volume. Methods： One hundred and twenty-five recruited men were equally divided into five groups according to their sperm concentration and clinical examination： fertile normozoospermia, oligoasthenozoospermia, non-obstructive azoospermia （NOA）, obstructive azoospermia （OA） and congenital bilateral absent vas deferens （CBAVD）. The patients＇ medical history was investigated and patients underwent clinical examination, conventional semen analysis and estimation of seminal plasma laminin by radioimmunoassay. Results： Seminal plasma laminin levels of successive groups were： 2.82 ± 0.62, 2.49 ± 0.44, 1.77 ± 0.56, 1.72 ± 0.76, 1.35 ± 0.63 U/mL, respectively. The fertile normozoospermic group showed the highest concentration compared to all infertile groups with significant differences compared to azoospermic groups （P 〈 0.05）. Testicular contribution was estimated to be approximately one-third of the seminal laminin. Seminal plasma laminin demonstrated significant correlation with sperm concentration （r = 0.460, P 〈 0.001） and nonsignificant correlation with age （r = 0.021, P = 0.940）, sperm motility percentage （r = 0.142, P = 0.615） and semen volume （r = 0.035, P = 0.087）. Conelusion： Seminal plasma laminin is derived mostly from prostatic and testicular portions and minimally from the seminal vesicle and vas deferens. Estimating seminal laminin alone is not conclusive in diagnosing different cases of male infertility.     

Beta-endorphin in serum and seminal plasma in infertile men

Aim:To access beta-endorphin levels in serum as well as seminal plasma in different infertile male groups.Methods:Beta-endorphin was estimated in the serum and seminal plasma by enzyme-linked immunosorbent assay(ELISA)method in 80 infertile men equally divided into four groups:non-obstructive azoospermia(NOA),obstructive azoosper-mia(OA),congenital bilateral absent vas deferens(CBVAD)and asthenozoospermia.The results were compared tothose of 20 normozoospermic proven fertile men.Results:There was a decrease in the mean levels of beta-endorphin in the seminal plasma of all successive infertile groups(mean±SD:NOA 51.30±27.37,OA 51.88±9.47,CBAVD 20.36±13.39,asthenozoospermia 49.26±12.49 pg/mL,respectively)compared to the normozoospermicfertile control(87.23±29.55 pg/mL).This relation was not present in mean serum level of beta-endorphin betweenfour infertile groups(51.09±14.71,49.76±12.4,33.96±7.2,69.1±16.57 pg/mL,respectively)and the fertilecontrol group(49.26±31.32 pg/mL).The CBVAD group showed the lowest seminal plasma mean level of beta-endorphin.Testicular contribution of seminal beta-endorphin was estimated to be approximately 40%.Seminal beta-endorphin showed significant correlation with the sperm concentration(r=0.699,P=0.0188)and nonsignificantcorrelation with its serum level(r=0.375,P=0.185)or with the sperm motility percentage(r=0.470,P=0.899).Conclusion:The estimation of beta-endorphin alone is not conclusive to evaluate male reproduction as there aremany other opiates acting at the hypothalamic pituitary gonadal axis.(Asian J Androl 2006 Nov;8:709-712)     

Seminal plasma albumin: origin and relation to the male reproductive parameters

We wanted to investigate the origin of seminal plasma albumin and its relation to the male reproductive parameters. Semen samples from 916 men, under infertility assessment, were analysed according to guidelines of the World Health Organization. Seminal plasma constituents, i.e. albumin, markers of the epididymal (neutral alpha-glucosidase, NAG), prostatic (prostate-specific antigen, PSA, and zinc) and seminal vesicle function (fructose), as well as levels of reproductive hormones in plasma were measured. The sperm chromatin structure assay (SCSA) was applied on 267 of the 916 samples. A negative correlation was seen for seminal albumin and plasma follicle-stimulating hormone (r=-0.1, P=0.02) and a positive correlation for seminal albumin and serum inhibin B (r=0.2, P=0.004). Albumin exhibited positive correlations with the epididymal marker, NAG (r=0.5, P<0.001) and with the prostatic markers, PSA and zinc (r=0.1, P=0.001; r=0.2, P<0.001 respectively) as well as with age (r=0.2, P<0.001). A negative significant association was seen for seminal albumin and semen volume (beta=-0.60; 95% CI -0.80 to -0.30). The opposite trend was found regarding sperm concentration (beta=0.34; 95% CI 0.30-0.40), total sperm count (beta=0.30; 95% CI 0.20-0.40), and percentage morphologically normal spermatozoa (beta=0.70; 95% CI 0.10-1.0). No association was found between albumin and sperm motility, SCSA parameters, or fructose, the marker of seminal vesicles. Our results suggest testicular, epididymal and prostatic origin of seminal plasma albumin, in addition to the contribution from blood. This is the first study to demonstrate an association between seminal plasma albumin and sperm morphology. Further studies are needed to elucidate the role of seminal albumin in sperm morphology.