Localization of lactoferrin in the male reproductive tract

The immunohistochemical localization of lactoferrin in the normal human prostate, seminal vesicle, vas deferens, epididymis and testis was studied using the peroxidase-antiperoxidase method at the light and electron microscopical level. Lactoferrin immunoreactivity was localized in the glandular epithelial cells and granulocytes in the prostate and seminal vesicle. In the prostate, lactoferrin showed an uneven distribution; some of the glands contained exclusively positive cells and others were completely lactoferrin negative, while the rest contained scattered positive cells. The seminal vesicles were divided into three segments, and their lactoferrin content varied significantly although it was always epithelial. The ductus deferens, epididymis and testis contained no lactoferrin. In conclusion, lactoferrin was found in the prostate and seminal vesicles, but not in the testis.     

男性型秃发头发移植术后性激素受体的变化

目的探讨头皮性激素受体在男性型秃发(male pattern baldness，MPB)发生机制中的作用。方法2001年7月至2003年6月，采用荧光组织化学方法，对13例接受过自体头发移植术患者的供、受区头皮及头发对应组织中雌、雄激素受体进行检测，并分别进行对比研究。结果头发移植术后，各实验对象供区与受区相应移植组织中，其性激素受体的含量对比，差异无统计学意义。结论供体毛胚移植到受区(原脱发区)后，其局部组织性激素受体的含量不会发生改变。从另一角度佐证了头皮及头发性激素受体的含量异常，在MPB发生中起重要作用。     

雄激素、雌激素与男性骨质疏松症

近年研究发现男性骨质疏松症与体内雄激素和雌激素水平呈正相关.雄激素通过刺激成骨细胞增殖和发育来促进骨骼生长,对维持骨量和提高骨密度起重要作用.雌激素对骨的作用可能是降低骨吸收而非促进骨形成,通过与成骨细胞上的受体结合而间接调控成骨细胞功能.但有研究认为睾酮对雄激素受体的亲和力和活性相对较低.睾酮在5α还原酶作用下代谢为双氢睾酮,进而代谢为雌二醇,或在芳香化酶作用下直接转变为雌激素,与雌激素受体结合而发挥生理学作用.该文就雄激素和雌激在男性骨质疏松症中的作用机制及激素替代疗法临床应用进展作一综述.     

Deficiency of androgen receptors in male pseudohermaphroditism

A diagnosis of androgen receptor deficiency was made in a male with ambiguous genitalia during the neonatal period. Since the neonate had a small hypospadiac phallus with laboratory evidence of a receptor deficiency and clinical unresponsiveness to high levels of androgen, it was decided to assign a female gender. Bilateral orchiectomy and phallic recession were performed.     

Sperm protection in the male reproductive tract by Toll‐like receptors

Sperm function can be affected by infection. Our understanding of innate immune system molecular mechanisms has been expanded, by the discovery of ‘Toll‐like receptors’ (TLRs). It seems that these receptors could play a critical role in the protection of spermatozoa. This study seeks to examine the presence and distribution of TLRs in different parts of the human male reproductive tract and spermatozoa. So, TLR gene expression was examined by RT‐PCR. Quantitative real‐time PCR (Q‐PCR) analysis used to compare the expression of TLRs in all sections of the male reproductive tract and TLRs 2, 3 and 4 in testicular sperm extraction (TESE) samples, which contained spermatozoa (TESE+) and those that did not (TESE?). Results showed that all TLR genes were expressed in different parts of the human male reproductive tract and spermatozoa. Moreover, Q‐PCR indicated that the relative expression of TLRs did not significantly change in different parts of the male reproductive tract but this technique has shown only relative TLR2 expression in TESE? is lower than TESE+ samples. It could be concluded that TLRs may provide a broad spectrum of protection from infection in the male reproductive tract. Furthermore, TLRs may influence on the developmental process during spermatogenesis.     

Co-localization of androgen receptor with estrogen receptor beta in the lower urinary tract of the male rat.

PURPOSE: Androgens and estrogens influence voiding. In this study their target sites in the lower urinary tract of the male rat were identified. MATERIALS AND METHODS: Cryosections of the bladder body, bladder neck, prostatic urethra, mid proximal urethra and prostatic autonomic ganglia of adult male rats were immunostained with specific estrogen receptor alpha, estrogen receptor beta (ERbeta) or androgen receptor (AR) antibodies. The sections were then examined under conventional, fluorescence or confocal fluorescence microscopy. RESULTS: Co-expression of AR and ERbeta in the urothelium, bladder smooth muscle cells, proximal urethra striated muscle cells and neurons in the autonomic ganglia of the prostatic plexus suggests that estrogen and androgen have direct effects in the lower urinary tract. CONCLUSIONS: The local interaction of AR and ERbeta in the hormonal control of voiding is an intriguing possibility.     

Subtotal obstruction of the male reproductive tract

Bilateral obstruction of the male reproductive tract is suspected in men with azoospermia, normal testicular volume and normal FSH. A testicular biopsy is required to differentiate between an obstruction and a testicular insufficiency. Unilateral or subtotal bilateral obstructions and epididymal dysfunction may cause severe oligozoospermia in men with a normal spermatogenesis. However, information on spermatogenesis in oligozoospermic men is lacking, since testicular biopsy is not routinely performed. Men with a sperm concentration of <1 x 10(6) spermatozoa/ml were investigated for possible partial obstruction by performing a testicular biopsy under local anaesthesia. Spermatogenesis was determined by the Johnsen scoring method. A testicular biopsy was performed in 78 men with severe oligozoospermia. The medical history showed male accessory gland infection in 12.8%, previous hernia repair in 14.1% and a history of cryptorchidism in 12.8%. A normal or slightly disturbed spermatogenesis (Johnsen score >8) was present in 39/78 (50%) of the men. Hernia repair occurred more often in men with normal spermatogenesis. A varicocele was predominantly seen in men with a disturbed spermatogenesis. FSH was significantly lower ( P<0.0001) in men with normal spermatogenesis. Subtotal obstruction of the male reproductive tract is a frequent cause of severe oligozoospermia in men with a normal testicular volume and a normal FSH. In other cases, an epididymal dysfunction might explain the oligozoospermia in men with a normal testicular biopsy score.     

Inflammatory-associated obstructions of the male reproductive tract

A history of urogenital inflammation occurs in 5-12% of men attending infertility clinics. Usually, infection has a detrimental effect on sperm quality by reducing concentration and motility, and possibly affecting the number of morphological normal spermatozoa. In addition, infection may be the source of auto-antibodies against spermatozoa, found in about 8% of the infertile male population. In contrast to the situation in women, there is no clear evidence that male accessory gland infections can result in epididymal blockage or vassal obstruction, with the exception of genital tuberculosis. Although Chlamydia trachomatis is a well-documented source of chronic prostatitis, the infection does not seem to cause obstruction of the reproductive tract, as it does in women. If male urogenital infection causes obstruction it is most likely located at the level of the ejaculatory ducts. Chronic prostatitis has been proved to cause scarring of the prostatic and ejaculatory ducts, resulting in low seminal volume with low fructose and alpha-glucosidase. Many of these men present with severe oligozoospermia or azoospermia, normal size testis and normal gonadotrophins. We performed an excisional testicular biopsy in all men presenting with <1 million spermatozoa per millilitre and found that 39 of 78 (50%) had a normal spermatogenesis. A history of male accessory genital infection was found in 12% of the men and 10% had abnormalities found on transrectal ultrasound of the prostate (like oedema, dilatation of the seminal vesicles and ejaculatory ducts) intraprostatic calcifications and dilatation of the periprostatic venous plexus. Ejaculatory duct obstruction is a common cause of male infertility and infections are present in at least 22-50% of these men. Transurethral resection of the ejaculatory ducts may result in a significant improvement of the sperm quality and in spontaneous pregnancies in up to 25% of the couples. In case of failure sperm aspiration from the epididymis and intracytoplasmic sperm injection is the treatment of choice.     

Correlation of estrogen, progesterone, and androgen receptors in breast cancer

Breast cancer was induced in female Holtzman rats by intragastric administration of 7,12-dimethylbenz[a]antracene (DMBA). At tumor maturity, biopsies of viable tissue were obtained, frozen, and then assayed for estrogen, progesterone, and androgen receptor content. By simple linear regression analysis, progesterone receptor levels significantly correlated with both estrogen and androgen receptor levels, whereas estrogen and androgen receptor levels did not correlate with each other. Multiple regression analyses further substantiated the predictive value of the progesterone receptor for the other two hormone receptors. Knowledge of breast tumor androgen receptor levels may further enhance the value of the estrogen receptor and progesterone receptor in hormonal responsiveness. Further, the progesterone receptor may be the most sensitive of the steroid hormone receptors for selecting patients likely to respond to hormonal therapy.     

Suppression of androgen action and the induction of gross abnormalities of the reproductive tract in male rats treated neonatally with diethylstilbestrol

This study evaluated whether androgen action is altered in rats treated neonatally with diethylstilbestrol (DES) at a dose that induced reproductive tract abnormalities. Rats were treated on alternate days 2-12 with 10 microg DES and studied on Day 18. DES-induced abnormalities included a 70% reduction in testis weight, distension and overgrowth of the rete, distension and reduction in epithelial height of the efferent ducts, underdevelopment of the epididymal duct epithelium, reduction in epithelial height in the vas deferens, and convolution of the extra-epididymal vas. In DES-treated rats, androgen receptor (AR) immunoexpression was virtually absent from all affected tissues and the testis, whereas AR expression in controls was intense in epithelial and stromal cells. The DES-induced change in AR immunoexpression was confirmed by Western analysis for the testis. In rats treated neonatally with 1 microg DES, reproductive abnormalities were absent or minor, except for a 38% reduction in testis weight; loss of AR immunoexpression also did not occur in these rats. Treatment-induced changes in AR expression were paralleled by changes in Leydig cell volume per testis (91% reduction in the 10-microg DES group; no change in the 1-microg DES group). To test whether suppression of androgen production or action alone could induce comparable reproductive abnormalities to 10 microg DES, rats were treated neonatally with either a potent gonadotropin-releasing hormone antagonist (GnRHa) or with flutamide (50 mg/kg/day). These treatments reduced testis weight (68% for GnRHa, 40% for flutamide), and generally retarded development of the reproductive tract but failed to induce the abnormalities induced by 10 microg DES. GnRHa and flutamide caused no detectable change in AR immunoexpression in target tissues, with the exception of minor changes in the testes of flutamide-treated males. GnRHa treatment caused a reduction (83%) in Leydig cell volume comparable to that caused by 10 microg DES. Immunoexpression of estrogen receptor alpha (ER alpha) in the efferent ducts and of ER beta in all tissues studied were unaffected by any of the above treatments. Neonatal coadministration of testosterone esters (TE; 200 microg) with 10 microg DES prevented most of the morphological abnormalities induced by 10 microg DES treatment alone, though testis weight was still subnormal (46% reduction in DES + TE vs 72% in DES alone and 49% with TE alone) and some lumenal distension was still evident in the efferent ducts. Coadministration of TE with DES prevented DES-induced loss of AR immunoexpression (confirmed for testis by Western blot analysis). It is concluded that 1) reproductive tract abnormalities induced in the neonatal male rat by a high (10 microg) dose of DES are associated with reduced AR expression and Leydig cell volume; 2) these changes are largely absent with a lower dose of DES (1 microg); 3) treatments that interfere with androgen production (GnRHa) or action (flutamide) alone failed to induce reproductive tract abnormalities or alter AR expression as did 10 microg DES; 4) a grossly altered androgen:estrogen balance (low androgen + high estrogen) may underlie the reproductive tract abnormalities, other than reduced testis weight, induced by high doses of DES.     

Expression of estrogen and androgen receptors in children with hypospadias: preliminary report

This investigation was conducted to evaluate the presence of estrogen and androgen receptors in penile tissues of patients with hypospadias. The biopsy specimens from prepuce, glans, and urethral plate were sampled during the hypospadias surgery in five patients and were analyzed immunohistochemically. Twelve specimens were investigated for the presence of estrogen or androgen receptors (n: 24); the result was negative in 9 (37%) and positive in 15 (63%). Estrogen receptors were present in 10 specimens (42%) (prepuce: 5, glans: 3, and urethral plate: 2). Androgen receptors were present in 5 specimens (21%) (prepuce: 3, glans: 1, and urethral plate: 1). There was expression of both estrogen and androgen receptors in 5 specimens and only estrogen receptors in the remaining 5. Dominant expression of estrogen receptors in penile tissues of children with hypospadias may be the postnatal finding of disrupted estrogen and androgen receptor interaction during the intrauterine development of external genitalia.     

Localization of estrogen receptors in long bones and vertebrae of human fetuses

Summary In order to investigate the possible role of estrogen in the development of cartilage and bone we studied by immunofluorescence immunohistochemistry and autoradiography 26 human embryos and fetuses 7–22 weeks in gestational age associated with pregnancy interrupted for nonmedical reasons. In order to demonstrate the presence of estrogen receptors (ERs) in human fetal cartilage, cryostat sections of long bones and lumbar and thoracic vertebrae were prepared for (1) fluorescent immunocytochemistry using an antiidiotypic monoclonal antibody to antiestradiol receptor monoclonal Ab labeled with fluorescein isothiocyanate (FITC), (2) immunohistochemistry using monoclonal antihuman estradiol receptor antibody, labeled with strept. A-B immunoperoxidose, and (3) autoradiographic localization of estradiol using labeled (3 H) l7 estradiol. In fetuses aged 10 weeks or older, intranuclear and perinuclear localization of ER was demonstrated by all methods, mainly amongst chondrocytes of the proliferating and higher hypertrophic zones of the epiphyses and in the cartilage of vertebral bodies. These data suggest that estrogen acts directly on chondrocytes of human fetuses through an ER-mediated mechanism.     

G蛋白偶联的雌激素受体在雄性生殖中的作用

G蛋白偶联的雌激素受体(GPER),又称G蛋白偶联受体30(GPR30),是近年来发现的有别于雌激素经典核受体的功能性膜受体。该受体广泛表达于皮质、小脑、海马、心脏、肺、肝脏、骨骼肌及泌尿生殖器官等全身各个系统,与雌激素及其相关的衍生物结合,引起快速的非基因效应,参与全身各个系统的多种生理活动。本文主要对男性生殖中GPER的分子结构、亚细胞定位、信号传导、分布以及功能进行了综述。     

脂多糖通过Toll样受体对雄性生殖功能的影响

生殖道感染是影响男性生育的重要因素之一,然而其机制尚未完全明了。最近研究认为病原体模式识别受体之一Toll样受体(TLRs)及其诱导的信号通路在炎症导致雄性不育过程中发挥着重要作用。脂多糖(LPS)作为革兰阴性菌细胞壁组成成分,可以通过TLRs诱导相应的炎症反应。众多研究表明,TLRs在雄性生殖道广泛表达,并且LPS可通过TLRs诱导生殖道炎症反应,影响雄性生殖功能。本文就LPS通过其相关受体TLRs通路诱导生殖道炎症,影响睾丸、附睾功能及精子质量,导致雄性生殖功能受损的机制进行综述。