SEARCH · Search PubMed

Results for “testis”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,531 records · Page 85Linked to original sources

PubMed2001

Reduction of long-term effects of local heating of the testis by treatment of rats with a GnRH agonist and an anti-androgen.

Heating the testes of anaesthetized adult rats to 43 degrees C for 30 min in a waterbath was followed by a large decrease in testis and epididymis mass and number of spermatozoa 35 days later. These parameters had recovered to some extent, but not completely, by days 70 and 97 after heating, but had decreased again in rats examined on day 182. There were no consistent effects of heating on androgen status, as determined by the concentrations of testosterone in blood and testis fluids, or by seminal vesicle mass, and interstitial fluid volume was increased in the heated testes. Treatment of rats with an implant of a GnRH agonist and daily injections of an anti-androgen for 14 days (sufficient in itself to cause large temporary decreases in tissue mass, number of spermatozoa and androgen status) did not reduce the initial decrease in testis mass or number of spermatozoa seen after heating, but reduced the later decreases in mass and number of spermatozoa significantly. These findings indicate that, as well as causing damage to spermatocytes and spermatids, as previously reported, heating also reduces the ability of spermatogonia to repopulate the seminiferous tubules at longer intervals after heating. Furthermore, it appears that this effect on the spermatogonia can be reduced by treating the animals with a GnRH agonist and anti-androgen, a treatment similar to that shown by other authors to improve recovery of the testis from irradiation or drug treatment.

Androgen Antagonists↗

PubMed2002

A quantitative (stereological) study of the effects of experimental unilateral cryptorchidism and subsequent orchiopexy on spermatogenesis in adult rabbit testis.

The aim of this study was to examine the controversial effects of experimental unilateral cryptorchidism and subsequent orchiopexy on the number of germ cells and other morphometric characteristics of testicular and epididymal structures in adult rabbits. Unilateral cryptorchidism was induced in 11 mature male New Zealand white rabbits by returning one testis, together with the ipsilateral epididymis, to the abdominal cavity via a surgical procedure. After 3 months, testes and epididymides were removed from six animals (and from six age-matched control animals that did not undergo the surgery). Orchiopexy was performed on the five remaining animals and the testes and epididymides of these animals (and an additional six age-matched control animals) were removed 7 weeks later. A contemporary, unbiased and efficient stereological tool, the optical disector, was used to estimate the number of nuclei in the testis and epididymis using methacrylate-embedded sections of 25 micron in thickness. Cryptorchidism resulted in severe testicular atrophy and spermatogenic arrest: type A spermatogonia and Sertoli cells only were seen in the seminiferous epithelium, and the number of type A spermatogonia per testis was reduced by 84%. After orchiopexy, the testis remained atrophied and the number of type A spermatogonia returned to the near-normal range in four of five animals, but spermatogenesis was recovered only partially at the stage of early primary spermatocytes (one animal), late primary spermatocytes (two animals) or spermatids (one animal). In conclusion, cryptorchidism caused severe spermatogenic arrest that was potentially recoverable (in view of the restoration of the number of type A spermatogonia), but orchiopexy failed to induce full recovery of spermatogenesis.

Animals↗

PubMed2005

Germ cell fate and seminiferous tubule development in bovine testis xenografts.

Spermatogenesis can occur in testis tissue from immature bulls ectopically grafted into mouse hosts; however, efficiency of sperm production is lower than in other donor species. To elucidate a possible mechanism for the impaired spermatogenesis in bovine testis xenografts, germ cell fate and xenograft development were investigated at different time points and compared with testis tissue from age-matched calves as controls. Histologically, an initial decrease in germ cell number was noticed in xenografts recovered up to 2 months post-grafting without an increase in germ cell apoptosis. From 2 months onward, the number of germ cells increased. In contrast, a continuous increase in germ cell number was seen in control tissue. Pachytene spermatocytes were observed in some grafts before 4 months, whereas in the control tissue they were not present until 5 months of age. Beyond 4 months post-grafting spermatogenesis appeared to be arrested at the pachytene spermatocyte stage in most grafts. Elongated spermatids were observed between 6 and 8 months post-grafting, similar to the controls, albeit in much lower numbers. Lumen formation started earlier in grafts compared with controls and by 6 months post-grafting tubules with extensively dilated lumen were observed. A donor effect on efficiency of spermatogenesis was also observed. These results indicate that the low efficiency of sperm production in bovine xenografts is due to an initial deficit of germ cells and impaired meiotic and post-meiotic differentiation. The characterization of spermatogenic efficiency will provide the basis to understand the control of spermatogenesis in testis grafts.

Animals↗

PubMed2006

Germ cell development in equine testis tissue xenografted into mice.

Grafting of testis tissue from immature animals to immunodeficient mice results in complete spermatogenesis, albeit with varying efficiency in different species. The objectives of this study were to investigate if grafting of horse testis tissue would result in spermatogenesis, and to assess the effect of exogenous gonadotropins on xenograft development. Small fragments of testis tissue from 7 colts (2 week to 4 years of age) were grafted under the back skin of castrated male immunodeficient mice. For 2 donor animals, half of the mice were treated with gonadotropins. Xenografts were analyzed at 4 and 8 months post-transplantation. Spermatogenic differentiation following grafting ranged from no differentiation to progression through meiosis with appearance of haploid cells. Administration of exogenous gonadotropins appeared to support post-meiotic differentiation. For more mature donor testis samples where spermatogenesis had progressed into or through meiosis, after grafting an initial loss of differentiated germ cells was observed followed by a resurgence of spermatogenesis. However, if haploid cells had been present prior to grafting, spermatogenesis did not progress beyond meiotic division. In all host mice with spermatogenic differentiation in grafts, increased weight of the seminal vesicles compared to castrated mice showed that xenografts were releasing testosterone. These results indicate that horse spermatogenesis occurs in a mouse host albeit with low efficiency. In most cases, spermatogenesis arrested at meiosis. The underlying mechanisms of this spermatogenic arrest require further investigation.

Animals↗

PubMed2004

Rapid evolution of mammalian X-linked testis-expressed homeobox genes.

Homeobox genes encode transcription factors that function in various developmental processes and are usually evolutionarily conserved in their sequences. However, two X-chromosome-linked testis-expressed homeobox genes, one from rodents and the other from fruit flies, are known to evolve rapidly under positive Darwinian selection. Here we report yet another case, from primates. TGIFLX is an X-linked homeobox gene that originated by retroposition of the autosomal gene TGIF2, most likely in a common ancestor of rodents and primates. While TGIF2 is ubiquitously expressed, TGIFLX is exclusively expressed in adult testis. A comparison of the TGIFLX sequences among 16 anthropoid primates revealed a significantly higher rate of nonsynonymous nucleotide substitution (d(N)) than synonymous substitution (d(S)), strongly suggesting the action of positive selection. Although the high d(N)/d(S) ratio is most evident outside the homeobox, the homeobox has a d(N)/d(S) of approximately 0.89 and includes two codons that are likely under selection. Furthermore, the rate of radical amino acid substitutions that alter amino acid charge is significantly greater than that of conservative substitutions, suggesting that the selection promotes diversity of the protein charge profile. More interestingly, an analysis of 64 orthologous homeobox genes from humans and mice shows substantially higher rates of amino acid substitution in X-linked testis-expressed genes than in other genes. These results suggest a general pattern of rapid evolution of mammalian X-linked testis-expressed homeobox genes. Although the physiological function of and the exact selective agent on TGIFLX and other rapidly evolving homeobox genes are unclear, the common expression pattern of these transcription factor genes led us to conjecture that the selection is related to one or more aspects of male reproduction and may contribute to speciation.

Amino Acid Sequence↗

PubMed2005

Arrest of spermatogenesis at the early meiotic stage in the small testis mutant (Smt) mice.

A spontaneous mutant having small testes was found in a laboratory mouse strain of mixed origins. The testis size was 1/3-1/2 of normal size, but no significant difference was seen in body mass and weight of organs such as kidney and seminal vesicle, which are influenced by androgen. Small testis males were found to be infertile by the mating test, although formation of a vaginal plug was normally observed in their female partners. Histological and air-dried specimens revealed degeneration of zygotene or early pachytene spermatocytes and very few numbers of pachytene and diplotene spermatocytes, round and elongate spermatids and mature spermatozoa in the mutant testis. Therefore, it was concluded that spermatogenesis is disrupted at the zygotene to early pachytene stages of meiosis in the mutant males. Segregation ratios of normal and mutant males were in accord with the assumption that the small testis character is caused by an autosomal recessive mutation. This mutant may be useful for research that would contribute to the elucidation of genetic mechanisms controlling the process of spermatogenesis and as a model animal for male infertility in humans.

Animals↗

PubMed1994

Increase in testis weight of hereditary dwarf rats (rdw/rdw) with advancing age.

Testis weight and seminal vesicle weight (relative to total body weight) in rdw rats and N rats were compared with advancing age. The results obtained were as follows 1) The increase in testis weight became remarkable at 15-16 weeks of age. The weight remained constant up to 23-30 weeks of age and decreased thereafter with age. 2) Seminal vesicle weight increased rapidly in rdw rat at 15-16 weeks of age, reflecting elevated androgen secretion and sexual maturation. 3) From the viewpoint of histology, one of causes of the increase in testis weight may be edema. The increase in testis weight coincided with the increase in androgen secretion at 15-16 weeks of age as suggested by the relative increase in seminal vesicle weight.

Aging↗

PubMed1981

Investigations into the possible effects of naturally occurring steroids on biosynthesis of 16-androstenes and androgens in microsomes of boar testis.

The possible interactions between naturally occurring steroids and three enzymes of the biosynthetic pathways of 16-androstenes and androgens in the boar testis were investigated. High concentrations (1 mmol/1) of several steroids reduced the production of 5,16-androstadien-3 beta-ol when a microsomal fraction of boar testis was incubated with pregnenolone at pH 7.0 (the pH optimum of this reaction was found to be 6.6). When some of these inhibitors were investigated in more detail using Lineweaver-Burk analyses, the apparent inhibition constants, Kv increased in value with increasing concentrations of inhibitors. When testosterone was added to 5,16-androstadien-3 beta-ol synthetase assays, the apparent Ki for 0.1 mumol testosterone/1 was 0.165 mumol/1 whereas those for 1.0, 10.0 and 100.0 mumol testosterone/1 were 1.65, 16.5 and 48.7 mumol/1 respectively. The apparent Michaelis constant, Km, of the reaction was 0.6 mumol/1. Similar results were obtained when oestrone, 17 alpha-hydroxyprogesterone and 4,16-androstadien-3-one were added as effectors. At physiological concentrations, these steroids would not affect the biosynthesis of 5,16-androstadien-3 beta-ol in vivo. Similarly, both 5 alpha-androst-16-en-3 beta-ol, quantitatively the most important 16-androstene in the boar testis and 5,16-androstadien-3 beta-ol were examined for their effects on the 17 alpha-hydroxy-C21-steroid, C-17,20 lyase (C-17,20 lyase) and 17 beta-hydroxysteroid dehydrogenase (17 beta-OHSDH) enzymes of androgen biosynthesis. Neither of these enzymes was affected by the 16-androstene steroids even at concentrations of 100 mumol/1, and the apparent Km values were 3.3 and 26.0 mumol/1 for C-17,20 lyase and 17 beta-OHSDH respectively. This lack of interaction between these pathways implies that the high levels of 16-androstene steroids produced by the testis will not interfere with androgen production, and also that the two side-chain cleavage steps from C21 precursors to C19 steroids are catalysed by independent systems.

Androgens↗

PubMed1988

Accelerated recovery of Leydig cells of the immature rat testis after administration of the cytotoxic ethylene dimethanesulphonate.

A single injection of ethane-1,2-dimethanesulphonate (EDS; 100 mg/kg) selectively destroys Leydig cells in the testis of the adult rat; however, unconfirmed reports indicate that Leydig cells in the immature rat are not affected. In this study the effect of EDS was examined 2 days after treatment of rats aged 20, 25 or 35 days. There was a large reduction in the in-vitro binding of 125I-labelled human chorionic gonadotrophin (hCG) to the homogenates of testes from EDS-treated immature rats. EDS reduced the testosterone content of the testes at all ages studied, but 2 days after injection had only significantly lowered the serum testosterone concentration of 25- or 35-day-old animals. Light microscopic examination of the testis of the 22-day-old rat, 2 days after treatment with EDS, indicated that there were still many cells staining for 3 beta-hydroxysteroid dehydrogenase. The interstitium also contained numerous atypical cells which did not stain for 3 beta-hydroxysteroid dehydrogenase. Electron microscopy of testes from the 22-day-old EDS-treated rat showed that Leydig cells were still present in the interstitium together with macrophages and fibroblast-like cells. Six days after EDS treatment of 20-day-old rats, but not 35-day-old rats, there was an increase in the binding of 125I-labelled hCG to testis homogenate to 70% of control value. Testicular testosterone content 6 days after treatment of the 20-day-old rat had risen to 50% of the control testis value.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Hydroxysteroid Dehydrogenases↗

PubMed1989

Dynamics of testosterone secretion by the rat testis: implications for measurement of the intratesticular levels of testosterone.

Testosterone concentrations have been measured in testicular interstitial fluid (IF), and in blood plasma sampled from various parts of the rat testis and spermatic cord, to assess (1) the most accurate method for determination of the intratesticular levels of testosterone, and (2) the route of secretion of testosterone from the testis. In untreated adult rats, testosterone concentrations were highest in blood collected from veins on the surface of the testis (269.50 +/- 30.63 (S.E.M.) nmol/l), but were reduced by 56% on average in blood collected from veins at the proximal end of the spermatic cord (123.06 +/- 24.75 nmol/l), and were reduced considerably in peripheral venous blood (4.55 +/- 0.55 nmol/l). Similar changes occurred in adult rats in which steroidogenesis was either stimulated (by treatment with human chorionic gonadotrophin; hCG) or inhibited (by treatment with aminoglutethimide; AMG), and in rats of various ages during sexual maturation. The reduction in testosterone levels during passage of blood from the testis up the spermatic cord is probably due mainly to dilution by incoming arterial blood which transfers to venous blood via anastomoses in the spermatic cord. Venous-arterial transfer of testosterone in the cord contributed to this in only a minor way. Concentrations of testosterone in testicular IF were always greater than testicular venous concentrations in control, developing and hCG-stimulated rats, but were comparable in rats treated with AMG to suppress Leydig cell steroidogenesis. These and other results demonstrate that the method of drip-collection of IF results in over-estimation of the actual intratesticular levels of testosterone.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1996

Growth hormone-releasing factor expression is discordantly regulated in the hypothalamus and testis of streptozotocin-diabetic rats.

Growth hormone-releasing factor (GRF) mRNA expression in male rats occurs predominantly in the hypothalamus (mainly in the arcuate nucleus), and among extraneural sites primarily in the testis. Hypothalamic GRF is the physiological tropic stimulus to growth hormone secretion. However, the role of GRF in the testis is unknown. We have shown previously that hypothalamic GRF mRNA expression is significantly reduced in streptozotocin (STZ)-diabetic rats. This reduction is confined to the arcuate nucleus and probably accounts for the suppression of growth hormone pulsatility. The present studies were performed to evaluate GRF expression in the testis of streptozotocin (STZ)-diabetic rats. Diabetes was induced by injection of STZ (100 mg/kg i.p.). Seventeen to twenty days later diabetic rats were hyperglycemic compared with vehicle-injected controls and demonstrated growth failure. Insulin treatment reduced the glycemia and increased body weight towards normal. Total RNA was extracted from the hypothalamus and testis, and GRF mRNA levels estimated by solution hybridization/nuclease protection assay. Levels of hypothalamic somatostatin mRNA were measured to serve as control values. GRF mRNA was significantly (P < 0.001) decreased in the hypothalamus of STZ-diabetic rats (0.2 +/- 0.07 mean relative densitometric units, n = 8) compared with controls (1.0 +/- 0.19, n = 8) with no change in somatostatin mRNA expression. In contrast, testicular GRF mRNA was increased 70% (P < 0.05) in STZ-diabetic rats. Insulin treatment resulted in normalization of hypothalamic GRF mRNA levels (1.1 +/- 0.17, n = 5) with no effect on testicular GRF mRNA expression. In conclusion GRF gene expression is discordantly regulated in tissues of male STZ-diabetic rats. While reduced GRF expression may account for the low growth hormone state in this model, increased testicular GRF mRNA (with the previously reported reduction of insulin-like growth factor-I mRNA) resembles the response seen in growth hormone-sensitive tissue (especially the hypothalamus) to this growth hormone-deficient state.

Animals↗

PubMed1996

The testis is not the major source of circulating follistatin in the ram.

The aims of this study were to determine the plasma concentrations of follistatin in rams and to assess if the testis contributes to circulating follistatin and if there is uptake or production of follistatin by the head in rams. Catheters were inserted in the carotid artery, jugular vein and spermatic vein of intact rams during the non-breeding season (experiment 1; n = 5) and breeding season (experiment 2; n = 4). In experiment 1, blood samples were collected from 5 rams every 10 min for 4 h, commencing 20-60 min after surgery. After 2 h of sampling 1 microgram gonadotrophin-releasing hormone (GnRH) was injected intravenously. In experiment 2, blood samples were collected from 4 of the rams used in experiment 1 by venipuncture 30 and 15 min before surgery and every 15 min throughout surgery. Commencing 1 h after surgery, matched samples were taken from each of the vessels every 10 min for 4 h (1-4 h after surgery), then every hour for 20 h (4-24 h after surgery) and then every 10 min for 4 h (24-28 h after surgery). In both experiments, follistatin secretion was non-pulsatile and there were no significant differences between the concentrations of follistatin in any of the vessels. There was a significant (P < 0.05) increase in the concentrations of follistatin in each of the vessels throughout the 4 h of 10-min sampling in both experiments. In experiment 2 plasma concentrations of follistatin in the jugular vein were significantly (P < 0.05) lower before surgery than at other stages of the experiment. During the non-breeding season (experiment 1) the concentrations of follistatin in all vessels were about 2-fold higher (P < 0.001) than during the breeding season (experiment 2). Concentrations of follistatin were measured in the testicular tissue of the ram, bull, monkey and rat and were found to be 13.6, 2.1, 2.5, 0.8 ng/g testis respectively. In experiment 3, blood samples were collected every 15 min for 4 h from castrated rams (n = 6) in the absence of treatment with testosterone propionate (TP) and after 7 days of treatment with a physiological dose of TP during the breeding and non-breeding seasons. There was no effect of stage of breeding season or TP on the plasma concentrations of follistatin and these concentrations in the castrated rams were similar to the concentrations in the intact rams in experiment 2. In experiment 4, the function of Leydig cells was stimulated by administration of human chorionic gonadotrophin but this had no effect on plasma concentrations of follistatin. These experiments show that the concentrations of follistatin in the plasma of rams are measurable, that the testis is not the major contributor to circulating follistatin and that there is no significant uptake or production of follistatin by the head in rams. It appears that the contribution of the testis to circulating follistatin may vary with the stage of the breeding season, being greater during the non-breeding season than the breeding season. The gonadotrophins and testosterone do not appear to have a direct effect on the secretion of follistatin in rams. The increase in concentrations of circulating follistatin during surgery and more frequent blood sampling suggest a stress-related effect on the production of follistatin.

Animals↗

PubMed1999

LH down-regulates gonadotropin-releasing hormone (GnRH) receptor, but not GnRH, mRNA levels in the rat testis.

The demonstration of an inhibitory effect of gonadotropin-releasing hormone (GnRH) agonists upon steroidogenesis in hypophysectomized rats and the presence of mRNA coding for GnRH and GnRH receptors (GnRH-R) in rat gonads suggests that GnRH can act locally in the gonads. To assess this hypothesis, we investigated the effects of GnRH analogs, gonadotropins and testosterone on the levels of both GnRH and GnRH-R mRNA in the rat testis. Using dot blot hybridization, we measured the mRNA levels 2 to 120 h after the administration of the GnRH agonist, triptorelin. We observed an acute reduction of both GnRH and GnRH-R mRNAs 24 h after the injection (about 38% of control). However, the kinetics for testis GnRH-R mRNA were different from those previously found for pituitary GnRH-R mRNA under the same conditions. Initially, the concentrations of serum LH and FSH peaked, then declined, probably due to the desensitization of the gonadotrope cells. In contrast, the GnRH antagonist, antarelix, after 8 h induced a 2.5-fold increase in GnRH-R mRNA, but not in GnRH mRNA, while gonadotropins levels were reduced. Human recombinant FSH had no significant effect on either GnRH or GnRH-R mRNA levels. Inversely, GnRH-R mRNA levels markedly decreased by 21% of that of control 24 h after hCG injection. Finally, 24 h after testosterone injection, a significant increase in GnRH-R mRNA levels (2.3 fold vs control) was found, but a reduction in the concentration of serum LH, probably by negative feedback on the pituitary, was observed. In contrast, GnRH mRNA levels were not significantly altered following testosterone treatment. Since LH receptors, GnRH-R and testosterone synthesis are colocalized in Leydig cells, our data suggest that LH could inhibit the GnRH-R gene expression or decrease the GnRH-R mRNA stability in the testis. However, this does not exclude the possibility that GnRH analogs could also affect the GnRH-R mRNA levels via direct binding to testicular GnRH-R. In contrast, the regulation of GnRH mRNA levels appeared to be independent of gonadotropins. Taken together, our results suggest a regulation of GnRH and GnRH-R mRNA specific for the testis.

Analysis of Variance↗

PubMed1989

The blood vascular architecture of the rat testis: a scanning electron microscopic study of corrosion casts followed by light microscopy of tissue sections.

The blood vascular bed of the rat testis was studied by scanning electron microscopy (SEM) of corrosion casts and by light microscopy of tissue sections. The testicular artery penetrates the pampiniform plexus and gives rise to the intertubular arterioles. Each of these arterioles courses in the intertubular connective tissue column, and gives off intertubular and peritubular capillaries. The intertubular capillaries pass the intertubular connective tissue column, whereas the peritubular capillaries reach the peritubular connective tissue sheet. The intertubular and peritubular capillaries anastomose with each other and converge into the intertubular venules in the intertubular connective tissue columns. Thus, the blood vascular bed of the rat testis consists of hexago- or pentago-columnar capillary networks which commonly surround the seminiferous tubules. The Leidig's cells are preferentially observed in the intertubular connective tissue columns. One of the intertubular capillaries is consistently thick, and directly continues into the intertubular venules (arteriolo-venular capillary channels), which finally drain into the pampiniform plexus. These findings suggest that the male sex hormone, testosterone, as secreted by the Leidig's cells, is discharged into the intertubular capillaries and then mainly carried by the arteriolo-venular capillary channels and intertubular venules into the pampiniform plexus. This specialized drainage may ensure the presence of highly concentrated testosterone in the pampiniform plexus and allow the testosterone-exchange from the pamipiniform plexus to the testicular artery. The arteriolo-venular capillary channels may also eliminate blood congestion in the testis to enhance the efficiency of the heat-exchange mechanism between the testicular artery and pampiniform plexus. Many arterio-arterial and arterio-venous anastomoses occur, which may regulate the blood flow within the testis.

Animals↗

PubMed2005

Vitellogenin-immunohistochemistry in the liver and the testis of the medaka, Oryzias latipes, exposed to 17beta-estradiol and p-nonylphenol.

Vitellogenin (VTG) produced in male fish has been used for a biomarker to study endocrine disrupters. However, the characteristics of VTG produced in male fish have not been studied well. In this study, we investigated the localization of VTG in the liver and the testis of male medaka (Oryzias latipes) treated with 17beta-estradiol (E2) and p-nonylphenol (NP). The male fish were exposed to 1 microg/L E2 and 500 microg/L NP for 1-12 days. Control groups were kept in water including only vehicle. The frozen sections of the liver and the testis were stained with immunohistochemical methods using an antiserum against medaka VTG as the first antibody. In the E2 and NP treated liver, the hepatocytes showed immunoreactivity. In particular, the cytoplasm close to the cell membrane surrounding the sinusoids was strongly immunopositive. In the testis of both treatments, the interstitial tissues and the cells (spermatocytes) in the seminiferous tubules were immunopositive. The concentration of VTG became gradually higher in both tissues with longer treatments. These results suggest that germ cells in the testis treated with E2 and NP are able to incorporate and accumulate VTG.

Animals↗

PubMed2006

Expression of orphan receptors TR2, TR3, TR4, and p53 in heat-treated testis of cynomolgus monkeys (Macaca fascicularis).

To investigate the possible role of testicular orphan receptors (TR) TR2, TR3, and TR4 in the process of germ cell apoptosis in the heat-treated testis of monkey, we have examined the spatiotemporal expression of the 3 TR mRNAs in relation to p53 mRNA levels in the monkey testis by in situ hybridization and reverse transcription polymerase chain reaction techniques. The results showed that TR2 mRNA was confined to spermatocytes; TR4 and TR3 mRNAs were expressed in both spermatocytes and spermatids. The heat treatment did not change TR2 mRNA level but significantly reduced TR4 mRNA expression in spermatocytes on days 3 and 8 after the heat treatment. TR3 mRNA expression was affected by the heat treatment in a time-dependent manner, with the lowest level on day 30 after the heat shock. Low to moderate signal for p53 mRNA was detected in spermatocytes before treatment, which increased dramatically on days 3, 8, and 30 after the heat shock. The coincident expression of the testicular TR3 and p53 mRNA, spatially and time dependently, implied that the decrease in TR3 expression in the heat-treated testis might be closely related to the p53 signal pathway, whereas the temporal decrease in TR4 production in the testis at the early stage indicated that this orphan receptor might be also involved in germ cell apoptosis. The data suggest that TR3, TR4, and p53 could be important regulators of germ cell apoptosis induced by the heat treatment, whereas TR2 might not be a key regulator in this process.

Animals↗

PubMed2006

Susceptibility of human testis to human immunodeficiency virus-1 infection in situ and in vitro.

Semen represents the main vector for human immunodeficiency virus (HIV) dissemination worldwide and has been shown to harbor replication-competent virus despite otherwise effective highly active anti-retroviral therapy, which achieves undetectable viral load in plasma. Despite this, the origin of seminal HIV particles remains unclear, as does the question of whether the male genital tract organs contribute virus to semen. Here we investigated the presence of HIV receptors within the human testis using immunohistochemistry and quantitative real-time polymerase chain reaction. We also analyzed the infectivity of a dual tropic HIV-1 strain in an organotypic culture, as well as the impact of viral exposure on testosterone production. Our study establishes that CXCR4+, CCR5+, CD4+, and DC-SIGN+ cells are present within the interstitial tissue of human testis and that these molecules persist throughout our organotypic culture. Our data also reveal that the human testis is permissive to HIV-1 and supports productive infection, leaving testosterone production apparently unaffected. Infected cells appeared to be testicular macrophages located within the interstitial tissue. That the testis itself represents a potential source of virus in semen could play a role in preventing viral eradication from semen because this organ constitutes a pharmacological sanctuary for many current antiretrovirals.

DNA, Viral↗

PubMed1994

Serum cholesterol concentration of mice selected for litter size and its relationship to litter size and testis mass.

This study assessed the genetic relationship between litter size and serum cholesterol concentration and between litter size and testis mass in mice. Mice were from a long-term experiment in which selection had occurred for 21 generations in three replicated lines per criterion of selection (LS = selection to increase litter size based on number born; LC = unselected control). Thereafter, random mating within lines was practiced. Serum cholesterol concentrations were evaluated in female and male mice from two replicates at Generation 29 and one replicate at Generation 30. Body weights and blood samples were collected from primiparous females 8 d after weaning their pups. Data from males were collected as they came out of breeding cages. In addition, the testes were excised, stripped clean of connective tissue and the epididymides, and weighed. Means for body mass of females and males, serum cholesterol, number born, and testis mass were as follows: 35.2 vs 32.5 g (P < .09), 33.9 vs 30.7 g (P < .08), 117.5 vs 110.5 mg/dL (P < .08), 14.0 vs 10.3 pups (P < .04), and 126 vs 122 mg, respectively, for LS and LC. Serum cholesterol was greater in males than in females (133.3 vs 95.1 mg/dL; P < .001), but there was no interaction between sex and selection criterion. Serum cholesterol concentration was not correlated phenotypically to number born or body mass, but it had a small negative relationship with testis mass. Therefore, we concluded that selection for litter size tended to increase serum cholesterol in addition to the increase in number born but did not change testis mass.

Animals↗