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PubMed2006

Reducing estrogen synthesis in developing boars increases testis size and total sperm production.

The abundant production of testicular estrogens and the presence of both ESR1 and ESR2 within boar testes are consistent with a role for estrogen in testicular development and/or function in this species. This study was aimed at determining the role of endogenous estrogen in the regulation of testicular development and function, including the effects on testis weight, histology, sperm production (detergent-resistant spermatid numbers), Sertoli cell numbers, and Leydig cell volume in the boar. Twenty-eight littermate pairs of boars were assigned to groups as follows: 1 boar from each pair was assigned to the control group (vehicle) and the other was assigned to treatment and received 0.1 mg/kg body weight of an aromatase enzyme inhibitor (letrozole) orally each week beginning at 1 week of age until castration at 2, 3, 4, 5, 6, 7, or 8 months of age. Testes were weighed and testicular parenchyma was recovered for determination of histology and detergent-resistant spermatid numbers, and for determination of Sertoli cell number and Leydig cell volume by staining for GATA-4 and 17-alpha hydroxylase/17-20 lyase respectively. Testes of aromatase-inhibited boars initially exhibited delayed lumen formation, lower testicular weight, fewer detergent-resistant spermatids, and fewer Sertoli cells, but by 7 to 8 months, these boars had recovered and had larger testes, more detergent-resistant spermatids per testis, and more Sertoli cells. Total Leydig cell volume increased in proportion to testis size. Reducing endogenous estrogen is consistent with a delay in testicular maturation/puberty that allows for a longer window for the proliferation of Sertoli cells and maturation of Leydig cells, resulting in larger testes and higher spermatid production.

Animals↗
PubMedDate not supplied

In vivo model for chronic direct intratesticular drug administration.

The efficacy and toxicity of a new method for chronic direct intratesticular drug infusion were assessed in a rat model. To this end, luteinizing hormone (LH) or buffer was infused via miniosmotic pumps for 14 days directly into the parenchyma of Copenhagen rat testes. The surgical manipulation and direct infusion of buffer did not have any apparent adverse effect upon either spermatogenesis or steroidogenesis as measured by testis weight, homogenization-resistant spermatid count, and in vitro response of the testes to a maximally stimulating concentration of LH. Histologic studies revealed only a localized inflammatory response in the testis around the Silastic tubing leading from the mini-osmotic pump to the testis. The biologic efficacy of direct infusion into the testis was assessed by determining the ability of mini-osmotic pump-infused LH to maintain steroidogenesis for 14 days in animals whose pituitary function was suppressed by simultaneous subcutaneous placement of testosterone/estradiol capsules. Steroidogenesis was found to be maintained quantitatively in testes infused with an appropriate dose of LH. At a given LH dose, the directly infused testes were found to produce fivefold more testosterone than contralateral testes and 10-fold more testosterone than testes from rats receiving systemic administration of the same dose of LH. We conclude that the miniosmotic pump system is a useful means to chronically administer a high concentration of LH, and presumably other agents, to the testis without any significant adverse effects.

Animals↗
PubMed2001

Lupron depot prevention of antispermatogenic/antifertility activity of the indenopyridine, CDB-4022, in the rat.

The goals of this study were to determine the CDB-4022 dose-response relationship for induction of acute decreases in testicular weight and germ cell depopulation in rats; establish the threshold dose of CDB-4022 required to induce infertility; and investigate whether CDB-4022-induced testicular damage could be prevented by a GnRH agonist (Lupron Depot). Reduction of testis weight and germ cell depopulation were observed 7 days after a single oral dose of 1 mg CDB-4022/kg, whereas 0.5 mg/kg had no observable effect. These effects were maximal at 12.5 or 25 mg CDB-4022/kg. After a single oral dose of either 2.5 or 5 mg/kg, CDB-4022 induced infertility in five of five treated rats by Week 5, whereas only one of five males was rendered infertile at a dose of 1 mg/kg. Proven fertile male rats (6/group) were treated with vehicle, CDB-4022 alone (2.5 mg/kg on Day 0), CDB-4022 plus Lupron Depot (on Weeks -1, 2, 5, and 8), or Lupron Depot alone. Control males demonstrated normal fertility throughout a 32-wk cohabitation period. Five of six rats were rendered transiently infertile with Lupron Depot alone, but all recovered fertility. CDB-4022 treatment resulted in infertility in all six rats, and only one of six regained fertility. Combined treatment also caused infertility in all six rats, but four of six recovered fertility (P = 0.08 compared to CDB-4022 alone). Testicular weight was decreased in the three treatment groups compared to vehicle controls; testicular weights were ranked from highest to lowest as follows: vehicle > Lupron Depot > Lupron Depot + CDB-4022 > CDB-4022. The tubule differentiation index of Lupron Depot-treated rats (96 +/- 4%) was not different from vehicle-treated rats (100%). CDB-4022 treatment decreased the number of differentiating tubules (15 +/- 8%). Lupron Depot plus CDB-4022 treatment resulted in a greater number of differentiating tubules (53 +/- 12%) than CDB-4022 alone, but this was still lower than vehicle- or Lupron Depot-treated rats. These data indicate that 2.5 mg/kg of CDB-4022 was the oral threshold dose that caused testicular damage rendering the majority of adult male rats permanently infertile within the study interval; 12.5 mg/kg of CDB-4022 induced maximal testicular damage. Suppression of gonadotropins and/or testosterone production by treatment with Lupron Depot before and after CDB-4022 prevented the CDB-4022-induced irreversible testicular damage.

Animals↗
PubMed1978

Testosterone and 5alpha-dihydrotestosterone inhibit both growth and spermatogenesis in the remaining testis in partially castrated adult newts, Notophthalmus viridescens.

The testis of the newt, Notophthalmus viridescens, undergoes hypertrophy following partial castration. Injections of either testosterone or 5alpha-dihydrotestosterone are equally effective in inhibiting the increase in testis weight which follows partial castration. In addition, both of these androgens inhibit spermatogenesis, i.e., spermatogonia appear to be inhibited resulting in early cessation of spermatogenesis and a precocious division of the testis into separate spermatogonia and sperm compartments.

Animals↗
PubMed1998

Testing the gonadal regression-cytoprotection hypothesis.

Germinal damage is an almost universal accompaniment of cancer treatment as the result of bystander damage to the testis from cytotoxic drugs and/or irradiation. Cancer treatment for the most common cancers of the reproductive age group in men has improved such that most are now treated with curative intent, and many others are treated with likelihood of prolonged survival, so that the preservation of fertility is an important component of posttreatment quality of life. This has led to the consideration of developing adjuvant treatments that may reduce the gonadal toxicity of cancer therapy. One dominant hypothesis has been based on the supposition that the immature testis was resistant to cytotoxin damage. Hence, if hormonal treatment were able to cause spermatogenic regression to an immature state via an effective withdrawal of gonadotrophin secretion, the testis might be maintained temporarily in a protected state during cytotoxin exposure. However, clinical studies have been disappointing but have also been unable to test the hypothesis definitively thus far, due to the inability to completely suppress gonadotrophin secretion. Similarly, experimental models have also given conflicting results and, at best, a modest cytoprotection. To definitively test this hypothesis experimentally, we used the fact that the functionally hpg mouse has complete gonadotrophin deficiency but can undergo the induction of full spermatogenesis by testosterone. Thus, if complete gonadotrophin deficiency were an advantage during cytotoxin exposure, then the hpg mouse should exhibit some degree of germinal protection against cytotoxin-induced damage. We therefore administered three different cytotoxins (200 mg/kg procarbazine, 9 mg/kg doxorubicin, 8 Gy of X irradiation) to produce a range of severity in testicular damage and mechanism of action to either phenotypically normal or hpg mice. Testis weight and homogenization-resistant spermatid numbers were measured to evaluate the potential protective effects on spermatogenesis. Although the three cytotoxins produced a range of severity of spermatogenic damage, there was no evidence of cytoprotection in the hpg mice that were completely gonadotrophin deficient at the time of treatment. These findings cast doubt on the validity of the hypothesis that spermatogenic regression via gonadotrophin withdrawal can protect the mouse testis against cytotoxin-mediated spermatogenic damage.

Animals↗
PubMed1990

Gonadotoxic effects of 2-hexanone and 1,2-dibromo-3-chloropropane on the enzymatic activity of rat testicular 17 alpha-hydroxylase/C17,20-lyase.

In this study the gonadotoxic effects of 2-hexanone administered as a pretreatment and/or 1,2-dibromo-3-chloropropane administered as a challenge on the activity of several key steroidogenic enzymes in the rat testis were examined. Despite the absence of an effect when either treatment was administered individually, the pretreatment/challenge combination inhibited the steroidogenic capacity of the rat testis. The specific activity of testicular 17 alpha-hydroxylase was significantly reduced (P less than 0.05), with respect to the control, following the pretreatment/challenge combination. There were no significant differences between the control and the individual treatments. The inhibition of 17 alpha-hydroxylase activity occurred in the absence of significant differences in testis weight and testicular protein content. This inhibition of testicular steroidogenic enzyme activity was specific as the activity of another testicular enzyme, namely C17,20-lyase, was not affected by any treatment. The decline in rat testicular 17 alpha-hydroxylase activity 18 h after the 1,2-dibromo-3-chloropropane challenge precedes the reported alterations in the seminiferous epithelium following this same treatment. The results of the present study indicate that the steroidogenic cell of the testis, i.e. the Leydig cell, is a potential site for the primary toxic effects of these agents in the rat testis.

Animals↗
PubMed1988

A comparison of the effects of the three isomers of dinitrobenzene on the testis in the rat.

Sexually mature Alpk/AP (Wistar derived) rats were killed 5 days after a single oral dose of 50 mg/kg of the 1,2-, 1,3-, or 1,4-isomers of dinitrobenzene. Testis weight reductions accompanied by testicular lesions were observed in the animals dosed with 1,3-dinitrobenzene (1,3-DNB) while the 1,2- and 1,4-isomers were without effect on the testis. However, 1,4-dinitrobenzene, but not 1,2-dinitrobenzene, was of a potency similar to that of 1,3-DNB in producing cyanosis and splenic enlargement in these animals, indicating that different mechanisms are probably responsible for these two toxic effects. In a subsequent study the pathogenesis of the testicular damage resulting from a single oral dose of 5, 10, 15, or 25 mg 1,3-DNB/kg was studied in sexually mature rats. Animals were killed 6, 12, 24, 48, and 96 hr after dosing and a detailed histopathological examination of the testes and selected tissues was made. At 12 hr after a single oral dose of 25 mg/kg, 1,3-DNB produced testicular lesions limited to Stages VIII to XI of the spermatogenic cycle. By 24 hr widespread Sertoli cell damage was evident and in some tubules was associated with degeneration of primary spermatocytes. Ultrastructural examination at this time confirmed that there were effects on Sertoli cells in the absence of germ cell damage. Similar effects were seen 48 hr after a single oral dose of 15 mg 1,3-DNB/kg. Doses of 5 or 10 mg 1,3-DNB/kg were without effect on the testis. The Sertoli cell is implicated as the prime target for the toxic action of 1,3-DNB with germ cell damage a secondary event.

Administration, Oral↗
PubMed1999

Long-term irradiation of a marine fish, the plaice Pleuronectes platessa: an assessment of the effects on size and composition of the testes and of possible genotoxic changes in peripheral erythrocytes.

PURPOSE: Previous investigation showed the very significant effects of chronic gamma-radiation on plaice testes at mean absorbed dose rates as low as 1.3 mGy h(-1) given over a period of 168 days (accumulated dose 4.7 Gy). The present paper examines the effects on the testes of exposure to even lower dose rates of gamma-radiation given over periods of 73 days or 197 days. In addition, the use of micronucleus counts and flow-cytometric measurement of nuclear DNA content in samples of peripheral blood for monitoring genotoxic effects has been assessed. MATERIALS AND METHODS: In Experiment 1, adult male plaice were exposed at mean absorbed dose rates of 0.25, 0.5 or 1.2 mGy h(-1) for 73 days (mean accumulated doses of 0.43, 0.85 and 2.03 Gy, respectively) and in Experiment 2 to 0.24, 0.5 or 1.0 mGy h(-1) for 197 days (mean accumulated doses of 1.07, 2.24 and 4.57 Gy, respectively). At termination the testes were removed, weighed and sections were prepared and examined histometrically. In addition, in Experiment 2, blood samples were taken during exposure and at termination. Blood smears were scored for micronuclei and samples processed and examined for nuclear DNA content by flow cytometry. RESULTS: Significant reductions in testis weight were seen in all radiation groups after 197 days of exposure, which were predominantly due to decreased amounts of sperm. In plaice killed after 73 days (at an earlier stage of spermatogenesis), there were no significant differences in weight compared with controls but amounts of spermatogonia were significantly reduced in irradiated fish. CONCLUSIONS: Exposure to dose rates as low as 0.24 mGy h(-1) of gamma-radiation given over a period of 197 days significantly reduced the weights of plaice testes, this being consequent on reductions in the amounts of sperm. Although there was some evidence of radiation affecting the numbers of spermatogonia it was not possible to determine the primary target for radiation damage which eventually caused the sperm reductions. Along with the related work described by Greenwood and Knowles (1996) this is the first investigation of a marine fish and it indicates that plaice testes are probably more radiosensitive than those previously described in tropical fish and of a similar radiosensitivity to mammalian testes. Although significant effects were observed after the lowest dose rate used of 0.24 mGy h(-1), this is still a factor of about 400 times greater than the estimated absorbed dose rate to plaice testes in the north-east Irish Sea off Sellafield at the present time. Micronucleus counts and flow-cytometric analysis of blood DNA both failed to show any evidence of genotoxic damage.

Animals↗
PubMedDate not supplied

Studies on a long-term use of rapeseed products in diets for boars. Pathomorphological changes in the reproductive system, liver and thyroid gland.

Three feeding groups were used: the control (SOY) was fed diets without rapeseed products, and the two experimental groups were fed with either 10% rapeseed meal (RSM) or with 12% OO rape seeds (PFRS). Half of the boars from each group were slaughtered after 1 or 2 years. In RSM and PFRS boars steroid-3-beta-ol-dehydrogenase activity was high, whilst Leydig cells were not numerous after 1 year. Degeneration and necrosis of seminiferous epithelium resulting in atrophy of seminiferous tubules appeared in RSM boars after 2 years. In the PFRS group the lesions were stronger and proliferation of Leydig cells with high steroid-3-beta-ol-dehydrogenase activity was observed. In 1-year-old RSM and PFRS boars there were foci of necrosis in the epididymal epithelium. Thyroid weight in RSM boars and liver weight in PFRS boars were distinctly higher only during the first year. In these thyroid glands flattening of glandular epithelium and enlargement of colloid masses were observed, while in the livers, parenchymatic degeneration and structural transformation appeared. Testis weight increased after 2 years in RSM and PFRS boars; however, this had little effect on semen production.

Animal Nutritional Physiological Phenomena↗
PubMed1991

Effects of in utero ultrasound exposure on the development of the fetal mouse testis.

The effect on the developing fetal testis of in utero exposure to 1-MHz, continuous-wave ultrasound in the spatial peak, temporal average intensity range 0.5-10 W/cm2 for durations of 400-30 sec on Day 9, 12, or 15 of gestation was determined. Results show that two subtle, yet potentially deleterious, effects occurred: a reduction in the Sertoli cell population and an apparent delay in the cessation of gonocyte mitosis. An increase was also seen in the number of fetal resorptions and stillborn pups per number of implantation sites in the exposed specimens as compared to the sham and cage controls. Because the reduction in testis weight was proportional to decreased body weight and because there was no difference in Sertoli cell numbers due to day of treatment, the testicular effects may reflect a generalized delay in growth. Whether this effect of ultrasound on fetal testis will be translated into an equal reduction in germ cell numbers in the adult testis remains to be determined.

Animals↗
PubMed1982

Arterialization of the liver prevents testicular atrophy in portacaval shunted rats.

Portacaval anastomosis in male is known to induce testicular atrophy. The effect of liver revascularization by the right renal artery on the testes of portacaval shunted rats was examined. After shunting, there was a 75% decrease in testis weight compared to the control value and spermatogenesis was blocked in steps 8-9 of spermiogenesis. The in vitro binding of [125I]hCG was only 10% of the control value on a per testis basis and labelled areas in the interstitium of frozen sections subjected to topical autoradiography with [125I]hCG were also strikingly reduced. These parameters were maintained to normality in revascularized shunted rats which displayed also normal copulatory and fertilizing abilities. It is suggested that an adequate blood supply to the liver, as provided by arterialization, can preserve testicular integrity in shunted rats, even though the blood is arterial instead of portal.

Animals↗
PubMedDate not supplied

[Corticosterone and testosterone in the blood of adult rats: the effects of low doses and the times of the action of ionizing radiation during intrauterine development].

Corticosterone levels in the blood and adrenal weights in adult rat males were increased after low-dose gamma irradiation during the last third of their intrauterine development; an increase of the dose decreased them. Decrease in testosterone levels and testis weights were dose-dependent. External and internal irradiation of females on the 11-14 days of pregnancy inhibited adrenals and increased testosterone levels and seminal vesicles weights in offspring. The changes of hormonal balance in adult animals depend on dose and period of ionizing irradiation during intrauterine development.

Animals↗
PubMed2004

Effects of neonatal oxytocin manipulations on male reproductive potential in prairie voles.

Oxytocin (OT) modulates adult mammalian sexual behavior, sperm production and transport, and steroidogenesis; however, the consequences of developmental manipulations of oxytocin have received little attention. The purpose of this experiment was to determine whether neonatal exposure to OT, an oxytocin antagonist (OTA), saline (SAL), or handling (HAN)-only would have long-term effects on reproductive potential in male prairie voles (Microtus ochrogaster). Adult males were observed for 24 h with a sexually receptive female and sexual behavior was recorded. Females were subsequently lavaged and smears were examined for sperm. Reproductive parameters including motility of epididymal sperm, testis weight, and plasma androgen levels were in the normal range. OT-treated males that did not mate within the first 30 min did not mate at all, and in comparison to controls, a higher proportion of those OT-treated and OTA-treated males that did mate did not transfer sperm to the females. OTA-treated males also had significantly higher testicular sperm concentrations than HAN-only males, and significantly lower epididymal sperm concentrations. These differences suggest that in males, developmental manipulations of OT may have the potential to influence the subsequent expression of sexual behavior and sperm transport.

Androgens↗
PubMed1990

[Usefulness of male golden hamsters for experimental reproductive pathology].

Seventy two male Golden hamsters were maintained in normal laboratory conditions (12h light-dark cycle, 20 +/- 2 degrees C) for the annual cycle experiment. Every month 6 animals were sacrificed and testis weight, cauda epididymis weight, caudal sperm number, sperm morphology and body weight were determined. The period of high gonadal activity was found to be from March to the end of July. In September reproductive activity decreased and the low activity period, with azoospermia in some animals, lasted till the end of January. This annual reproductive cycle, shown for the male Golden hamsters, should be taken into consideration when designing new experiments and interpreting their results.

Animals↗
PubMed1982

Morphometric studies of compensatory testicular hypertrophy in the rat after hemicastration.

The quantitative nature of the compensatory testicular hypertrophy following unilateral castration was examined in groups of immature Wistar-derived male rats hemicastrated at 10, 20, 30, 40 and 50 days of age and completely castrated 20 days later. Hemicastration resulted in compensatory hypertrophy of the remaining testis and it decreased as the animals aged. In 30-day-old rats compensatory testicular hypertrophy was 33% while at 70 days of age hypertrophy was reduced to 2%. The increase in testis weight of hemicastrated rats was correlated with an increase in total seminiferous tubule length and a larger cross-sectional area which was due in part to the greater number of germ cells per testis. Sertoli cell number did not increase significantly in the hemicastrated testis but more germ cells were associated with each Sertoli cell.

Aging↗
PubMed1995

Identification and quantification of fluorine-containing metabolites of 1-chloro-2,2,2-trifluoroethane (HCFC133A) in the rat by 19F-NMR spectroscopy.

1-Chloro-2,2,2-trifluorethane (HCFC133a) causes a reduction in testis weight and germinal epithelial cell atrophy in the rat following exposure by inhalation at concentrations of 10,000 ppm and above. Following administration by gavage, an increased incidence of Leydig cell tumors of the testis was seen. The metabolism of HCFC133a has been investigated in respect to the known toxicity of this compound. Male rats were exposed by inhalation to an atmosphere of 50,000 ppm HCFC133a for a period of 6 hr. Analysis of urine, collected during the exposure period and up to 48 hr following exposure, by 19F-NMR spectroscopy identified 2,2,2-trifluoroethanol (TFE; and its beta-glucuronide), trifluoroacetaldehyde (TFAA; as its hydrate and urea adduct), and trifluoroacetic acid (TFA) as fluorine-containing metabolites of HCFC133a. Of the total amount of metabolite eliminated in urine, 83% was excreted within 24 hr postdose, establishing a rapid elimination of metabolites by this route. TFAA, an established testicular toxicant, was the major metabolite accounting for 57% of the total fluorinated metabolites eliminated in urine, whereas TFA and TFE accounted for 29% and 14%, respectively. The presence of these metabolites in urine is consistent with an oxidative route of metabolism of this fluorocarbon.

Animals↗
PubMed1980

Effect of immunization of male rabbits against androstenedione.

After active immunization of male rabbits against androstenedione and with increasing antibody titre the concentration of androstenedione and testosterone in peripheral blood increased more than 1000-fold resp. 20-fold above values of control animals. On histological examination of the testes a marked Leydig's cell hyperplasia was found, though there was no difference in testis weight.

Androstenedione↗
PubMed1987

On unilateral testicular and epididymal torsion: no effect on the contralateral testis.

It is often stated that unilateral testicular torsion results in damage to the contralateral testis; however, there are a growing number of experimental and clinical papers which suggest this is not so. Conflicting results from experimental studies confuse the issue and may be due, among other things, to some specifics of the experimental model. In the present paper, we have examined bilateral rat testes 30 and 60 days after 720 degrees torsion to determine 1) the effect of unilateral testicular torsion with and without the inclusion of epididymal torsion, 2) the effect of relatively chronic torsion (24 hr., 10 day) versus relatively acute torsion (two hr., four hr.), and 3) the effect of establishing the model using scrotal surgery versus using an abdominal approach. Bilateral testicular histology, testis wt. (gm.), cauda epididymal sperm concentrations (sp./ml.), and cauda sperm motility scores (0-4) were examined. Ipsilateral testicular torsion or testicular plus epididymal torsion of two hr. or four hr. duration significantly reduced (p less than .05) ipsilateral testis weights, sperm concentrations, and motility scores, and disrupted normal tissue histology. Contralateral testicles were not altered. Epididymal ischemia alone produced no significant ipsilateral or contralateral effects. Chronic torsion (one day, 10 days) also destroyed ipsilateral testis function without altering the contralateral testicles. The occult cryptorchidism associated with the scrotal approach to establishing the torsion model had no effect on contralateral testicles. In no group, using either Lewis rats or Sprague-Dawley rats, were contralateral testicles altered by unilateral testicular torsion. These results plus recent clinical reports indicate that contralateral testicular damage due to ipsilateral torsion is hardly a proven phenomenon, let alone a significant factor contributing to male infertility.

Animals↗