Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Testis weight”

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.

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

At least 217 records · Page 12Linked to original sources
PubMed1990

Pachytene pairing and sperm counts in mice with single Robertsonian translocations and monobrachial compounds.

Data on testis weights, sperm counts, and synaptonemal complexes are presented for mice carrying the following Robertsonian translocations: Rb(6.15)lAld; Rb(4.6)2Bnr; Rb(4.15)4Rma; Rb(6.15)lAld/Rb(4.6))2Bnr, which is male-sterile; and Rb(6.15)lAld/Rb(4.15)4Rma, which is male-fertile. In RblAld/Rb2Bnr sperm were absent or sparse, whereas the sperm count in RblAld/Rb4Rma was just over 50% of the parental value. The translocated chromosomes appeared as fully paired bivalents in homozygotes, as trivalents in single heterozygotes, and as quadrivalents in compounds. About 20-40% of trivalents had unsynapsed ends. The proportion of quadrivalents with unsynapsed ends was about 85% in the male-sterile compound, compared with 75% in the male-fertile compound. The proportion of quadrivalents associated with XY was about 70% in both. Testis weights, but not sperm counts, were found to differ in two of three reciprocal crosses. It is concluded that, in addition to pairing failure and autosome/XY association, the effect of translocations on spermatogenesis is affected by other factors, including genetic background, inbreeding, and perhaps environmental factors. It remains to be elucidated whether pairing failure and XY association are primary or secondary effects.

Animals↗
PubMed1983

Studies on seminiferous tubule fluid production in the adult rat: effect of hypophysectomy and treatment with FSH, LH and testosterone.

Seminiferous tubule fluid production in adult rats was studied using the technique of unilateral efferent duct ligation (EDL), the production rate representing the difference in testis weight over the time since ligation. Following EDL, fluid production increases linearly for 6 h and linearly at a slightly slower rate for a further 18 h with a sharp decrease thereafter. No differences in fluid production were noted for rats aged between 90-310 days. Forty-eight hours after hypophysectomy there was a significant fall (26%) in fluid production prior to any significant decrease in testis weight. Fluid production continued to decline with time after hypophysectomy eventually reaching a plateau 16-44 days later at levels approximately 15% of those found in control rats. Treatment of rats hypophysectomized 4 days earlier with ovine FSH for 3 days did not restore fluid production, but treatment with ovine LH, testosterone propionate (TP) or FSH together with TP for a similar duration all restored fluid production to normal. On the other hand, treatment of intact adult rats with ovine LH significantly increased fluid production but the effect of treatment with testosterone alone did not reach significance. The results indicate that in the adult rat, seminiferous tubule fluid production is controlled principally by testosterone secreted by the Leydig cell in response to LH stimulation.

Animals↗
PubMed2005

[Changes of cycle and apoptosis of spermatogenic cells and antioxidant capacity in male rats with diabetes mellitus].

OBJECTIVE: To explore the changes of cycle and apoptosis of spermatogenic cells and antioxidant capacity of the serum and testis in male rats with diabetes mellitus. METHODS: Thirty male rats were divided into two groups, 10 for normal control and 20 for the diabetes group. The rats were injected intraperitoneally with streptozocin (TZ) to develop diabetes, and 12 weeks later, their survival rate and testis weight were recorded. The percentage of G0/G, S and G2/M phases and apoptosis in spermatogenic cells were measured with flow cytometry (FCM). Malondialdehyde (MDA) and nitric oxide (NO) levels, superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and NO synthase (NOS) activities in the serum and testis were measured with thiobarbituric acid reactive substances (TBARs), nitric acid reoxidized enzyme, xanthine oxidative enzyme, 5,5 Dithiobis (2,2 nitrobenzoate) (TNB) and visible light photometer methods, respectively. RESULTS: Twelve weeks after the male rats got diabetes, their survival rate, body weight and testis weight were significantly lower (p < 0.05), and the percentages of G0/G1 phases and apoptotic spermatogenic cells were obviously higher (P < 0.05) than the normal control. At the same time, the percentage of S and G2/M phases spermatogenic cells decreased. So the spermatogenic cells were arrested in G0/G1 phase. In the diabetic rat serum and testis, especially in the testis, MDA levels were distinctly higher and SOD activities were significantly lower than those in the control. Serum GSH-Px activities of the diabetic rats were significantly lower (p < 0.05), while testis GSH-Px activities were significantly higher than those in control group (P < 0.01). NO contents in the serum and testis of the diabetic rats (P < 0.01) increased significantly, particularly the former, while NOS activities in the serum decreased significantly as compared with the control (P < 0.5). CONCLUSION: The increase in testis and serum MDA levels and NO contents and the decrease in the antioxidant enzyme activity of the diabetic rats may be relevant to spermatogenic disorder caused by the increase of G0/G1 phases arrest and spermatogenic cells apoptosis.

Animals↗
PubMed1993

Spermatic cord torsion: loss of spermatogenesis despite return of blood flow.

Previous work in animal models has recapitulated and refined the clinical observation that longer periods of testicular torsion are associated within increased damage to the testis. Minimum times of damage-inducing torsion have not been established, however, nor has it been established to what degree blood flow returns to the testis on examination several hours or days after the torsion repair. Adult male rats were subjected to 0.5-h or 1.0-h 720 degrees torsion and examined for effects on testis weight, histology, and daily sperm production (DSP). None of the parameters examined were affected by 0.5-h, but all were affected by 1.0-h torsion. In a subsequent experiment, adult rats were subjected to unilateral, 1-h, 720 degrees torsion, and bilateral testicular blood flow as measured by radiolabeled microsphere distribution was determined during torsion and 4 h, 24 h, 2 days, 7 days, 15 days, and 30 days after repair of torsion. Ipsilateral testicular blood flow was reduced 94% during torsion. Blood flow was not significantly different from control or contralateral values by 4 or 24 h after repair of torsion. In spite of this return of blood flow, testis weights were significantly reduced by half by 7 days after torsion repair and spermatogenesis was clearly disrupted upon histological examination 30 days after torsion repair. Increasing the time of torsion to 2 or 4 h did not inhibit return of blood flow to the testis as measured 48 h after torsion repair. Unless the testis is infarcted, testicular blood flow in the rat model returns to normal after torsion repair.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2000

The relative biological effectiveness of low doses of 14 MeV neutrons in steady-state murine spermatogenesis as determined by flow cytometry.

The relative biological effectiveness of 14 MeV neutrons in the low-dose range < or =1 Gy has been determined in differentiating and differentiated spermatogonia. Male NMRI mice were exposed to single doses of 2 cGy to 3 Gy of (60)Co gamma rays or neutrons. The ratios of testicular S-phase cells, 4c primary spermatocytes, and elongated spermatids were quantified by DNA flow cytometry 2 to 70 days after irradiation and were found to decrease. Histological samples and testis weight were analyzed in parallel. Doses of 2-5 cGy neutrons and 10-50 cGy gamma rays significantly (P<0.05) decreased the proportions of S-phase cells, spermatocytes and elongated spermatids at 4, 14 and 28 days postirradiation. For S-phase cells, the biphasic shape of the cell survival curves was described with a D(50) of 5 cGy neutrons. The D(50) for (60)Co gamma rays and the relative biological effectiveness could not be determined. The relative biological effectiveness of neutrons at 50% reductions of testis weight, primary spermatocytes, and elongated spermatids were 2.5, 10.0 and 6.1, respectively. This in vivo assay is interesting because of its sensitivity at dose ranges that are relevant for exposures in the environment, the workplace and radiotherapy.

Animals↗
PubMed1992

Central sites mediating reproductive responses to melatonin in juvenile male Siberian hamsters.

Juvenile male Siberian hamsters received infusions of varying doses of melatonin (MEL), or saline vehicle, via microdialysis probes implanted in brain regions which have previously been shown to contain MEL receptors. Daily infusions were 10 h in length and occurred during exposure to constant light on days 22-34 of age. All animals were sacrificed on day 35 and paired testis weights recorded prior to preparation of the brain tissue for histological evaluation of the infusion site. Some animals were also blood-sampled prior to sacrifice for determination of circulating levels of prolactin (PRL). Saline infusions did not have a significant effect upon gonadal maturation, regardless of the infusion site, when compared with unoperated control animals reared under similar photoperiod conditions. In contrast, animals which received infusions of 75 pg MEL into the suprachiasmatic nucleus (SCN), paraventricular nucleus of the thalamus, or nucleus reuniens regions, showed a marked inhibition of gonadal growth. Infusions of this dose of MEL into various other neural regions (e.g. lateral hypothalamus, ventromedial nucleus of the hypothalamus, paraventricular nucleus of the hypothalamus) did not result in decreased testis weights at the time of sacrifice. Daily administration of 20 pg MEL inhibited gonadal maturation and resulted in decreased circulating PRL levels only when infused into the SCN region. For animals receiving the 7.5 pg dose, infusions into the midline thalamic nuclei were not successful in inhibiting testis growth, and infusions in the SCN region had only a marginal effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Genetic injury in hybrid male mice exposed to low doses of 60Co gamma-rays or fission neutrons. I. Response to single doses.

Young adult male B6CF1 mice were exposed to single whole body doses of fission neutrons or 60Co gamma rays. Postspermatogonial dominant lethal injury, incidence of reciprocal chromosome translocations induced in spermatogonia, incidence of abnormal epididymal sperm 4-6 weeks after exposure, and testis weight loss 3-6 weeks after exposure were all measured. Emphasis is on response to neutron doses between 1 and 40 rad, and gamma-ray doses between 22.5 and 145 rad, although more limited data from a 4-fold higher dose range were integrated into the analysis. Significant effects were seen at 1 and 2.5 rad of neutrons consistent with extrapolation from higher doses, with the exception of dominant lethal mutations, which occurred in significant excess of expectation. Dose-response functions were linear or linear-quadratic, depending upon end point, radiation quality, and dose range. For translocation frequencies, the D2 term was negative for neutron and positive for gamma-ray irradiations. RBE values varied with dose and end point. For testis weight loss and abnormal sperm over the full dose range, the RBEs were between 5 and 6. They were between 7 and 9 at lower doses (less than 10 rad) for translocations. RBEs for postimplantation and total dominant lethal rates were 5-6 above 10 rad and 10-14 below 10 rad. The RBEs for preimplant losses were between 15 and 25 above 10 rad and possibly higher below 10 rad, although the data are statistically "noisy". The tentative interpretations of unusual results at lowest doses involve variation in cell sensitivity, cell selection, probability of neutron traversal per cell, variance of magnitude of the energy deposition events, dose rate, and DNA repair.

Animals↗
PubMed1996

Relationship among hormonal treatments, suppression of spermatogenesis, and testicular protection from chemotherapy-induced damage.

To further elucidate the mechanism by which hormonal pretreatment protects the rat testis from damage by procarbazine, we investigated the relationship between the suppression of hormone levels and spermatogenesis and the recovery of spermatogenesis from stem spermatogonia. LBNF1 rats were implanted with capsules containing testosterone or testosterone plus estradiol. After hormone treatment, rats were injected with procarbazine, and recovery of spermatogenesis was assessed. Testosterone (2 cm) plus estradiol (0.5-cm) reduced serum LH levels causing intratesticular testosterone (ITT) to fall to 3% of control levels within 2 weeks, but testis weights and sperm head counts were not appreciably suppressed until 4 weeks. Two weeks' hormone pretreatment, only slightly enhanced spermatogenesis recovery, but 4 weeks markedly increased it. Testosterone (2 cm) alone produced slower suppression of spermatogenesis and less protection from procarbazine than did testosterone plus estradiol implants, despite equivalent suppression of LH and ITT. Long testosterone implants (24-cm) partially maintained ITT at 14% of control despite undetectable LH levels, prevented any decline in sperm counts, and nearly completely abrogated the protective effect of the hormone treatment. Protection appeared to be best correlated with the testis weight reduction by hormone treatment. Thus, recovery of spermatogenesis after chemotherapy is dependent on the degree of suppression of spermatogenesis caused by the reduction of ITT levels at the time of chemotherapy and likely involves cells, such as the Sertoli cells, that are both androgen-responsive and affected by the numbers of germ cells present.

Animals↗
PubMedDate not supplied

Environmental temperature and cryptorchidism: effects on pregnenolone-sulfatase of mice testicular tissue.

This study examined the capacity of abdominal organs, such as the scrotal testis, exposed to environmental temperature to hydrolyze pregnenolone sulfate. The cryptorchid state of exposure to 34 degrees C during 14 days decreased testis weight by 38 and 23%. But the enzymatic activity (nanomoles of free steroid/testis) was significantly higher (p < .05) compared with the control. Moreover, a rise in the environmental temperature combined with cryptorchidism in mice, two conditions that induced testicular damage, has been related to the elaboration of factors capable of modifying, through paracrine mechanism, the androgen biosynthesis. The presence of this factor could lead to an increase in the hydrolysis of pregnenolone sulfate, but as for cryptorchidism or high environmental temperature exposure, when cryptorchid mice were exposed to temperatures of 34 degrees C an apparent synergism of both conditions produced a decrease of 66% in testis weight. It would appear that the steroid sulfatase is predominantly located in the interstitial epithelium. This study suggests that cryptorchidism and hyperthermia damage the tubular epithelium by different mechanisms.

Animals↗
PubMed2001

Correlation between inhibin secretion and damage of seminiferous tubules in a model of experimental autoimmune orchitis.

The aim of the present study was to evaluate inhibin secretion in rats with autoimmune orchitis. As we have previously described, experimental autoimmune orchitis (EAO) induced in rats by active immunization with testis homogenate and adjuvants is characterized by an interstitial mononuclear cell infiltrate and sloughing of the germinal epithelium. At 120 days after the first immunization 60% of the rats exhibited a severe orchitis with large areas of aspermatogenic seminiferous tubules in which only spermatogonia and Sertoli cells with cytoplasmic vacuolization remained attached to the tubular wall. None of the untreated (N) or control (C) rats revealed pathological alterations. Sixty percent decrease in testis weight was observed in rats with EAO compared with N or C groups. A 3-fold increase in serum FSH levels was observed in rats with EAO compared with N or C groups (19.8+/-3.7 vs 5.6+/-0.3 and 5.9+/-0.1 ng/ml respectively). A significant decrease in inhibin B levels was observed in rats with EAO when compared with N or C groups (40+/-4.6 vs 207+/-38.8 and 221.4+/-28.6 pg/ml respectively). An inverse correlation between inhibin B and FSH serum levels and a direct correlation between inhibin B and testis weight were found. Strong expression of the inhibin alpha-subunit in Sertoli cells of untreated and control rats was observed; this subunit was undetectable or poorly detectable in rats with orchitis. Positive staining for the inhibin alpha-subunit was also observed in Leydig cells of all groups studied. In conclusion, using a model of autoimmune orchitis our results show that circulating inhibin B levels and inhibin alpha-subunit expression in Sertoli cell cytoplasm closely correlate with the degree of damage of the germinal epithelium.

Analysis of Variance↗
PubMed1986

Hormonal effects of ketoconazole in vivo in the male rat: mechanism of action.

Ketoconazole, an antifungal agent, has been shown to lower serum testosterone (T) in man. Measurements of circulating precursors of T suggest that ketoconazole may inhibit 17,20-desmolase activity in the testis. To further elucidate its mechanism of action in vivo, we studied its effects on the pituitary-gonadal axis in the male rate. Two groups of normal male Sprague-Dawley rats were treated with either oil or 25 mg ketoconazole in oil by im injection every 8 h for 21 days. Serum ketoconazole concentrations in the rat 2 h after the 25-mg dose were similar to those after oral administration of a much lower (1/33rd) dose to man. Ketoconazole treatment led to 50% suppression of serum T and prostate and seminal vesicle weights. Testis weights were not significantly affected. Intratesticular T concentrations showed a 50% decrease below the control level. Testicular 17 alpha-hydroxylase, 17,20-desmolase, and 17 beta-hydroxysteroid dehydrogenase activities in the ketoconazole-treated animals were significantly decreased in proportion to the decreases in serum and intratesticular T concentrations. Elevations of serum LH and FSH concentrations in the ketoconazole-treated rats were not proportionate to the decline in serum T concentration. Therefore, to exclude an additional inhibitory effect of ketoconazole at the pituitary level, we treated two groups of castrated male Sprague-Dawley rats with the same dose of ketoconazole or oil for 3 days. Serum LH and FSH concentrations were not significantly different in the two groups. In separate experiments, combined treatment of intact rats with GnRH agonist and ketoconazole for 21 days led to lower mean serum T concentrations and accessory organ weights than those achieved with either agent alone. We conclude that ketoconazole inhibits T synthesis, primarily by inhibiting the activity of multiple enzymes in the T biosynthetic pathway and has no direct effect at the pituitary level; ketoconazole metabolism in the rat is considerably different from that in man; and ketoconazole enhances the inhibitory effects of GnRH agonist.

Aldehyde-Lyases↗
PubMed1981

The effects of radiation dose-rate and quality on the induction of dominant lethals in mouse spermatids.

Hybrid male mice were given 3 Gy (300 rad) doses of X- or gamma-irradiation at dose-rates of either 0.6 or 0.002 Gy/min for each radiation. Germ-cells treated as spermatids were tested for dominant lethality. Effects on spermatogonia were evaluated by studying testis-weight, sperm-count and sperm abnormalities. The rate of induction of dominant lethal mutations was 2.1 times as high after acute X-irradiation as after protracted gamma-irradiation. Most of this difference resulted from the change in radiation quality, since the relative effectiveness of X- versus gamma-irradiation was 1.9 at low and 1.6 at high dose rates. For each radiation, however, fewer dominant lethals were induced at low dose-rates than at high (low/high ratios of 0.8 and 0.9 respectively) although differences did not reach a significant level. There were no statistically significant effects of dose rate on testis-weight or sperm-count in the X-ray series, but there were significantly less severe effects on both with protraction of the gamma-irradiation. Evidence for effects of radiation quality on these characters was conflicting. Frequencies of abnormal spermatozoa were markedly increased 7 weeks after irradiation but there were no consistent effects of radiation intensity or quality.

Animals↗
PubMed1990

Evaluation of the effect of experimental cyclosporine toxicity on male reproduction and renal function. Reversal by concomitant human chorionic gonadotropin administration.

Administration of cyclosporine to rats has been shown to impair testicular function, resulting in a decrease in sperm counts and fertility. In order to determine whether or not the deleterious effects of CsA could be reversed by hormonal therapy, mature male Sprague Dawley rats were treated with CsA (40 mg/kg/day, s.c.) alone or in combination with human chorionic gonadotropin (hCG) (5 micrograms/day/r; s.c.) for 14 days. Cyclosporine administration decreased the body weight (290 +/- 5.30 vs. 339 +/- 8.7 g; P less than 0.05) and reproductive organ weights (testis 1.49 +/- 0.42 vs. 1.60 +/- 0.03 g; epididymis 0.41 +/- 0.02 vs. 0.49 +/- 0.002 g; seminal vesicle 0.61 +/- 0.09 vs. 1.60 +/- 0.05 g; prostate 0.28 +/- 0.04 vs. 0.60 +/- 0.06 g; P less than 0.05) testicular sperm counts (5.80 +/- 0.42 vs. 8.49 +/- 0.48 x 10(7)/100 mg tissue; P less than 0.05) and epididymal sperm counts, (28.2 +/- 0.95 vs. 51 51.62 +/- 2.17 x 10(7)/100 mg tissue; P less than 0.05) and fertility (25% vs. 100%). Serum levels of LH were elevated (101.98 +/- 21.48 vs. 25.6 +/- 5.18 ng/ml; P less than 0.05) and testosterone was decreased (0.48 +/- 0.07 vs. 2.06 +/- 0.56 ng/ml; P less than 0.05). The administration of hCG to the CsA-treated rats restored the reproductive organ weights (testis 1.56 +/- 0.043 g; seminal vesicle 1.04 +/- 0.05 g; prostate 0.70 +/- 0.06 g) and sperm counts (testicular 7.88 +/- 1.0 x 10(7)/100 mg tissue; epididymal 59.86 +/- 4.16 x 10(7)/100 mg tissue; P less than 0.05) Serum levels of testosterone (18.63 +/- 4.45 ng/ml) and LH (431.65 +/- 31.41 ng/ml) were significantly elevated, as compared with control and CsA-treated groups (P less than 0.05). All the rats in the gonadotropin-treated group were fertile, as compared with 25% in the CsA-treated group. CsA reduced the kidney weight (1.17 +/- 0.02 vs. 1.27 +/- 0.03 g; P less than 0.05) and increased the levels of serum creatinine (0.97 +/- 0.07 vs. 0.59 +/- 0.03 mg/dl; P less than 0.05): these changes were ameliorated by the administration of hCG (kidney weight 1.35 +/- 0.03 g; creatinine 0.76 +/- 0.09 mg/dl).

Animals↗
PubMed2005

Understanding the role of thyroid hormone in Sertoli cell development: a mechanistic hypothesis.

More than a decade of research has shown that Sertoli cell proliferation is regulated by thyroid hormone. Neonatal hypothyroidism lengthens the period of Sertoli cell proliferation, leading to increases in Sertoli cell number, testis weight, and daily sperm production (DSP) when euthyroidism is re-established. In contrast, the neonatal Sertoli cell proliferative period is shortened under hyperthyroid conditions, but the mechanism by which thyroid hormone is able to negatively regulate Sertoli cell proliferation has been unclear. Recent progress in the understanding of the cell cycle has provided the opportunity to dissect the molecular targets responsible for thyroid-hormone-mediated effects on Sertoli cell proliferation. In this review, we discuss recent results indicating a critical role for the cyclin-dependent kinase inhibitors (CDKI) p27(Kip1) and p21(Cip1) in establishing Sertoli cell number, testis weight, and DSP, and the ability of thyroid hormone to modulate these CDKIs. Based on these recent results, we propose a working hypothesis for the way in which thyroid hormone regulates the withdrawal of the cell cycle by controlling CDKI degradation. Finally, although Sertoli cells have been shown to have two biologically active thyroid hormone receptor (TR) isoforms, TRalpha1 and TRbeta1, experiments with transgenic mice lacking TRalpha or TRbeta illustrate that only one TR mediates thyroid hormone effects in neonatal Sertoli cells. Although significant gaps in our knowledge still remain, advances have been made toward appreciation of the molecular sequence of events that occur when thyroid hormone stimulates Sertoli cell maturation.

Animals↗
PubMedDate not supplied

Impaired germ cell development in the testes of immature rats with neonatal hypothyroidism.

The induction of neonatal hypothyroidism from day 1 to day 25 postpartum using 6-propyl-2-thiouracil (PTU) resulted in a 45% and 77% reduction of testis weight on days 20 and 30, respectively, and an increase in Sertoli cell number. The present study evaluated the effect of neonatal hypothyroidism on the developing germ cell population during the first 30 days postnatally. Qualitative and quantitative studies using the optical disector method were undertaken on the testes of control and hypothyroid rats, on days 10, 20, and 30 after birth. Germ cell development was obviously impaired in the hypothyroid rats, as shown by decreased primary spermatocyte and round spermatid numbers in day 20 and day 30 testes, and the persistence of gonocytes on days 10 and 20. These reductions obviously accounted for the reduced testis weight, absolute volume, and diameter of the seminiferous cords/tubules, especially on days 20 and 30. The failure to establish a seminiferous tubule lumen in hypothyroid rats probably reflects decreased fluid production and a functional immaturity of the Sertoli cells. The delay in germ cell maturation and increased degeneration may be because of the immature state of the Sertoli cell or result from the low follicle-stimulating hormone and thyroxine levels known to occur in the hypothyroid rats.

Aging↗
PubMed1998

Testicular cycles in three species of Korean frogs: Rana nigromaculata, Rana rugosa, and Rana dybowskii.

Seasonal changes in testicular structure and function in three species of Korean frogs (Rana nigromaculata, R. rugosa, and R. dybowskii) having different breeding seasons and habitats were examined throughout the year. R. nigromaculata live in rice fields and breed in early May. Their gonadosomatic index (GSI) and testis weight decreased slightly from May until July, but increased markedly from August to high levels through December. The diameter (cross-sectional area) of seminiferous tubules changed little from January until August, increased sharply from September through October, and decreased thereafter. In seminiferous tubules, the number of primary spermatogonia (I SPG) was low from January-March, increased from April to maximum levels by May-June, and decreased subsequently. The number of spermatids (SPT) was highest from November to March, decreased to nondetectable levels in May, and increased markedly from September to November. Spermiation was most active during March and April. R. rugosa, which live in streams and breed during May-June, exhibited no changes in GSI, testis weight, or seminiferous tubule size throughout the year. The number of I SPG was high during May-August and that of secondary spermatogonia (II SPG) was highest in August. The number of SPT increased to high levels in November-December. Active spermiation occurred from January to April in this frog. In R. dybowskii, which live in the mountains and breed from late February to early March, the number of I SPG gradually increased from April through August; however, essentially no other spermatogenic cells were observed from January to July. A marked increase in early spermatogenic cells appeared during August-September and was followed by an increase in SPT from November to December. From December to March the number of spermatozoa increased and spermiation occurred. In general, testicular testosterone levels were high in the winter and low in summer in all three species, and positively correlated with the number of interstitial cells and the size of their nucleus.

Analysis of Variance↗
PubMed1986

Pituitary gonadal function in adult male rats subjected to crowding.

The effect of crowding on the pituitary-gonadal axis was studied in adult male rats. Crowding reduced body weight gain, did not alter relative adrenal weight and increased relative testis weight. Neither basal levels of corticosterone nor its response to acute stress were altered by crowding. Likewise, LH secretion was similar in control and crowded rats. Prolactin levels tended to be lower in crowded than control rats, but they did not reach statistical significance. In contrast, impaired testosterone secretion was observed in crowded rats, at least in part due to reduced Leydig cell responsiveness to gonadotropin release. In addition, some mechanisms other than pituitary-adrenal hyperactivity might be responsible for reduced testosterone secretion during crowding.

Adrenal Glands↗
PubMed1986

Genetic toxicology of phthalate esters: mutagenic and other genotoxic effects.

The effects of DEHP on sperm morphology and on peripheral blood micronuclei were studied for 12 weeks following five subacute IP injections of DEHP at 1/6, 1/12, and 1/60 of the LD50 per day. Sperm morphology was examined in both adult mice and rats, while peripheral blood micronuclei were scored in mice up to 4 weeks after treatment. In mice, DEHP at 1/6 LD50 significantly depressed body weight gain for up to 12 weeks after treatment, and reduced epididymal sperm number by 4 weeks. Numbers of morphologically abnormal sperm did not differ from controls in the 12 weeks following treatment. In addition, DEHP did not increase the numbers of peripheral blood micronuclei. Studies in the rat indicated that exposure to doses of 1/6 and 1/12 of the LD50 per day of DEHP resulted in a reduced gain in body weight compared to controls. Testis weight, sperm number, and numbers of morphologically abnormal sperm were unaffected by DEHP following treatment. In separate experiments, DEHP did not induce sister chromatid exchange (SCE) or DNA damage in Chinese hamster ovary (CHO) cells. Although DEHP is known to cause testicular atrophy in rats and to a lesser extent in mice, it did not cause an increase in abnormal sperm in either species. Together with the CHO and micronucleus data, these findings suggest that DEHP has a low probability of causing genetic damage capable of being transmitted through the male germ line.

Animals↗