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PubMed1993

The effects of prenatal administration of azo dyes on testicular development in the mouse: a structure activity profile of dyes derived from benzidine, dimethylbenzidine, or dimethoxybenzidine.

In mice and rats, prenatal exposure to the dye Congo red permanently reduces the number of germ cells in male and female offspring. In the current investigation, nine other dyes structurally related to Congo red were examined for developmental testicular toxicity. In this study, the structural component of the dyes responsible for the prenatal induction of germ cell aplasia was identified. We found that only benzidine-based dyes altered testicular development and caused hypospermatogenesis in mice during adulthood. Dimethyl- and dimethoxybenzidine-based dyes were without effect. Pregnant mice were dosed orally on Days 8-12 of gestation with a benzidine-, dimethylbenzidine-, or a dimethoxybenzidine-based dye and the testes of 45- to 50-day-old male offspring were examined. The testes of postpubertal male offspring exposed to the benzidine-based dyes, Congo red, diamine blue, and Chlorazol Black E, were small and contained some tubules completely devoid of germ cells, but the dimethylbenzidine-based dyes, trypan blue, Evans blue, and benzopurpurin 4B, and the dimethoxybenzidine-based dye, Chicago sky blue, did not alter testicular development in this manner. Azoic diazo component 48, a dimethoxybenzidine congener, and two other diazo dyes, naphthol blue black and Sudan III, were also without effect on the germ cells. Experiments with Chlorazol Black E (CBE) indicate that the period of susceptibility in the male fetus is limited to the period of primordial germ cell migration and division. When CBE was administered on Days 8-10 of gestation it reduced testis weight after puberty by 30%, while treatment after Day 13 did not affect testicular function.(ABSTRACT TRUNCATED AT 250 WORDS)

Abnormalities, Drug-Induced↗
PubMed2005

Morphometric studies on the testis of Korean ring-necked pheasant (Phasianus colchicus karpowi) during the breeding and non-breeding seasons.

The purpose of this study was to obtain detailed quantitative information on all cell types in the testis interstitium of Korean ring-necked pheasants and to combine these data with changes in the steroidogenic function of the testis during the breeding and non-breeding seasons. For animals collected during the breeding season, their testis weights, sperm production, serum testosterone levels and leuteinizing hormone (LH)-stimulated testosterone secretion were significantly (p < 0.01) increased compared to the non-breeding season. Testes of the pheasants during the non-breeding season displayed a 98% reduction in testis volume that was associated with a decrease in the absolute volume of seminiferous tubules (98% reduction), tubular lumen (100%), interstitium (90%), blood vessels (84%), lymphatic spaces (97%), Leydig cells (79%), mesenchymal cells (51%) and myoid cells (61%) compared to the breeding season. The numbers of Leydig cells, mesenchymal cells and myoid cells per testis in the breeding season were much higher than in the non-breeding season. Although the mean volume of a Leydig cell was 74% lower in the non-breeding season, the mean volumes of myoid and mesenchymal cells remained unchanged. These results demonstrate that there are striking differences in the testicular structure of the Korean ring-necked pheasant during the breeding and non-breeding seasons. Every structural parameter of the Leydig cell was positively correlated with both testosterone serum levels and LH-stimulated testosterone secretion. The correlation of changes in hormonal status with the morphometric alterations of Leydig cells suggests that the Korean-ring necked pheasant may be used as a model to study structure-function relationships in the avian testis.

Animals↗
PubMed1993

Hydroxyurea exposure alters mouse testicular kinetics and sperm chromatin structure.

The effects of hydroxyurea (HU) on testicular cell kinetics and sperm chromatin differentiation were investigated in mice. Whole testis, minced testicular cell suspensions and caudal epididymal sperm cells were obtained at 8 and 29 days after i.p. injections containing 0, 25, 50, 100, 200, 400 and 500 mg/kg HU x 5 days. Testis weights were unaffected by 25 mg/kg HU while 500 mg/kg caused up to a 50% loss of testicular weight by 29 days. Flow cytometrically measured acridine-orange (AO) stained testicular cells revealed altered population ratios at the highest dosages at 8 days and for all dosages except 25 mg/kg HU at 29 days. At 8 days, 400-500 mg/kg HU caused a near depletion of tetraploid cells. Flow cytometry of AO stained sperm, previously treated with acid to potentially induce DNA denaturation, was used to follow the shift from normal chromatin structure to an abnormal form with increased sensitivity to DNA denaturation in situ. The extent of DNA denaturation was quantitated for each cell by the computer-derived value alpha t, alpha t = [red/(red+green) fluorescence]. The flow cytometry measures, standard deviation of alpha t (SD alpha t), mean of alpha t (X alpha t) and cells outside the main peak of alpha t (COMP alpha t), gave similar dose response curves to the sperm head morphology assay. SD alpha t was more sensitive than the X alpha t as a measure of HU-induced alteration of chromatin structure. The major conclusions reached are that HU inhibits DNA synthesis, probably by inhibiting ribonucleotide reductase, causing maturation depletion of pachytene spermatocytes and, subsequently, depletion of meiotic daughter cells and differentiated cell types leading to mature sperm. This inhibition of DNA synthesis is related to an alteration of sperm chromatin structure and abnormal sperm head morphology.

Animals↗
PubMed2004

Effects of 60 Hz electromagnetic field exposure on testicular germ cell apoptosis in mice.

AIM: To evaluate the effects of 60 Hz extremely low frequency (ELF) elelctromagnetic field (EMF) exposure on germ cell apoptosis in the testis of mice. METHODS: Adult male BALB/c mice (7 weeks of age) were exposed to a 60 Hz EMF of 0.1 mT or 0.5 mT for 24 h/day. A sham-exposed group served as the control. After 8 weeks of exposure, the mice were sacrificed. Germ cell apoptosis in the testis was assessed by histopathological examination, the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay (TUNEL) and flow cytometric examination of isolated spermatogenic cells stained with 7 aminoactinomycin D (7-AAD). RESULTS: EMF exposure did not significantly affect the body and testis weights, but significantly increased the incidence of germ cell death. The distinguishing morphological feature of EMF exposure was a decrement in the number of well organized seminiferous tubules. Quantitative analysis of TUNEL-positive germ cells showed a significantly higher apoptotic rate in the 0.5 mT exposed mice than that in the sham controls (P<0.05), while the difference between the two exposed groups was insignificant. The TUNEL-positive cells were mainly spermatogonia. In flow cytometry analysis, the percentage of live cells [forward scatter count (FSC)(high)7-AAD(-)] was lower in the exposed groups than that in the controls (Figure 5A), but the decrease in viability was not statistically significant. CONCLUSION: Continuous exposure to ELF EMF may induce testicular germ cell apoptosis in mice.

Animals↗
PubMed2001

Diethylstilbestrol-treated adult rats with altered epididymal sperm numbers and sperm motility parameters, but without alterations in sperm production and sperm morphology.

In this study, we characterized estrogenic effects of diethylstilbestrol (DES) on reproductive parameters in male rats to identify a minimal dose level that alters epididymal and sperm functions but has little or no effect on sperm production and/or spermatogenesis. Adult rats (five animals/group) received s.c. injections of 0.2 ml of corn oil containing DES at a rate of 1.0 mg, 200 microg, 40 microg, 8 microg, 1.6 microg, or 320 ng x rat(-1) x day(-1) for 12 days. The control group received corn oil only. DES effects were similar in the 8-microg group and higher dose groups and included significant (P < or = 0.05) reductions in 1) absolute and relative weights of the head and body of the epididymis (EP), tail of the EP, and seminal vesicle, 2) numbers of sperm in both regions of the EP, and 3) motility characteristics in sperm collected from the tail of the EP. Conversely, no significant changes were observed in relative testis weight, daily sperm production, spermatogenesis, seminiferous epithelial height in stage VII, and sperm morphology. All of the above parameters in the 1.6-microg group (except seminal vesicle weight) and 320-ng group were comparable to those of controls. Plasma testosterone (T) level was reduced to an almost undetectable level in the > or = 8-microg groups and to a very low level in the 1.6-microg group (0.35 vs. 2.36 ng/ml in controls or 320-ng group), but LH level was unaltered. In a parallel fertility study, males received DES at a rate of 40, 8, or 1.6 microg x rat(-1) x day(-1) for 12 days prior to and 12 days during cohabitation (1:1) with untreated females. Of the 15 females cohabited with treated males (5 females/dose), none in the 40-microg and 8-microg groups and 1 in the 1.6-microg group formed a copulatory plug and delivered 8 pups, in contrast to 5/5 copulatory plugs and 13-15 pups/litter in the controls. DES at a rate of 8 microg x rat(-1) x day(-1) for 12 days reduced EP weights, sperm numbers in the EP, and sperm motility patterns but caused minimal to no alterations in daily sperm production, spermatogenesis, or sperm morphology. Factors other than T, or in addition to lower T, may be responsible for DES-induced reproductive disorders (despite lower T, sperm contents and sperm motility patterns in the EP were normal in the 1.6-microg group). Deficits in EP sperm functions and/or sexual behavior (as evident from absence of copulatory plugs) probably accounted for reduced fertility in treated males.

Animals↗
PubMed1988

Effects of local heating of the testes on the concentration of testosterone in jugular and testicular venous blood of rats and on testosterone production in vitro.

Heating both testes of rats to between 39 degrees C and 41 degrees C for 30 min was apparently without effect 21 days later, but heating to between 41.5 degrees C and 43 degrees C for 30 min resulted in a significant drop in testis weight accompanied by significant rises in the serum levels of LH and FSH. There were no changes in serum testosterone concentration in the peripheral circulation although there were increases in the concentration in testicular venous blood. The ability of the heated testis to secrete testosterone in vivo in response to maximal stimulation by hCG was reduced, as judged by testosterone levels in peripheral blood, while there was a supranormal increase in testosterone levels in testicular venous blood. Maximally stimulated testosterone production in vitro by the heated testis was supranormal whereas the basal production of testosterone per testis was not different from control values. Therefore, it appears that the testosterone produced by Leydig cells from heated testes may not be secreted as effectively as in normal testes.

Animals↗
PubMedDate not supplied

Effects of heat stress on mouse testicular cells and sperm chromatin structure.

Scrotal regions of mice were exposed to a 38.0, 40.0, or 42.0 degrees C (+/-0.1) H2O bath for 60 minutes to determine the effects of elevated temperatures on testicular cells and sperm chromatin structure. Mice were killed on various days after exposure, and ratios of acridine orange-stained testicular cell populations were determined by flow cytometry. Testicular weights of mice exposed to 42.0 degrees C decreased significantly day 1 (P < 0.01) through 35 (P < 0.001). Also, a significant relative decrease in testicular haploid cells was seen on days 3-35 (P < 0.001) with a corresponding increase in the diploid population (P < 0.001). Testicular analyses of mice exposed to 38.0 degrees C were not significantly different from control values. Testis weights of mice exposed to 40.0 degrees C were not affected, but a relative decrease in percent haploid cells occurred on days 11 and 14 (P < 0.001). The sperm chromatin structure assay (SCSA) was used to measure the susceptibility of cauda epididymal sperm DNA to in situ denaturation at low pH. Caudal epididymides of mice exposed to 42.0 degrees C had no sperm. Caudal epididymal sperm from mice exposed to 40.0 degrees C were most susceptible to acid-induced DNA denaturation on days 3 (P < 0.05), 7, 11, and 14 (all P < 0.001). The 38.0 degrees C exposed mice showed some minor sperm chromatin abnormalities at later time points (days 11-35). When compared to sperm head morphology measurements, SCSA parameters were more sensitive indicators of heat-induced sperm abnormalities. These results show that mouse spermatogenesis is disrupted by scrotal exposure to environmental temperatures several degrees over normal physiological temperature and, of more biological interest, that some thermal ranges above normal allowed production of sperm with compromised nuclear chromatin structure.

Acridine Orange↗
PubMed1991

Evaluation of 2-methoxyacetic acid toxicity on mouse germ cells by flow cytometry.

Flow cytometric (FCM) DNA content measurements were carried out on testicular monocellular suspensions obtained from mice exposed per os to a single dose of 50, 100, 300, 600, and 900 mg/kg body weight (b.w.) of 2-methoxyacetic acid (MAA) in order to investigate its cytotoxic action on germ cells. The effects of MAA were evaluated 2, 7, 14, 28, and 45 d after treatment in terms of altered cell type ratios in FCM fluorescence distribution histograms. Testis weight and histological tissue sections were also analyzed. MAA induced marked changes in the relative percentages of tetraploid and haploid cells, indicating the occurrence of cytotoxic damage on primary spermatocytes. Multiparameter FCM analysis showed that, besides its action on nucleic acid synthesis, MAA can also affect the cellular energy metabolism reflected in an altered mitochondrial mass distribution on round spermatids surviving the MAA treatment. This study demonstrates that rapid and unique FCM procedures can be usefully applied in reproductive toxicology.

Acetates↗
PubMed2003

Effect of vitamin E deficiency on the growth and secretory function of the rat prostatic complex.

Increased intake of vitamin E has been suggested to be protective against prostate cancer in men, but the effects of vitamin E on prostate growth and function remain poorly defined. The purpose of this study was to determine the effects of vitamin E deficiency on pubertal growth and maturation of the prostate in the rat. Animals were placed on a vitamin E deficient diet at 28 days of age and were followed for 15 and 26 weeks. Vitamin E deficient rats had a circulating vitamin E level of less than 1% of control animals and experienced a decrease in body and testis weight. The deficiency did not alter the weights of the ventral and dorsal lobes of the prostate. However, there was an increase in weight, DNA, and protein contents of the lateral lobe in control and vitamin E deficient rats from 15 to 26 weeks of treatment, but these increases were significantly lower in vitamin E deficient 26-week treated rats. The volume of secretion per milligram tissue was greater in the ventral than lateral or dorsal lobes. The volume of secretion and activity of the secretory 26 kDa protease in the ventral prostate was lower in vitamin E deficient rats at 15 weeks, but not at 26 weeks of treatment. In contrast, the relative protein content of lateral lobe secretion increased in both control and vitamin E deficient rats from 15 to 26 weeks of treatment. The lateral, but not ventral or dorsal, lobes of both control and vitamin E deficient rats were affected by chronic prostatitis as evidenced by infiltration of inflammatory cells. The lateral lobes also showed markedly elevated activities of the matrix metalloproteinases gelatinase A (MMP-2) and gelatinase B (MMP-9). These data indicate that vitamin E deficiency does not alter the growth of the prostatic lobes, nor the onset and extent of lateral lobe specific prostatitis, but it may delay some differentiated functions such as secretion of specific proteins in the ventral lobe. Thus, the effects of vitamin E in the prostate of the rat appear to be selective.

Animals↗
PubMed2005

The resin monomer triethylene glycol dimethacrylate exhibits reproductive toxicity in male mice.

The present study evaluated the effect of triethyleneglycol dimethacrylate (TEGDMA) on mouse fertility. Adult male mice were administered TEGDMA (0, 25 and 100 microg kg(-1)) intragastrically daily for 28 days and then allowed to mate for 10 days with sexually mature untreated female mice; fertility was assessed after a further 10 days. Females mated by males that had been treated with TEGDMA had a significant reduction in pregnancy rate, as well as a significant increase in the total number of resorptions as a percentage of the total number of implantations. Furthermore, the number of animals in which resorption occured was increased significantly. Males treated with TEGDMA exhibited a significant reduction in bodyweight, testis weight and the weight of the seminal vesicles and preputial glands. Testicular and epididymal sperm counts, as well as the efficiency of sperm production, were also significantly reduced in TEGDMA-treated males. The results suggest that TEGDMA has adverse effects on the fertility and reproductive system of male mice.

Animals↗
PubMed1992

Developmental regulation of ornithine decarboxylase (ODC) in rat testis: comparison of changes in ODC activity with changes in ODC mRNA levels during testicular maturation.

These studies were undertaken to analyze the changes in testicular ornithine decarboxylase (ODC) mRNA levels and ODC activity in rats from birth to maturity. Levels of ODC mRNA were initially low in animals aged 10-17 days. Beginning at 21 days, ODC mRNA levels began to rise, reaching maximal levels by 40 days (p less than 0.01). The size of the 2.2- and 2.6-kb ODC mRNAs did not appear to change with age, as determined by Northern blot analysis. The increase in ODC mRNA that began at 21 days paralleled the increase in testis weight. This increase in ODC mRNA preceded the appearance of rat protamine-1 mRNA, a germ cell-specific mRNA found in round spermatids, which was first detected on Day 40. In contrast, levels of sulfated glycoprotein-2 mRNA, which, in the testis, is found exclusively in Sertoli cells, were highest at Day 17 and thereafter declined gradually with age. Unlike the increase in ODC mRNA levels, ODC activity was highest in 10-day-old animals and thereafter declined steadily with age, reaching minimal levels by 40 days (p less than 0.01). Thus, the increase in testicular ODC mRNA levels was in marked contrast to the decrease in testicular ODC activity. Incubation of cytosolic extract from 40-day-old animals with that from 10- or 17-day-old animals inhibited ODC activity approximately 50%, when compared to cytosols from 10- or 17-day-old animals. Dialysis of cytosol from 40-day-old animals prior to incubation with cytosol from 10-day-old animals relieved this inhibition.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2002

Wild intersex roach (Rutilus rutilus) have reduced fertility.

Endocrine-disrupting chemicals, known to be present in the environment, have great potential for interfering with reproductive health in wildlife and humans. There is, however, little direct evidence that endocrine disruption has adversely affected fertility in any organism. In freshwater and estuarine fish species, for example, although a widespread incidence of intersex has been reported, it is not yet known if intersexuality influences reproductive success. The purpose of this study was, therefore, to determine gamete quality in wild intersex roach (Rutilus rutilus) by assessing sperm characteristics, fertilization success, and ability to produce viable offspring. The results clearly demonstrate that gamete production is reduced in intersex roach. A significantly lower proportion of moderately or severely feminized fish (17.4% and 33.3%, respectively) were able to release milt compared with normal male fish from contaminated rivers (in which 97.6% of the males were able to release milt), reference male fish (97.7%), or less severely feminized intersex fish (experiment 1: 85.8%, experiment 2: 97%). Intersex fish that did produce milt produced up to 50% less (in terms of volume per gram of testis weight) than did histologically normal male fish. Moreover, sperm motility (percentage of motile sperm and curvilinear velocity) and the ability of sperm to successfully fertilize eggs and produce viable offspring were all reduced in intersex fish compared with normal male fish. Male gamete quality (assessed using sperm motility, sperm density, and fertilization success) was negatively correlated with the degree of feminization in intersex fish (r = -0.603; P < 0.001) and was markedly reduced in severely feminized intersex fish by as much as 50% in terms of motility and 75% in terms of fertilization success when compared with either less severely feminized intersex fish or unaffected male fish. This is the first evidence documenting a relationship between the morphological effects (e.g., intersex) of endocrine disruption and the reproductive capabilities of any wild vertebrate. The results suggest that mixtures of endocrine-disrupting substances discharged into the aquatic environment could pose a threat to male reproductive health.

Animals↗
PubMedDate not supplied

Demonstration of direct effect of estrogen on rat spermatogenesis.

The presence of an estrogen receptor in Leydig cell cytosol suggests that estrogen could have a direct action on Leydig cell function. We have shown earlier the direct effect of estradiol on testosterone biosynthesis. We report in this communication effect of estradiol on spermatogenesis using hypophysectomized rats treated daily for four days with 400 IU hCG/Pregnyl) and 1 IU FSH (Pergonal), a model that eliminates the possibility of feedback effects of estradiol on gonadotropin secretion. Estradiol was administered in subcutaneous silastic capsules. The control animals had empty capsules. The inhibition of spermatogenesis, after estradiol treatment, was marked by the presence of multinucleated giant cells, disorganization of the germinal elements, accumulation of cellular debris and the absence of late spermatid and spermatozoa. These changes in the histoarchitecture of testis were accompanied by the reduction in the diameter of the seminiferous tubules and the thickness of the basement membrane. Morphologically Leydig cells were, however, normal. Inhibition of spermatogenesis was in relation to the amount of estrogen available/administered as estradiol capsule of 0.25 cm did not evoke significant changes in the histology of the testis whereas estradiol capsule of 4 cm caused maximum damage to the spermatogenesis. Similarly progressive damage to the spermatogenesis was quite apparent as the number of days increased after estradiol capsule implantation. Neither high (1600 IU/day/4 days) nor low /5.25 IU/day) doses of hCG synergized the effect of estradiol on spermatogenesis. Testis weight was significantly reduced after estradiol treatment but weight of the epididymis and accessory sex organs did not change. Body weight was also not effected by estradiol treatment.

Animals↗
PubMedDate not supplied

Role of early GnRH administration in sexual behavior disorders of rat pups perinatally exposed to lead.

The effects of maternal exposure to lead (Pb) during the perinatal (1% and 0.1% Pb) periods of sexual brain differentiation were studied in adult male offspring. Maternal Pb levels were measured after treatment. Behavioral (open field and sexual behavior), physical (sexual maturation, body and organ weights), and biochemical (testosterone levels and hypothalamic monoamine and respective metabolite levels) data were assessed in perinatally exposed offspring. The effects of gonadrotopin-releasing hormone (GnRH) administration to pups at birth on puberty and sexual behavior were also investigated in offspring postnatally exposed to the metal. Results showed that perinatal administration of the two Pb concentrations did not modify maternal weight gain; 1% Pb exposure reduced offspring body weight during the 7 days of treatment while no changes were observed after 0.1% Pb exposure; neither Pb concentration altered offspring sexual maturation; the higher Pb concentration improved sexual behavior while the 0.1% concentration reduced it; exposure to 0.1% Pb caused decrease in testis weight, an increase in seminal vesicle weight and no changes in plasma testosterone levels; hypothalamic VMA levels were increased compared to the control group; GnRH administration reversed the effects of 0.1% Pb administration on male sexual behavior. These results show that perinatal exposure to Pb had a dose-dependent effect on the sexual behavior of rats and that a decrease in GnRH source in the offspring was probably involved in the reduction of their sexual performance.

Animals↗
PubMed1993

Effect of prenatal and postnatal photoperiod on spermatogenic development in the Djungarian hamster (Phodopus sungorus sungorus).

The effect of the pre- and postnatal daylength on the start of spermatogenesis and further testicular development from day 4 up to day 127 was investigated in Djungarian hamsters. Hamsters were either gestated under long (16 h light:8 h dark) photoperiod and reared under long or short (4 h light:20 h dark) photoperiod after birth (L/L and L/S hamsters, respectively), or gestated under short photoperiod and transferred to long photoperiod after birth (S/L hamsters). In L/L and L/S hamsters, spermatogenesis started between day 4 and day 5 (day of birth = day 1), when the first gonocytes entered the S-phase. A, Intermediate and B spermatogonia were first observed on days 6, 8 and 9, respectively. The proliferation pattern of gonocytes and Sertoli cells, studied between day 4 and day 9, did not differ between L/L and L/S hamsters. Hence, the duration of the postnatal photoperiod had no effect on the start of spermatogenesis. The first effect of postnatal photoperiod on spermatogenic development was observed on day 15, when testis weights and tubular diameters were reduced in L/S animals. From day 22 onwards, spermatogenesis was arrested mainly at the mid-pachytene stage, no tubular lumen was formed, and the number of preleptotene spermatocytes was reduced. The ultimate number of Sertoli cells per testis was not affected by postnatal short photoperiod. The duration of the prenatal photoperiod had a clear effect on spermatogenesis after birth. In S/L hamsters, the number of gonocytes per tubular cross-section was reduced on day 4 and 4.5. Gonocyte proliferation was reduced on day 5 and spermatogenesis started one day later. Consequently, A and Intermediate spermatogonia appeared on day 7 and 9, respectively. Sertoli cell proliferation was also shifted to later ages, but the ultimate number of Sertoli cells did not differ from L/L or L/S hamsters. From day 29 onwards, the number of preleptotene spermatocytes was increased in S/L hamsters, indicating that the Sertoli cells in these animals could support more germinal cells. In conclusion, a short postnatal photoperiod does not affect spermatogenesis before day 15 after birth, when further testicular development becomes arrested. A short prenatal photoperiod delays the start of spermatogenesis by one day, alters the proliferation pattern of Sertoli cells, and from day 29 onwards, enables the Sertoli cells to support more germinal cells. The duration of the pre- and postnatal photoperiod did not affect the ultimate number of Sertoli cells.

Animals↗
PubMed1981

The reproductive cycle in the male hedgehog (Erinaceus europaeus L.): a study of endocrine and exocrine testicular functions.

Seasonal changes in testicular and accessory gland weights, histological testicular structures, fructose and citric acid concentrations in two accessory glands and plasma testosterone levels were determined in adult male hedgehogs living in middle western France. Testicular activity started in winter (from December to February) during the last part of the hibernation period. During this resumption period, testis weights as well as all the testicular structural features (Leydig cell volume; length, diameter and volume of seminiterous tubules) increased. These changes were correlated with similar variations in plasma testosterone concentrations and accessory gland features (weight, fructose and citric acid contents). However, maximal development of endocrine testicular function was reached about one month before the completion of spermatogenesis and the maximal development of androgen target organs. Testicular activity was high from February-March to August-September, according to the year. After the spring peak corresponding to the main breeding period, a decrease in testicular activity was always noted in May-June. The values of the testicular features then remained high or increased again and a second breeding period always occurred. Finally, involution began at the end of summer but the endocrine function of the testis decreased before the exocrine function. All the gonadal functions were depressed from September to November. Our results show that in middle western France, one of the southern-most countries characterized by a mild, temperate climate, the testis of Erinaceus europaeus L. is activated earlier and the breeding season lasts longer than in any of the other European countries cited in the literature.

Animals↗
PubMed1989

Long-term effects of triethylenemelamine exposure on mouse testis cells and sperm chromatin structure assayed by flow cytometry.

The toxic and potentially mutagenic actions of triethylenemelamine (TEM) on mouse body and testis weights, testicular cell kinetics, sperm production, sperm head morphology, and sperm chromatin structure were assessed in two experiments. The first experiment examined effects of four dose levels of TEM, assayed 1, 4, and 10 wk after toxic exposure. In the second study, effects from five dosage levels were measured at 1, 4, and 10 wk, and the highest dosage level was evaluated over 44 wk. TEM produced an expected dose related loss of spermatogenic activity and subsequent recovery as determined by dual-parameter (DNA, RNA) flow cytometry (FCM) measurements of testicular cells. Both testicular weights and caudal sperm reserves remained generally below controls after 44 wk recovery following exposure to the highest (1.0 mg/kg daily x 5) dosage. Chromatin structure alterations, defined as increased susceptibility to DNA denaturation in situ, and sperm head morphology were highly correlated (.87-.93, P less than .001) with dose and with each other. Data obtained from the sperm chromatin structure essay (SCSA) on fresh sperm was highly correlated with measurements of aliquots of the same sample collected over 44 wk, frozen, and then measured on the same day. Sperm head morphology and sperm chromatin structure remained abnormal at 44 wk for the 1.0 mg/kg TEM dosage, suggesting that the abnormalities, present long after the initial toxic response, may be a result of mutation. This study demonstrates that flow cytometry provides a unique, rapid, and efficient means to measure effects of reproductive toxins and potential mutagens.

Animals↗
PubMed1999

Effects of lead on the male reproductive system in mice.

The effect of environmental lead on the male reproductive system has been a major area of concern for several years. Lead toxicity to the male reproductive system of sexually mature male CF-1 mice was investigated by administering two concentrations of lead (0.25% and 0.5%) via drinking water for 6 wk. The low lead dose significantly reduced the number of sperm within the epididymis, while the high dose reduced both the sperm count and percentage of motile sperm and increased the percentage of abnormal sperm within the epididymis. There was no significant effect on testis weight; however, the high-dose treatment significantly decreased the epididymis and seminal vesicle weights as well as overall body weight gain. Plasma luteinizing hormone (LH), follicle-stimulating hormone (FSH), and testosterone (T) levels were not affected by lead administration indicating that in adult male CF-1 mice, lead targets testicular spermatogenesis and sperm within the epididymis to produce reproductive toxicity rather than acting at other sites within the hypothalamic-pituitary-testicular axis.

Administration, Oral↗