Desquamation Of Germ Cells Research Articles

Impact of Perinatal Coexposure to Chlorpyrifos and a High-Fat Diet on Kisspeptin and GnRHR Presence and Reproductive Organs.

Emerging evidence has indicated the involvement of extrahypothalamic Kisspeptin and GnRHR in reproductive function. In this study, we evaluate if maternal exposure to the pesticide chlorpyrifos (CPF) and/or a high-fat diet (HFD) has an impact on the expression of Kisspeptin and GnRHR in the reproductive organs of rats' offspring. A total of 16 pregnant rats are divided into four groups: a control group (n = 4), CPF group (4 rats exposed daily to 1/mg/kg/day), HFD group (4 rats randomly fed a 5.25 kcal/g HFD), and coexposed group (4 rats exposed to CPF and HDF). At postnatal development postnatal day (PND) 60, male and female offspring were sacrificed. The reproductive organs (ovary and testis) were removed, and histological and immunohistological analysis and in silico quantification (TissueGnostics software 6.0.1.102, TissueFAXS, HistoQuest) were applied to investigate the impact of different treatments on Kisspeptin and GnRHR expression in reproductive organs. The main outcomes of the study showed a significant decrease in rat offspring's body weight in the CPF group from PND30 and PND60 (p < 0.05 and p < 0.01, respectively). Histological analysis showed a significant increase in the atretic follicle and abnormal testis structure with germ cell desquamation in the CPF-exposed group. The immunodetection quantification of protein shows a significant decrease in GnRHR and Kisspeptin in the HFD and CPF exposed groups, respectively, in testis rat offspring. Perinatal exposure to CPF and HFD exposure affect the reproduction function of rat offspring.

Supplementation of feedlot lambs with cactus cladodes as strategy to improve testicular function

The aim of this study was to evaluate the effects of diets containing cactus cladodes genotypes on plasma testosterone levels, testicular histopathological and histomorphometric parameters, and oxidative stress markers in lambs. Thirty-six male, intact Santa Inês lambs (22.0 ± 2.9 kg initial body weight), were to feedlot for 86 days. A completely randomized design was used with three dietary treatments (control diet with Tifton-85 hay as the only roughage; and two more diets with Miúda or OEM cactus cladodes partially replacing hay) and twelve replicates. There was no influence of the diets on the testicular weight (P = 0.414) and gonadosomatic index (P = 0.384) of lambs. The testosterone serum concentrations were almost twice as higher in lambs fed Miúda cactus cladodes compared to control treatment. There was greater incidence and severity of lesions in the testicular parenchyma of animals that received control diet: loosening of germ cell epithelium, germ cell desquamation and vacuolization of Sertoli cells. The seminiferous tubule diameter and height of the seminiferous epithelium were higher in lambs fed OEM cactus cladodes (P = 0.003). The tubular volume and Leydig cells volume were higher in animals fed with cactus cladodes (P < 0.05). The levels of malondialdehyde were higher in the lambs of control group compared to OEM group (P = 0.039) and the testicular concentration of nitric oxide was higher in control group (P = 0.009). The diet containing OEM cactus cladodes increased the levels of superoxide dismutase. Our results indicate that diets containing cactus cladodes promote antioxidant protection to the testicular parenchyma and preserve the spermatogenic process of lambs.

Морфологический анализ семенников в оценке фертильности мышей после однократного острого γ-облучения разными дозами

Introduction. Radiation therapy for malignant neoplasms can have detrimental effects on male reproductive health. Little is known about the role of morphological changes in the testes when assessing the fertility after exposure to lethal and sublethal doses. The research aimed to investigate the impact of acute γ-irradiation at various doses on testicular morphology, spermatozoa, and fertility potential in mice through a comparative morphological analysis. Materials and methods. We subjected BALB/c mice to acute γ-irradiation at doses of 1 and 6 Gy using the IGUR device (Cs137, dose rate of 0.85 Gy/min). We studied the structural state of the testes and spermatozoa. Morphological examination was performed using optical microscopy of histological slides with digital microphotography (n=180). Fertility potential was assessed by mating irradiated males (n=200) with intact mature females (n=400). Results. During the course of the experiment, which lasted from 16 to 120 days, we observed significant morphological changes in the testes and spermatozoa of the experimental groups. On day 62, the number of seminiferous tubules exhibiting destruction at 1- and 6-Gy doses was the highest. This destruction was characterized by a 2- to 4-fold increase in the desquamation of germ cells, a 3- to 6-fold increase in the desquamation of the spermatogenic epithelium, and a 2- to 10-fold increase in the desolation of the seminiferous tubules, respectively. The maximum decrease in the number of spermatozoa was to 68 and 44% at doses of 1 and 6 Gy, respectively. The number of live spermatozoa decreased to 62% and 25%; sperm motility dropped by 21% and 100%. We detected an increase in the number of pathological forms of spermatozoa by 40% and 3 times at doses of 1 and 6 Gy, respectively. An increase in the total embryonic and induced post-implantation mortality in females fertilized by irradiated males was noted at all stages of spermatogenesis (p&lt;0.05). At a 6-Gy dose, we detected a temporary sterility at the stages of spermatids and spermatocytes. Conclusion. The degree and depth of morphological changes in the testes and spermatozoa are dose-dependent, the most pronounced changes being at a 6-Gy dose causing temporary sterility. A compensatory-restorative reaction from spermatogenesis was revealed. Keywords: γ-irradiation, spermatogenesis, spermatozoon, fertility

Saponins derived from the stems and leaves of Panax ginseng attenuate scrotal heat-induced spermatogenic damage via inhibiting the MAPK mediated oxidative stress and apoptosis in mice.

Heat stress (HS) reaction is a stress response caused by adverse conditions. Currently, the incidence of reproductive malignancies particularly in males has been constantly increasing. This work investigated the effects of saponins derived from the stems and leaves of Panax ginseng (GSLS) on testicular injury induced by scrotal hyperthermia in mice. GSLS (150, 300 mg/kg) were administered intragastrically to mice for 14 days, then exposed to a single scrotal heat treatment at 43°C for 18 min on seventh day. HS induced a significant loss of multinucleate giant cells, desquamation of germ cells in destructive seminiferous tubules. Moreover, HS reduced the serum testosterone, testicular tissue superoxide dismutase activity and glutathione (GSH) content, while significantly enhanced the production of malondialdehyde (p < .05). GSLS exhibited the protective potential against HS-induced injury not only by modulating Bcl-2 family and caspase protease family, but also by suppressing the protein levels of heme oxygenase-1 (HO-1), heat shock protein 70 (HSP70), hypoxia inducible factor-1α (HIF-1α) and activation of Mitogen-activated protein kinase (MAPK) signaling pathways (p < .05). In conclusion, we clearly demonstrated that GSLS exhibited a significant protective effect against HS-induced testicular dysfunction, mainly the inhibition of oxidative stress associated apoptosis partly via regulation of the MAPK signaling pathway.

Sertoli Cell Alterations in Peripubertal Varicocelized Rats: Evidence of Primary Damage on Spermatogenesis.

Idiopathic varicocele is closely associated with male infertility or subfertility. Sertoli cell is a very important regulator of spermatogenesis. We investigated the morphofunctional alterations in the Sertoli cell and its possible involvement in the establishment of testicular primary lesion in experimental left-sided varicocele, induced from peripuberty. Twenty-five male peripubertal rats (44 days postpartum [dpp]) were distributed into two groups: control (C) and varicocele (V). Experimental left varicocele was induced in rats through the partial ligature of the left renal vein. Euthanasia was performed at 100 dpp. Testicular histopathology and testosterone plasmatic level were evaluated. Transferrin and vimentin proteins were, respectively, used as immunomarkers of Sertoli cell function and structure. Significant reductions in vimentin and transferrin expressions were noticed in androgen-dependent stages (VII and VIII) of the seminiferous epithelium cycle in V rats; testosterone plasmatic level was also reduced. Bilateral testicular histopathological alterations were found in V rats, mainly massive germ cell desquamation. The histological damage and changes in protein expressions occurred bilaterally. The relevant impairment of the functional and structural characteristics of the Sertoli cell, together with the typical massive germ cell desquamation, indicates that Sertoli cell changes can primarily contribute to the significant testicular dysfunction associated with varicocele.

20(R)-ginsenoside Rg3, a product of high-efficiency thermal deglycosylation of ginsenoside Rd, exerts protective effects against scrotal heat-induced spermatogenic damage in mice

Heat stress (HS) reaction can lead to serious physiological dysfunction associated with cardiovascular and various organ diseases. Ginsenoside Rg3 (G-Rg3) is a representative component of ginseng rare saponin and can protect against multiple organs, also used as functional food to adjust the balance of the human body, but the therapeutic effect and molecular mechanism of G-Rg3 on male diseases under HS are underexplored. The aim of the present study, G-Rg3 was prepared through the efficient conversion of ginsenoside Rd and investigate the contribution of G-Rg3 to testicular injury induced exposure to HS. All mice were divided into four groups as follows: normal group, HS group, and HS+G-Rg3 (5 and 10 mg/kg) groups. G-Rg3 was administered orally for 14 days, then exposed to a single scrotal heat treatment (43°C, 18min) on the 7th day. After HS treatment, the morphology of testis and epididymis changes, and caused a significant loss of multinucleated giant cells, desquamation of germ cells in destructive seminiferous tubules, and degenerative Leydig cells, further destroying the production of sperm. After administration G-Rg3 (5 and 10 mg/kg/day) for 2 weeks, the spermatogenic-related indexes of testosterone levels and superoxide dismutase (SOD) activity, glutathione (GSH) content significantly (p < 0.01) increase compared with the HS group. Moreover, G-Rg3 treatment effectively ameliorated the production of malondialdehyde (MDA) (p < 0.05 or p < 0.01). Importantly, G-Rg3 exhibited the protective potential against HS-induced injury not only suppressing the protein levels of heme oxygenase-1 (HO-1), hypoxia-inducible factor-1α (HIF-1α), and heat shock protein 70 (HSP70) but also modulating the Bcl-2 family (p < 0.01 or p < 0.001) and activation of mitogen-activated protein kinase (MAPK) signaling pathways (p < 0.01). For most of the parameters tested, the HS+G-Rg3 (10 mg/kg) group exhibited potent effects compared with those exhibited by the low dose (5 mg/kg) group. In conclusion, the present study demonstrated that G-Rg3 exerted protective effects against HS-induced testicular dysfunction via inhibiting the MAPK-mediated oxidative stress and apoptosis in mice.

Prenatal exposures to bisphenol A and di (2-ethylhexyl) phthalate disrupted seminiferous tubular development in growing male rats

Endocrine-disrupting compounds (EDCs) are found in the environment due to their use in industrial and manufacturing activities. Exposure of the population to bisphenol A (BPA) and di (2-ethylhexyl) phthalate (DEHP) is significant because they are present in many consumer products. EDCs target the reproductive tract because they express high levels of steroid hormone receptors, which act as transcriptional factors to regulate reproductive development. In the present study, timed-pregnant Long-Evans female rats (n = 8–10) were administered BPA and DEHP by oral gavage at 2.5 or 25 μg/kg body weight and 5 or 50 μg/kg body weight, respectively. Exposures to chemicals were limited to the period between gestational days 12 and 21 followed by assessment of testicular development in male offspring in the postnatal period. Leydig cells and Sertoli cells are the two major somatic cells present in the testis. The 17β-hydroxysteroid dehydrogenase (17β-HSD) steroidogenic enzyme is a marker for Leydig cell maturation, whereas transferrin is a marker for Sertoli cell differentiation. At day 10 post-partum, testes were obtained from cohorts of control and chemical-exposed male rats and processed to measure 17β-HSD and transferrin expression levels in western blots. Compared to control, 17βHSD enzyme protein was increased in BPA-treated rats but levels were decreased in animals exposed to DEHP (P < 0.05). Transferrin protein was decreased in male rats exposed to both BPA and DEHP compared to control animals (P < 0.05). To assess qualitative cellular changes within the spermatogenic epithelium, testes were obtained from separate cohorts of male rats at 35 days of age and processed for histopathological analysis. Results showed that prenatal exposures of male rats to BPA and DEHP caused disruption of the spermatogenic epithelium evident as disorganization and atrophy of seminiferous tubules as well as desquamation of germ cells into the tubular lumen. Together, results from the present study support the view that developmental exposures to environmentally relevant levels of BPA and DEHP are associated with disruptions of testicular cell development, which have implications for endocrine and exocrine functions of testis.

REPRODUCTIVE TOXICITY AND ENDOCRINE DISRUPTION OF ORAL AND DERMAL EXPOSURE TO PESTICIDE MIXTURE IN MALE RATS

The current study was performed to assess the risk and hazards of oral & dermal exposure to chlorpyrifos & cypermethrin mixture based on some reproductive & endocrine impaired parameters as well as histopathological alterations & histomorphometric study. Eighty-five Wister male rats (weighing 130-150g) were randomly classified into four groups (a, b, c and d). Each of group (a) and (b) were further subdivided into 5 subgroups used for determination of the oral and dermal LD50. While group (c) and (d) were classified into 3 subgroups which were used for oral and dermal treatments respectively. The first subgroups of (c) and (d) were considered as control. Rats of two subgroups (c) treated orally by 2 doses 4.26 mg/kg (1/20 LD50) and 2.84 mg/kg(1/30 LD50). Rats of two subgroups (d) treated by dermal application of 2 doses70.85mg/kg (1/30 LD50) and 42.51 mg/kg (1/50 LD50). The experiment was conducted for 65 consecutive days. The results revealed that, the tested pesticides mixture caused a significant reduction in reproductive organs weights, sperm count, sperm motility percent, alive sperm percent, pseudocholinesterase and serum testosterone levels in all treated groups especially the dermally treated groups (P≤0.05), moreover there was azoospermia in most of the group of rats treated with high dermal dose. The treated groups showed a significant increase in sperm abnormalities and composite score which represent sperm DNA fragmentation. Moderate to severe histopatholoical alterations were detected in testis and epididymis of treated rats in a dose and route dependant manner in the form of germ cell desquamation, multinucleated giant cells formation and leydig cell vacuolization with disturbance in spermatogenesis. Moreover the histomorphometric parameters analysis detected significant (P≤0.05) reduction of diameter, thickness, endothelium height & lumen of seminiferous tubules and also significant reduction of sertoli cell population. There was significant increase of blood vessel wall thickness. These results indicated that the tested formulation had synergistic effects and induced significant harmful effects on male reproductive system which were more pronounced with dermal exposure.

Late reproductive analysis in rat male offspring exposed to nicotine during pregnancy and lactation.

We previously observed that nicotine, administered to rats (Wistar) during pregnancy and lactation periods, provokes, in the progeny, late morphofunctional alterations in Leydig cell, body weight increase in adulthood (90 days post partum, dpp) as well as seminiferous epithelium injury. Aiming to investigate whether the spermatogenic damage previously observed in adult progenies from pregnant and lactating nicotine-exposed rat dams are maintained or whether it is worsened in older rats, we analyzed the morphological testicular alterations after up to two complete periods of spermatogenesis (53 days each), spermatic parameters, and sperm DNA fragmentation. Pregnant and lactating rats were nicotine-exposed (2 mg/kg/day) through an osmotic minipump implanted on the first day of pregnancy and replaced after birth. Absolute Control (no minipump) and Sham Control (minipump without nicotine) groups were established. The offspring were killed at 90, 143, and 196 dpp. Significant alterations in morphometric and stereological testicular parameters, such as concentration of sperm number, daily sperm production, and plasma and intratesticular levels of cholesterol and testosterone were not observed in nicotine-exposed rats. Testicular histopathological analysis showed small intraepithelial vacuolization and an accentuated germ cell desquamation in exposed rats. However, the offspring from nicotine-exposed dams exhibited higher frequency of morphologically abnormal spermatozoa and lower sperm motility in comparison with control groups. In addition, nicotine-exposed groups showed a significant reduction in sperm mitochondrial activity and an increased sperm DNA fragmentation (Comet assay). These results indicate a late reproductive damage in the male progeny caused by maternal nicotine exposure, related to the decrease in sperm quality.

Enhanced Protective Effects of Combined Treatment withβ-Carotene and Curcumin against Hyperthermic Spermatogenic Disorders in Mice

Scrotal hyperthermia leads to oxidative stress and apoptosis in spermatogenic cells, which subsequently causes male infertility. In this study, we examined the effects of β-carotene and/or curcumin on heat-stress- (HS-) induced testicular injuries in mice. ICR male mice (8 weeks old) were consecutively treated with β-carotene (10 mg/kg) and/or curcumin (20 mg/kg) orally once a day for 14 days and then subjected to single exposure with scrotal HS at 43°C for 15 min on day 7. HS induced a significant reduction in testicular weight, appearance of multinucleated giant cells, and desquamation of germ cells in destructive seminiferous tubules, as well as degenerative Leydig cells. Moreover, HS reduced the superoxide dismutase (SOD) activity and mRNA levels of mitochondrial SOD, phospholipid hydroperoxide glutathione peroxidase, B-cell lymphoma-extra-large, and 3β-hydroxysteroid dehydrogenase, with increases in lipid peroxidation levels and mRNA levels of BCL2-associated X protein and caspase-3 relative to those of the control group. However, these changes were significantly recovered by combined treatment with β-carotene and curcumin after HS. These findings indicate that the combined treatment with β-carotene and curcumin might be a valuable protective agent to ameliorate hyperthermic spermatogenic disorders via its potent antioxidative, antiapoptotic, and androgen synthetic effects.

Protection of murine spermatogenesis against ionizing radiation-induced testicular injury by a green tea polyphenol.

Epigallocatechin-3-gallate (EGCG), a bioactive polyphenol in green tea, exerts antiapoptotic activity and prevents tissue damage against different stimuli. Herein, we investigated the effects of EGCG treatment to simultaneously improve spermatogenesis following ionizing radiation (IR) (at a dose of 2 Gy). Mice were intraperitoneally injected with 50 mg/kg EGCG or vehicle control 3 days prior to the irradiation, and the treatment lasted intermittently for 24 days. Supplement with exogenous EGCG protected against short-term germ cell loss and attenuated IR-elicited testicular oxidative stress. Mechanistically, prosurvival effects of EGCG treatment upon IR stress were regulated, at least in part, via the mitogen-activated protein kinase/BCL2 family/caspase 3 pathway. Consistently, at post-IR Day 21, histological analyses revealed tubule damage, desquamation of germ cells, and impairment of caudal parameters in irradiated testis, which could be significantly improved by intermittent EGCG treatment. In addition, long-term EGCG application ameliorated the IR-induced blood-testicular barrier permeability and suppressed testicular steroidogenesis, thus exerting a stimulatory effect on the spermatogenic recovery. Collectively, EGCG appeared to efficiently prevent germ cells from radiation-induced cell death via multiple mechanisms. Employment of this bioactive polyphenol should be an attractive strategy to preserve fertility in males exposed to conventional radiation therapy and warrants further investigation.

Meiotic Chromosome Behavior in a Human Male t(8;15) Carrier

Reciprocal translocation is one of the most common structural chromosomal rearrangements in human beings; it is widely recognized to be associated with male infertility. This association is mainly based on the abnormal chromosome behavior of the translocated chromosomes and sex chromosomes during meiosis prophase I in reciprocal translocation carriers. However, the underlying mechanisms are not completely known. Here we report a reciprocal translocation carrier of t(8;15), who is oligozoospermic due to apoptosis of primary spermatocytes and to premature germ cell desquamation from seminiferous tubules. Further analysis showed abnormal synapsis and recombination frequency in this patient, indicating a connection between chromosome behavior and apoptosis of primary spermatocytes. We also compared these observations with recently reported findings on spermatogenesis defects in reciprocal translocation carriers, and discuss the possible mechanisms underlying both common and unique phenotypes of reciprocal translocations involving different chromosomes with the aim of further understanding the regulation of human spermatogenesis.

Endocrine and testicular changes induced by olanzapine in adult Wistar rats

Olanzapine is an atypical antipsychotic drug that has been increasingly used in acute treatment of, and therapeutic support for, schizophrenia, bipolar disorder and other psychoses. Considering that olanzapine acts on the dopaminergic receptor and this receptor is detected in germ cells, the present study aims to investigate the effects of treatment with different doses of olanzapine on spermatogenesis, plasma testosterone and weight of androgen-dependent organs in rats. Results showed reduced plasma testosterone levels, and reduced testis, epididymis and prostate weights. Histopathologic and histomorphometric analysis of spermatogenesis indicated testicular degeneration. Furthermore, germ cell desquamation, syncytial multinucleated cells, Sertoli cell vacuolization and presence of necrotic and apoptotic germ cells wwew observed. Olanzapine treatment in rats promoted endocrinological changes and lesions in the testis, leading to a disturbance in spermatogenesis.

Disruption of sexual function, FSH secretion, and spermiogenesis in rabbits following developmental exposure to vinclozolin, a fungicide

We studied sequelae of prenatal plus infantile exposure of male rabbits to vinclozolin, because it is ingested by women and children. Female Dutch-Belted rabbits (7-10/group) were treated daily per orum from gestation day 15 through post-natal week 4 to provide 0, 7.2, or 72 mg vinclozolin/kg dam's body weight/day. Vinclozolin had no effect on maintenance of pregnancy, growth of pups, age at testicular descent or weight of organs. Concentrations of serum LH or testosterone at 6, 12, or 24 weeks of age were unaffected. However, FSH was lower (P < 0.05) in both vinclozolin groups at all three ages. Following injection of GnRH at 12 or 24 weeks, the increase in FSH was less (P < 0.05) in both vinclozolin groups, as was testosterone at 12 weeks of age. After full sexual maturity, 2 of 7 low dose rabbits were uninterested in female or male teasers and never achieved erection or ejaculation. Overall, rates of ejaculation failure were: control 0% (0/48), low dose 29% (12/42), and high dose 5% (3/60). Daily sperm production per gram of testis and total number of sperm per ejaculate in both vinclozolin groups were similar (P > 0.1) to controls. However, semen from vinclozolin rabbits contained over two times more (P < 0.05) morphologically abnormal spermatozoa, mostly nuclear and acrosomal defects, than semen from controls. Seminiferous tubules with degenerative changes were more frequent (P < 0.05) in vinclozolin rabbits than in controls. Lesions included syncytia of spherical spermatids and desquamation of germ cells. Hence, developmental exposure to vinclozolin caused presumably permanent changes in copulatory ability, secretion of FSH, and spermiogenesis.

PARTIAL REVERSAL OF ETHANOL OF ETHANOL-INDUCED MALE REPRODUCTIVE PATHOLOGY FOLLOWING ABSTINENCE

To date, no longitudinal studies have been carried out to determine the recovery of ethanol-related reproductive failure subsequent to moderate periods of abstinence. An animal model (C57B1 mouse) was utilized to examine the effectiveness of abstinence for reversal of ethanol-induced reproductive failure. After treatment with either a 5% (v/v) ethanol diet (10 weeks) or a 6% (v/v) ethanol diet (5 weeks), ethanol-treated animals and their pair-fed controls were electroejaculated and hemicastrated (right testis and accessory organs); their reproductive tracts and epididymal spermatozoa were examined. Ingestion of the 5% and 6% ethanol diets resulted in significantly (P less than 0.05) decreased weights of testes (24% and 28%, respectively) and seminal vesicles/prostate (20%, 6% diet only), increased frequencies of germ cell desquamation (480% and 400%), inactive seminiferous tubules (186% and 567%), sperm dysmorphology (31% and 119%) and inhibition of in vitro fertilization of mouse oocytes by epididymal spermatozoa (26% and 62%), as compared to their respective pair-fed control values. Also observed were significant decreases in epididymal sperm content (72%, 6% diet only), total motile spermatozoa (85%, 6% diet only) and seminal vesicles epithelial cell height (13% and 29%). No abnormal semen parameters were observed after treatment with the 5% ethanol diet; however, in animals treated with the 6% diet, significant decreases were noted in coagulum weight (50%), sperm count (85%) and acid phosphatase content (53%). Improvement in all parameters was observed in the contralateral half of the reproductive tract subsequent to 10 weeks abstinence. Only germ cell desquamation remained significantly elevated (100% as compared to control) in animals that ingested the 5% diet. In contrast, significant abnormalities persisting 10 weeks after treatment with the 6% ethanol diet included increased germ cell desquamation (200%), inactive seminiferous tubules (157%) and sperm dysmorphology (39%) and decreased forward progression (17%) of epididymal sperm, as compared to values. These findings are discussed in relation to the influence of alcohol consumption on male reproductive function in man.

Spontaneous recovery from ethanol-induced male infertility

Chronic ethanol ingestion by the male is associated with reproductive impairment. No longitudinal studies have been carried out to determine the recovery of ethanol-related reproductive failure subsequent to moderate periods of abstinence. An animal model (C57B1 mouse) was utilized to examine the effectiveness of abstinence for reversal of ethanol-induced reproductive failure. After treatment with either a 5% ethanol diet (10 weeks) or a 6% ethanol diet (5 weeks), animals were hemicastrated (right testis and accessory organs); their reproductive tracts and epididymal spermatozoa were examined. Ingestion of the 5% and 6% ethanol diets resulted in significantly ( p<0.05) decreased testicular weights (24% and 28%, respectively) and seminal vesicle/prostate weights (20%, 6% diet only), increased frequencies of germ cell desquamation (480% and 400%), inactive seminiferous tubules (186% and 567%) and inhibition of in vitro fertilization of mouse oocytes by epididymal spermatozoa (26% and 62%), as compared to their respective pair-fed control values. Also observed was a significant decrease in total motile spermatozoa (85%, 6% diet only). Improvement in all parameters was observed in the contralateral reproductive organs subsequent to ten weeks abstinence. Only germ cell desquamation remained significantly elevated (100% as compared to control) in animals that ingested the 5% diet. In contrast, significant abnormalities persisted ten weeks after treatment with the 6% ethanol diet, including increased germ cell desquamation (200%) and inactive seminiferous tubules (157%); decreased forward progression (17%) of epididymal sperm also persisted. If these data can be applied clinically, male alcoholic patients with reproductive disorders could have a prognosis of at least partial recovery following moderate periods of abstinence from ethanol.

Differential susceptibility to experimental autoimmune orchitis in BALB/c substrains.

Experimental allergic orchitis (EAO) is an organ specific autoimmune disease which can be readily induced in a susceptible mouse strain by a single injection of mouse testicular homogenate (MTH) emulsified in complete Freund’s adjuvant with either Bordetella pertussis organisms (Pokorna et al 1963; Bohme 1965; Hargis et al 1968; Bernard et al 1978; Sato et al 1981) or an extract enriched in pertussigen prepared from the spent media of B. pertussis cultures (Kohno et al 1983). Murine EAO is manifest as inflammation in the testis (orchitis), epididymitis, and vasitis (Kohno et al 1983). The histopathologic evidence of autoimmune orchitis first appears 10–15 days after immunization with maximal disease involvement occurring by day 20–25. Testicular lesions are characterized by varying degrees of interstitial, peritubular, and intratubular infiltration of eosinophils, neutrophils, lymphocytes, and macrophages. In severe disease, global necrosis may be seen. In the seminiferous tubules desquamation of germ cells leading to aspermatogenesis occurs concomitantly with the development of autoimmune orchitis.