Unilateral obstruction or injury to the vas deferens can result in significant injury to the contralateral testicle. Although various pathways have been proposed, the mechanism of contralateral testicular deterioration remains controversial. The present animal study was performed to evaluate the effects of unilateral vasectomy on ipsilateral and contralateral testicular histology and fertility in rats that were chemically sympathectomized neonatally. The study comprised 40 male albino rats: 20 received a placebo and the other 20 underwent chemical sympathectomy neonatally. When 60 days old, each group of 20 rats was divided into two groups that underwent either a sham operation or an operation to create unilateral left vasectomy. Eight weeks after surgery, each male rat was housed with two known fertile female rats for 25 days, and then their testes were harvested. Mean seminiferous tubular diameters (MSTD) and mean testicular biopsy scores (MTBS) were determined for each testis. Although MSTD and MTBS were not significantly different between groups, chemical sympathectomy prevented the decrease in total fertility rates of the rats with unilateral left vasectomy in our study. Prevention of this decrease by chemical sympathectomy suggests that the sympathetic nervous system may play a role in the testicular degeneration associated with vasectomy.
Animals ; Female ; Fertility/*drug effects ; Male ; Oxidopamine/toxicity ; Rats ; *Sympathectomy, Chemical ; Testis/drug effects/*pathology ; *Vasectomy

OBJECTIVETo investigate the protective effect of L-carnitine on the testis and epididymis against ornidazole (ORN)-induced injury in male rats.

METHODSForty male SD rats weighing 200 -230 g were randomly divided into 5 groups, Group A treated with 0.5% sodium carboxymethyl cellulose, and Groups B, C, D and E with ORN at the daily dose of 400 mg/kg, 800 mg/kg, 400 mg/kg plus LC 100 mg/kg and 800 mg/kg plus LC 100 mg/kg, respectively, all by oral gavage for 20 days continuously. Twenty-four hours after the last administration, all the rats were put to death, their testes and epididymides harvested, weighed and subjected to HE staining. The indexes of the testes and epididymides were obtained and their histopathological changes observed.

RESULTSCompared with Group A, Groups B and C showed significant decreases in the indexes of the testis and epididymis (P < 0.05 and P < 0.01), while Group D exhibited no difference and Group E extremely significant difference (P < 0.01). HE staining revealed that the spermatogenic cells at all levels of testicular seminiferous tubules were neatly arranged in Group B, caduceus in some seminiferous tubules, with decreased number of sperm and sporadic spermatogenic cells in the epididymal duct. Necrotic and caduceus spermatogenic cells were observed in the seminiferous tubules of Group C, with significantly decreased number of sperm and lots of non-sperm cell components in the epididymal duct. No obvious changes were found in the testicular seminiferous tubules, nor evident reduction in the number of sperm in the epididymal duct of Group D. Group E showed decreased number of sperm in the testicular seminiferous tubules, necrotic and caduceus spermatogenic cells, obviously reduced number of sperm and a lot of non-sperm cell components in the epididymal duct.

CONCLUSIONORC can induce histopathological changes in the testis and epididymis of male rats, and L-carnitine plays a role in protecting the testis and epididymis from ORN-induced injury in male rats.

Animals ; Carnitine ; pharmacology ; Epididymis ; drug effects ; pathology ; Male ; Ornidazole ; adverse effects ; Rats ; Rats, Sprague-Dawley ; Testis ; drug effects ; pathology

OBJECTIVETo establish an oxidative stress model induced by cumene hydroperoxide (cHP) in testis and epididymis of rats in vivo, and to understand the peroxidative damage of oxidative stress in testis, epididymal sperm and its propensity to induce nuclear DNA damage during spermatogenesis and sperm maturation in vivo.

METHODSAn organic hydroperoxide, cHP, 70% aqueous, diluted by 0.9% NaCl, was employed as model prooxidant. Ninety-day-old male Wistar rats were divided into a control and three cHP groups, and were administered intraperitoneally 0, 1/10, 1/6 and 1/4 LD50 cHP per day respectively at a dose of 2 ml/kg, for 7 consecutive days and were observed for any toxic symptoms and mortality. Twenty-four hours after the last dose, rats were sacrificed and induction of oxidative stress was ascertained by monitoring the degree of lipid peroxidation expressed as nano molar of malondialdehyde (MDA) in testicular homogenate and epididymal sperm. Nuclear DNA damage in testes and epididymal sperms was determined by comet assay. Motility of caudal sperms was counted and the morphology of testes and epididymis was observed under light microscope.

RESULTSRats of cHP administered groups were less vigorous than those of the control, but there were not death of rats during treatment. 1/10 LD50 per day for 7 consecutive days resulted in only a marginal increase in testicular MDA levels. However, 1/6 and 1/ 4 LD50 per day for 7 days of cHP administered to adult rats induced marked oxidative stress in testis and epididymal sperms as evidenced by a marked increase in MDA or nuclear DNA damage in testis and caput sperms, as well as significant decreases both in the body weight-and motility of caudal sperms. While the nuclear DNA damage caput sperms of 1/6 and 1/4 LD50 cHP administered rats increased significantly, nuclear DNA damage in caudal sperms showed no treatment related alterations.

CONCLUSIONOxidative stress in testis and epididymal sperms can be safely induced by applying multiple doses of cHP (1/6 and 1/4 LD50 per day for seven consecutive days). DNA damage caused by cHP induced oxidative stress may occurred mainly in testes.

Animals ; Benzene Derivatives ; toxicity ; DNA Damage ; Epididymis ; drug effects ; pathology ; Lipid Peroxidation ; drug effects ; Male ; Rats ; Rats, Wistar ; Sperm Count ; Spermatozoa ; drug effects ; pathology ; Testis ; drug effects ; pathology

OBJECTIVETo study the effect of ethane dimethane sulfonate (EDS) injection on the volumes of different histological structures in the seminal vesicles of adult rats.

METHODSTwenty-seven male SD rats aged approximately 90 days were randomly divided into a control group (n = 14) and an EDS group (n = 13) to receive one intraperitoneal injection of normal saline and EDS (75 mg/kg bodyweight), respectively. At 7 and 12 days after treatment, the unilateral seminal vesicles were removed, methacrylate resin-embedded sections prepared and the total volumes of various structures in the seminal vesicles estimated using stereological methods.

RESULTSEDS treatment almost completely destroyed the Leydig cells in the testis, resulting in a drastic testosterone deficiency. The volume of the seminal vesicle (including the coagulating gland attached to the vesicle) was decreased by 53% in the 7 d EDS group (n = 6) in comparison with the 7 d control group (n = 7) ([138.2 +/- 12.9] vs [64.9 +/- 3.6] mm3, P < 0.01), but showed no significant difference between the 7 d and the 12 d EDS (n = 7) groups ([64.9 +/- 3.6] vs [55.4 +/- 7.7] mm3, P > 0.05). The total volumes of the glandular lumen, glandular epithelium, smooth muscular layer and adventitia were decreased by 96.7, 80.3, 57.6 and 67.0%, respectively, in the 12 d EDS group as compared with the 12 d control group (n = 7).

CONCLUSIONEDS induces drastic testosterone deficiency in adult rats, and significantly reduces the total volumes of the seminal vesicle lumen, glandular epithelium, smooth muscular layer and adventitia.

Animals ; Leydig Cells ; drug effects ; Male ; Mesylates ; pharmacology ; Organ Size ; drug effects ; Rats ; Rats, Sprague-Dawley ; Seminal Vesicles ; drug effects ; pathology ; Testis ; cytology ; drug effects ; pathology

OBJECTIVETo investigate the pathological changes of major organs in rats that have inhaled methyl ethyl ketone peroxide (MEKP) aerosol and to provide clues to the oxidative damage mechanism of MEKP.

METHODSA total of 100 Sprague-Dawley rats (male-to-female ratio = 1:1) were randomly and equally divided into blank control group, solvent control group, and 50, 500, and 1000 mg/m(3) MEKP exposure groups to inhale clean air, solvent aerosol, or MEKP for 6 h per day, 5 d per week, for 13 weeks. A rat model of subchronic MEKP exposure was established. The clinical manifestations during exposure were recorded. The organ coefficients of the kidney, thymus, and testis were calculated. The histopathological changes of the lung, liver, and testis were observed by HE staining.

RESULTSThe male rats in 1000 mg/m(3) MEKP exposure group had significantly lower organ coefficients of the kidney and testis than those in blank control group, solvent control group, and 50 and 500 mg/m(3) MEKP exposure groups (P < 0.05). The rats in 1000 mg/m(3) MEKP exposure group had a significantly lower organ coefficient of the thymus than those in blank control group and solvent control group (P < 0.05). Some rats in 500 and 1000 mg/m3 MEKP exposure groups had significant damage to the lung, liver, and testis, which demonstrated a worsening trend as the dose increased. Pulmonary hyperinflation, hyperemia, bleeding, interstitial pneumonia, and even lung abscess were seen in the damaged lung. Nuclear enrichment, hepatocyte steatosis, and mild cellular edema in the portal area were seen in the damaged liver. Variable degeneration, necrosis, and dysplasia of spermatogenic cells and significant decrease in sperms in spermatogenic cells were seen in the damaged testis. The female rats in blank control group, solvent control group, and 50, 500, and 1000 mg/m(3) MEKP exposure groups showed no pathological changes in the ovary.

CONCLUSIONInhalation of MEKP aerosol can cause oxidative damage to the liver, lung, kidney, thymus, and testis in rats, particularly to the testis in male rats.

Animals ; Butanones ; administration & dosage ; toxicity ; Female ; Inhalation Exposure ; Kidney ; drug effects ; pathology ; Liver ; drug effects ; pathology ; Lung ; drug effects ; pathology ; Male ; Rats ; Rats, Sprague-Dawley ; Testis ; drug effects ; pathology ; Thymus Gland ; drug effects ; pathology

OBJECTIVETo explore the effects of Di (2-ethylhexyl) phthalate (DEHP) on the testis and testicular gubernaculum of fetal KM mice in vivo and to investigate the mechanism of DEHP-induced cryptorchidism.

METHODSThirty healthy pregnant KM mice were randomly and equally divided into a blank control group, a corn oil control group and a DEHP group. The pregnant mice in the latter group were exposed to DEHP by gavage at the dose of 500 mg/kg body weight per day from gestation day 12 (GD12) through gestation day 19 (GD19). The effects of DEHP were observed on the number of fetuses per pregnancy, the ratio of male to female pups, the weight of the testis, the morphology and location of the testis and gubernaculum, the relative testis-bladder neck distance (TBD) and cranial suspensory ligament (CSL) residual. The expressions of the androgen receptor (AR), estrogen receptor (ER) and actin and proliferating cell nuclear antigen (PCNA) in the gubernaculum were detected by immunohistochemistry.

RESULTSDEHP reduced the testis weight and TBD, induced different degrees of testis maldescent, but produced no obvious effect on the body weight, the number of fetuses per pregnancy, the sex ratio and the testis gubernacular morphology. Under the light microscope, hypotrophy was seen in all the testis seminiferous tubules, spermatogenic cells and Sertoli cells, marked Leydig cell hyperplasia was noted, and the positive expression of AR in the gubernaculum was decreased in the DEHP group (P < 0.01).

CONCLUSIONDEHP could cause dysfunction of the testis gubernaculum via its anti-androgen effect, induce cryptorchidism, and cause dysplasia and dysfunction of Sertoli cells, Leydig cells and spermatogenic cells in fetal mice.

Animals ; Diethylhexyl Phthalate ; pharmacology ; Female ; Fetus ; drug effects ; Leydig Cells ; drug effects ; Male ; Mice ; Mice, Inbred Strains ; Pregnancy ; Sertoli Cells ; drug effects ; Testis ; cytology ; drug effects ; pathology

OBJECTIVETo investigate the effects of neonatal exposure of DNA methylation inhibitor, Cadmium and PCB153 on DNA methylation, apoptosis and spermatogenesis in SD rats.

METHODSNeonatal SD rats were randomly divided into 10 groups and received oral administrations of PCB153 (0.025, 0. 250, 2.500 mg/kg), or Cadmium (1, 2, 4 mg/kg), or positive control 5-Aza-CdR (0.025, 0.250 mg/kg), or vehicle control for five days from PND3. Half of the rats were killed 24 h after the last administration. The remains were fed until 12 weeks. Sperm numbers, apoptosis and DNA methylation levels in testis were investigated.

RESULTSThe daily sperm production was significantly decreased in each neonatal exposed group (P < 0.05). Neonatal rats exposed to 5-Aza-CdR and Cadmium reduced the global DNA methylation level, increased apoptosis, while PCB153 exposure did not significantly change DNA methylation and apoptosis.

CONCLUSIONNeonatal rats exposed to chemicals could reduce spermatogenesis via multiple pathways. Lower DNA methylation and increased neonatal apoptosis were suggested as one of the causes.

Animals ; Animals, Newborn ; Apoptosis ; drug effects ; Cadmium ; toxicity ; DNA Methylation ; drug effects ; Male ; Polychlorinated Biphenyls ; toxicity ; Rats ; Rats, Sprague-Dawley ; Spermatogenesis ; drug effects ; Testis ; drug effects ; metabolism ; pathology

Acrylonitrile ; toxicity ; Animals ; Male ; Mice ; Mice, Inbred Strains ; Testis ; drug effects ; pathology

AIMTo investigate the effect of formaldehyde (FA) on testes and the protective effect of vitamin E (VE) against oxidative damage by FA in the testes of adult rats.

METHODSThirty rats were randomly divided into three groups: (1) control; (2) FA treatment group (FAt); and (3) FAt + VE group. FAt and FAt + VE groups were exposed to FA by inhalation at a concentration of 10 mg/m(3) for 2 weeks. In addition, FAt + VE group were orally administered VE during the 2-week FA treatment. After the treatment, the histopathological and biochemical changes in testes, as well as the quantity and quality of sperm, were observed.

RESULTSThe testicular weight, the quantity and quality of sperm, the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and glutathione (GSH) were significantly decreased whereas the level of malondialdehyde (MDA) was significantly increased in testes of rats in FAt group compared with those in the control group. VE treatment restored these parameters in FAt + VE group. In addition, microscopy with hematoxylin-eosin (HE) staining showed that seminiferous tubules atrophied, seminiferous epithelial cells disintegrated and shed in rats in FAt group and VE treatment significantly improved the testicular structure in FAt + VE group.

CONCLUSIONFA destroys the testicular structure and function in adult rats by inducing oxidative stress, and this damage could be partially reversed by VE.

Animals ; Antioxidants ; pharmacology ; Epididymis ; drug effects ; pathology ; Formaldehyde ; toxicity ; Male ; Oxidative Stress ; drug effects ; physiology ; Rats ; Rats, Sprague-Dawley ; Sperm Count ; Testis ; drug effects ; pathology ; Vitamin E ; pharmacology

OBJECTIVETo determine whether testosterone-induced intra-testicular testosterone withdrawal and therefore spermatogenic impairment is associated with looser arrangement of spermatogenic cells in rats.

METHODSAdult male SD rats received intramuscular injection of testosterone undecanoate at 19 mg/(kg x 15 d) for 130 days, and then testicular tissue blocks were obtained for the preparation of methacrylate resin-embedded sections and observation of the changes in testicular histology.

RESULTSApart from such changes as impaired spermiogenesis and spermiation, apparently looser arrangement of spermatogenic cells was seen in 11.5% of the seminiferous tubule profiles, with radial cracks (empty spaces) running towards the tubule lumen being formed between lines, bundles or groups of spermatogenic cells (mainly spermatids and spermatocytes).

CONCLUSIONLooser arrangement of spermatogenic cells is one of the key histological changes resulting from intra-testicular testosterone withdrawal in rats.

Animals ; Male ; Rats ; Rats, Sprague-Dawley ; Seminiferous Tubules ; cytology ; drug effects ; Spermatogenesis ; drug effects ; Testis ; cytology ; drug effects ; pathology ; Testosterone ; administration & dosage ; adverse effects