Polychlorinated biphenyls (PCBs) are a class of persistent organic pollutants with estrogen-like effects that exist widely in the environment, and its male reproductive toxicity is arousing more and more attention. Studies indicate that different types of cells in the testis respond differently to PCBs exposure. This article presents an overview on the toxicity of PCBs to testicular germ cells, Leydig cells, Sertoli cells and male offspring. We suggest that deeper studies focus on the mechanism of PCBs according to the results of investigations on male reproductive epidemiology. An insight into the intercellular junctions of Sertoli cells might produce a breakthrough in the studies of the testicular toxicity of PCBs.
Animals ; Leydig Cells ; drug effects ; Male ; Polychlorinated Biphenyls ; toxicity ; Sertoli Cells ; drug effects ; Testis ; drug effects

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

This paper summarizes the research progress of reproductive toxicity of Tripterygium wilfordii from 1979,and the toxicity characterization,damage mechanism,and attenuated measures are summarized. It was found that,the reproductive toxicity caused by T. wilfordii is mainly distributed on components of Tripterygium glycosides,triptolide,tripchlorolide,and clinically preparations,such as Leigongteng Tablets and Tripterygium Glycosides Tablets. Adverse reactions to male reproductive system caused by Tripterygium preparations mainly include decreased sperm motility,oligospermia or spermatozoa,decreased fertility or infertility,etc. Long-term drug use may also lead to testicular atrophy and decreased sexual desire. Adverse reactions to women are mainly manifested as menstrual disorders,decreased menstrual volume or even amenorrhea,decreased sexual desire,infertility,etc. The reproductive toxicity of T. wilfordii is related to apoptosis of reproductive cells,disturbance of spermatogenesis or oogenesis,damage of testis and ovary in reproductive target tissues,and changes of internal environment in gonad tissues( hormones,hormone synthesis rate-limiting enzymes and energy metabolism). Drug compatibility,hormone replacement,medication duration and dosage form changes can help reduce the damage of T. wilfordii to the reproductive system. In addition,in view of the existing problems in the current study,the author proposes new directions in clinical studies,pharmacological metabolism mechanism,preparation quality standards and new therapeutic effects,etc.,to provide a basis for the safe and reasonable clinical application of T. wilfordii.
Drugs, Chinese Herbal ; toxicity ; Female ; Genitalia ; drug effects ; Humans ; Male ; Ovary ; drug effects ; Testis ; drug effects ; Tripterygium ; toxicity

OBJECTIVETo evaluate effects of cypermethrin on the testis histology and testosterone, LH and FSH in adult male Sprague-Dawley rats.

METHODSThe intact adult male rats were randomly divided into five groups and were treated with cypermethrin at doses of 0, 7.5, 15, 30, or 60 mg/kg per day by oral gavage for 15-days. After the treatments, serum was collected for hormone assays. The testes, epididymides, seminal vesicles, and prostates were excised and weighed. The right testis was frozen for daily sperm production and the left one was processed for histopathology.

RESULTSDaily sperm production decreased significantly in 30 and 60 mg/(kg•day) groups. Testicular structure abnormalities included atrophic and distorted seminiferous tubules, deformed and disordered arrangement of germ cells, reduced germ cells, Sertoli cells and Leydig cells, vacuolization and multinucleated formations of spermatids in the cypermethrin-treated rats. Vacuolization was found in Sertoli cells and the deformed nucleus was noted in Leydig cells. Serum testosterone reduced significantly in 30 and 60 mg/(kg•day) groups. Serum FSH increased significantly in 60 mg/(kg•day) group.

CONCLUSIONCypermethrin induces impairments of the seminiferous tubules structure and spermatogenesis in the rats. The damages of the male reproductive system may be attributed to the imbalance of circulating testosterone.

Animals ; Epididymis ; drug effects ; Male ; Prostate ; drug effects ; Pyrethrins ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Seminal Vesicles ; drug effects ; Spermatogenesis ; drug effects ; Testis ; drug effects ; Testosterone ; blood

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

Animals ; Dose-Response Relationship, Drug ; Hydroxylamine ; toxicity ; Male ; Rats ; Rats, Wistar ; Spermatozoa ; drug effects ; Testis ; cytology ; drug effects

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

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 Anthocyanin (Ay) on Cadmium-Induced Mouse testis Damage.

METHODSMouse testis damage model were constructed and testis malonaldehyde (MDA) and protein carbonxyl content (PCO), as well as catalase (CAT) and superoxide dismutase (SOD) were determined.

RESULTSThe intoxication of cadmium can cause the increase of MDA and PCO content in mouse testis (P < 0.05), however, the activities of SOD and CAT were altered (P < 0.01).

CONCLUSIONAy have the strong potent to scavenge free radicals, owing to its special chemical structures, and act as a protector to inhibit the oxidative stress induced by cadmium.

Animals ; Anthocyanins ; chemistry ; pharmacology ; Cadmium ; toxicity ; Catalase ; drug effects ; Male ; Malondialdehyde ; analysis ; Mice ; Oxidative Stress ; Protein Carbonylation ; drug effects ; Superoxide Dismutase ; drug effects ; Testis ; drug effects

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