Elimination of spermatogenic cells via apoptosis occurs spontaneously under normal physiologic conditions and is often aggravated after chemical-induced testicular impairment. A great amount of pollutants is released into the environment by modern industry, and many of these substances have been confirmed possessing reproductive toxicity, which can affect the reproduction and development of organism. These chemicals have been categorized to endocrine disrupting chemicals(EDCs). Studying spermatogenic cell apoptosis induced by EDCs will enrich and expand the pathway to identify EDCs, and will put forward new expounding of its mechanism. It has important meaning in the field of reproduction toxicology and male fertility.
Apoptosis ; Endocrine System ; cytology ; drug effects ; Environmental Pollutants ; toxicity ; Humans ; Male ; Reproduction ; drug effects ; Spermatogenesis ; drug effects

AIMTo further clarify the changes occurred in the testicular capsulotomized rats.

METHODSIn testicular capsulotomized and sham-operated rats, the cross sectional area, the nucleus diameter and the number of Leydig cells were morphologically analyzed by the Vidas Image Processing System connected to a microscope.

RESULTSIn the capsulotomized animals, the cross sectional area of Leydig cells was gradually increased from 30 days onwards. There was no obvious change in the nucleus diameter of Leydig cells. However, The Leydig cell number was significantly increased from day 30 onwards.

CONCLUSIONIn rats, testicular capsulotomy may induce hyperplasia/hypertrophy of Leydig cells in the testis.

Animals ; Cell Count ; Cell Nucleus ; Image Processing, Computer-Assisted ; Leydig Cells ; cytology ; Male ; Rats ; Rats, Sprague-Dawley ; Testis ; cytology

OBJECTIVETo explore the relationship between germ cell apoptosis and the expression as well as the distribution of Sertoli cell vimentin induced by local exposure to heat.

METHODSLocal short-term exposure of prepubertal male rats testis to heat (43 degrees C for 15 min). Histochemical method was used to observe morphological characteristics of seminiferous tubule. The distribution and expression of Sertoli cell cytoskeletons were analyzed by immunohistochemistry and germ cell apoptosis was evaluated by TUNEL technique at different hour-intervals.

RESULTSAfter 2 h and 4 h heat exposure, the disattachment phenomenon between Sertoli cell and spermatogonia occurred. Spermatogonia arranged in disorder and displaced away from the basement membrane of seminiferous tubules. Immunohistochemical staining showed that vimentin positive staining was seen radiating from the Sertoli cell perinuclear region with apical "spoke-like" pattern in controls. There was an intense vimentin immunoreactivity surrounding Sertoli cell nuclei along with the collapse of the apical extensions in 2 h group, but no significant difference compared with the controls. The expressions of vimentin in 12 h and 24 h groups were higher than those of the controls (P <0.01), respectively. TUNEL showed that incidence of apoptosis was observed to increases markedly in 12 h and 24 h groups, but it was found that the incidences of apoptotic events were decreased in these two groups compared with the controls.

CONCLUSIONThe changes of expression and distribution of Sertoli cell vimentin filaments correlate with the increased germ cell apoptosis. Local heat may disrupt spermatogenesis by injuring Sertoli cell directly.

Animals ; Apoptosis ; Hot Temperature ; In Situ Nick-End Labeling ; Male ; Rats ; Rats, Sprague-Dawley ; Sertoli Cells ; metabolism ; Spermatozoa ; pathology ; Vimentin ; biosynthesis

OBJECTIVETo investigate the effects of prepubertal continuous exposure to dibutyl phthalate (DBP) on the testis development in SD rats.

METHODSTwenty-one-day-old weanling prepubertal male SD rats were randomly divided into a control (n = 24) and an experiment group (n = 54), gavaged daily with corn oil vehicle or corn oil + DBP at the repeated dose of 0 mg/(kg x d) (control), 50 mg/(kg x d) (low-dose), 200 mg/(kg x d) (medium-dose) and 600 mg/(kg x d) (high-dose) for 14, 21 and 28 days, and then sacrificed by decapitation on PND35, PND42 and PND49. The body weight gain, the testis weight and volume and the weight of accessory sex organs were measured, the serum testosterone level assayed by chemoluminescence technique, the testis tissues stained by H&E and observed under the light microscope for morphological alteration, the mean diameter of the seminiferous tubules determined and testicular biopsy scores obtained.

RESULTSDisordered arrangement of spermatogenic cells was found in some seminiferous tubules on PND35 in the low-dose group, but testis development and spermatogenesis were normal on PND42 and PND49. In the medium-dose group, disordered arrangement and decreased number of spermatogenic cells were observed on PND35 and PND42, but without testicular atrophy, and various grades of spermatogenic cells and sperm were seen on PND49. High-dose DBP slowed down the body weight gain, decreased serum T levels and induced degeneration of seminiferous tubules, arrest of spermatogenic epithelium development and necrosis of spermatogenic cells. The pubertal rats (PND49) showed testicular atrophy, azoospermia and delayed development of accessory sex organs.

CONCLUSIONPrepubertal continuous exposure to DBP induces damages to testicular development and spermatogenesis in a dose-dependent manner, and those induced by high-dose DBP cannot be recuperated in the phase of prepubertal development, while the slight adverse effects on the testis induced by low- and medium-dose DBP could be completely or partly reversible before PND49.

Animals ; Dibutyl Phthalate ; toxicity ; Environmental Exposure ; Growth ; drug effects ; Male ; Rats ; Rats, Sprague-Dawley ; Testis ; drug effects ; growth & development

The Y chromosome contains genes and gene families that play critical roles in the process of testis determination and differentiation. Male infertility can be induced by many factors, and extensive studies have strongly indicated that Y chromosome microdeletions are closely related to male reproductive dysfunction. Because most of the Y chromosome does not participate in sexual recombination, it has degenerated both in size and gene content, in comparison with the X chromosome. Consequently males may be faced with survival problems in the future. This article reviews the role of the Y chromosome in male infertility and the fate of the male in the future.
Chromosomes, Human, Y ; Humans ; Infertility, Male ; genetics ; Male

Objective To clarify the clinical features,therapeutic strategy and prognosis of lipid storage myopathy (LSM).Methods The clinical data and therapeutic effects of 42 LSM patients were summarized retrospectively.All patients were followed up to evaluate their prognosis.Results Data of short-term therapeutic results of all the 42 patients were available.Thirty-three cases were placed in low- doses prednisone and 9 cases in riboflavin.All patients showed marked and quick improvement of symptoms within one month.Among thirty-two patients followed up for more than one year,26 cases had a full recovery and 6 remained to have intolerance to heavy exercise.Thirteen patients had relapses of muscle weakness in various degrees and most of which were induced by exertion,exposure to coldness and upper respiratory tract infection.In 5 patients the symptoms were recurred for more than one time.Among 13 cases with relapses, 7 had family history.Conclusions Our data suggest that LSM is a treatable disease and well responsive to low-doses prednisone.The disease tends to recur,especially in patients with family history.Glutaric aciduria type Ⅱ should be considered in LSM patients who are responsive well to riboflavin,indicating drug therapeutic strategy for LSM should be based on the etiology of the disease.

OBJECTIVESTo study the effect of testicular local heating on spermatogenic cell apoptosis in rat.

METHODSSeventy male SD rats were divided into heat treatment group (43 degrees C) and control group (22 degrees C). Each group was further divided into seven sub-groups respectively according to the time of 12 hours and 1 days, 3 days, 6 days, 10 days, 50 days and 80 days after testicular local treatment. The spermatogenic cell apoptosis in all sub-groups was examined by means of electron microscopy, flow cytometry and terminal deoxynucleotidyl transferase-mediated dUDP-nick end labeling(TUNEL) method.

RESULTSIn the groups of heat treatment, spermatogenic cell apoptosis was detected by electron microscopy; flow cytometry showed that the percentage of cells with sub-haploid increased(P < 0.01); the percentage of positive TUNEL cells in the heat treatment groups was higher than that in the control group(P < 0.01). Initiation of spermatogenic cell apoptosis after testicular heating was not random but was highly selective.

CONCLUSIONSLocal testicular heating could increase the spermatogenic cell apoptosis. The most sensitive cell is spermatocyte. Spermatid and sperm also display apparent changes. Heating can increase the apoptosis of spermatogonia in a long period.

Animals ; Apoptosis ; Flow Cytometry ; Hot Temperature ; In Situ Nick-End Labeling ; Male ; Microscopy, Electron ; Rats ; Rats, Sprague-Dawley ; Spermatogonia ; cytology ; ultrastructure ; Testis ; pathology ; ultrastructure

OBJECTIVETo investigate the effects of diet-induced obesity on the developmental process of testes in pubertal rats.

METHODSEighty 21-day-old male SD rats were randomly divided into a control group (n=32) and an experiment group (n=48), and fed respectively on a normal diet and a high-fat diet. And changes in the body weight, Lee's index, testis weight and epididymis weight were measured at the end of the 3rd, 4th, 5th and 6th week after the treatment, that is, when the rats were 6, 7, 8 and 9 weeks old. The concentrations of testosterone and estradiol were determined by Access immunoassay system and the morphological alterations in testis development observed by HE staining.

RESULTSThe body weight of the high-fat group obviously increased at the end of the 3rd week (P < 0.05), 26.6% heavier than that of the control by the end of the 6th week (P < 0.01), and Lee's index was also obviously increased (P < 0.01). Compared with the controls, the testicular coefficient declined in the high-fat group at the end of the 5th and 6th week (P < 0.05), plasma TG and TC remarkably increased, the testosterone level obviously decreased (P < 0.05), estradiol concentration lowered at the end of the 3rd, 4th and 5th week but dramatically increased at the 9th, with significant difference between the two groups (P < 0.01). Microscope examination showed that spermatogenic epithelial cells were arranged in disorder, the spermatogenic cell layers reduced and the number of mature sperms reduced.

CONCLUSIONHigh-fat diet can induce nutritional obesity in pubertal rats, which in turn may lead to the underdevelopment of the testis and the abnormal level of gonadal hormones.

Animals ; Body Fat Distribution ; Body Weight ; Diet Fads ; Epididymis ; growth & development ; pathology ; Male ; Obesity ; pathology ; physiopathology ; Organ Size ; Rats ; Rats, Sprague-Dawley ; Testis ; growth & development ; pathology

It has been demonstrated that insulin-like growth factor-1 (IGF-1) stimulates the proliferation and division of cells, facilitates the individual growth and development and regulates the material metabolism. Furthermore, it regulates male reproductive development and testicular endocrine functions. IGF-1 can stimulate the expression of GnRH gene in the hypothalamus of prepubertal male mice. However, it has no effect on or even inhibits GnRH gene expression in adult mice. IGF-1 may influence the growth, maturation and differentiation of GnRH neurons. It also accelerates LH and FSH secretion in hypophysis. IGF-1, produced locally in the testis and combined with its specific receptor, can regulate the proliferation and differentiation of adult Leydig cells, cause Sertoli cells to play different functions and control the biosynthesis of testicular hormones.
Animals ; Gene Expression Regulation ; Gonadotropin-Releasing Hormone ; biosynthesis ; Hypothalamo-Hypophyseal System ; metabolism ; physiology ; Insulin-Like Growth Factor I ; physiology ; Leydig Cells ; physiology ; Male ; Mice ; Sertoli Cells ; physiology ; Testis ; metabolism ; physiology

OBJECTIVETo establish the rat model of estradiol valerate medication in early pregnancy, and to investigate the effects of estradiol valerate on the development of the reproductive system of the first filial generation (F1) male rats by evaluating the anogenital distance (AGD) and the development of the testis and epididymis.

METHODSPregnant SD rats were divided at random into a blank control group and a low dose, a medium dose and a high dose medication group to receive intragastric estradiol valerate at 0.2 mg/kg, 0.5 mg/kg and 0.8 mg/kg, respectively. The newborn F1 male rats were normally fed. Their anogenital distances were measured on postnatal day (PND) 3 and 21, the organ coefficients of the testis and epididymis (testicular and epididymal weight g/body weight 100 g) were obtained on PND 60, the morphological changes of spermatogenic cells were observed by testis biopsy, and the diameter of the seminiferous tubule and epithelial height were measured.

RESULTSThere was no significant difference between the control and medicated F1 male rats in AGD on PND 3 and 21 (P > 0.05), nor in the organ coefficients of the testis and epididymis on PND 60 (P > 0.05), nor in the diameter of the seminiferous tubule and epithelial height.

CONCLUSIONMedication of estradiol valerate (0.2 -0.8 mg/kg) to rats in early pregnancy neither significantly affects the reproductive system development, nor induces obvious histological changes of the testis in the sexual maturation period of their F1 males.

Animals ; Estradiol ; analogs & derivatives ; pharmacology ; Female ; Male ; Maternal Exposure ; Pregnancy ; Rats ; Rats, Sprague-Dawley ; Sexual Maturation ; drug effects ; Testis ; drug effects ; growth & development