AIMto investigate the effects of crude garlic on adult male rat reproductive functions.

METHODSThirty male rats were divided into five groups: group 1 (untreated) and groups 2, 3, 4 and 5 were fed for 30 days with 5%, 10%, 15% and 30% crude garlic, respectively. Testes and accessory organs were weighed and some markers were assessed. Light and electron microscopy observations were also performed.

RESULTSA significant decrease was observed in the body weight of groups 4 (14%; P < 0.01) and 5 (20%; P < 0.01); of the prostate weight in group 5 (29.1%; P < 0.05) and of seminal vesicle weight in groups 3 (14.4%; P < 0.01), 4 (18.3%; P < 0.01) and 5 (27.3%; P < 0.01). In contrast, testis and epididymis weights were unchanged. In epididymis tissue, the alpha glucosidase activity and the spermatozoa density were unchanged. The treatment resulted in a significant decrease in testosterone serum levels in groups 3 (77.3%; P < 0.01), 4 (77.3%; P < 0.01) and 5 (90.9%; P < 0.01), associated with a significant increase in LH serum levels (P < 0.01). Testicular histology showed a dose-dependent increase in the percentage of empty seminiferous tubules. Moreover, testicular function was affected; a significant decrease in phosphatase acid activity (P < 0.01) and testosterone (P < 0.05) contents were observed.

CONCLUSIONCrude garlic consumption during 1 month reduced testosterone secretion and altered spermatogenesis at 10%, 15% and 30% doses.

Animals ; Dose-Response Relationship, Drug ; Epididymis ; drug effects ; physiology ; Garlic ; adverse effects ; Leydig Cells ; drug effects ; physiology ; Luteinizing Hormone ; blood ; Male ; Plant Preparations ; pharmacology ; Prostate ; drug effects ; physiology ; Rats ; Rats, Wistar ; Reproduction ; drug effects ; physiology ; Seminal Vesicles ; drug effects ; physiology ; Sertoli Cells ; drug effects ; physiology ; Sperm Count ; Spermatogenesis ; drug effects ; physiology ; Testis ; cytology ; drug effects ; metabolism ; Testosterone ; blood

Animals ; Dose-Response Relationship, Drug ; Male ; Mice ; Mice, Inbred Strains ; Nickel ; toxicity ; Oxidative Stress ; physiology ; Testis ; drug effects ; metabolism

AIMTo evaluate the effect of oxidative stress on the spermatogenesis and lactate dehydrogenase-X (LDH-X) activity in mouse testis.

METHODSFor creating different levels of oxidative stress in mice, three selenium (Se) level diets were fed in separate groups for 8 weeks. Group 1 animals were fed yeast-based Se-deficient (0.02 ppm) diet. Group 2 and Group 3 animals were fed with the same diet supplemented with 0.2 ppm and 1 ppm Se as sodium selenite, respectively. After 8 weeks, biochemical and histopathological observations of the testis were carried out. LDH-X levels in the testis were analyzed by western immunoblot and ELISA.

RESULTSA significant decrease in testis Se level was observed in Group 1 animals, whereas it was enhanced in Group 3 as compared to Group 2. The glutathione peroxidase (GSH-Px) activity was significantly reduced in both the liver and testis in Group 1, but not in Group 2 and 3. A significant increase in the testis glutathione-S-transferase (GST) activity was observed in Group 1, whereas no significant change was seen in Groups 2 and 3. Histological analysis of testis revealed a normal structure in Group 2. A significant decrease in the germ cell population in Group 1 was observed as compared to Group 2 with the spermatids and mature sperm affected the most. Decrease in the lumen size was also observed. In the Se-excess group (Group 3), displacement of germ cell population was observed. Further, a decrease in the LDH-X level in testis was observed in Group 1.

CONCLUSIONExcessive oxidative stress in the Se deficient group, as indicated by changes in the GSH-Px/GST activity, affects the spermatogenic process with a reduction in mature sperm and in turn the LDH-X level.

Animals ; Diet ; Glutathione Transferase ; metabolism ; Isoenzymes ; drug effects ; metabolism ; L-Lactate Dehydrogenase ; drug effects ; metabolism ; Male ; Mice ; Mice, Inbred BALB C ; Oxidative Stress ; drug effects ; physiology ; Selenium ; deficiency ; pharmacokinetics ; pharmacology ; Spermatogenesis ; physiology ; Testis ; drug effects ; enzymology ; pathology ; physiology

The testicular gubernaculum plays an important role in testicular descent and development. Its differentiation and development are affected by many factors. Androgens, calcitonin gene-related peptide (CGRP), insulin-like factor 3 (INSL3), Müllerian inhibiting substance (MIS), epidermal growth factor (EGF) and environmental estrogens (EEs) are involved in gubernacular development. The effect of CGRP, INSL3 and especially EEs on genital system has been attracted more attention.
Animals ; Calcitonin Gene-Related Peptide ; physiology ; Estrogens ; pharmacology ; Humans ; Insulin ; physiology ; Male ; Mice ; Proteins ; physiology ; Rats ; Testis ; drug effects ; embryology ; physiology

OBJECTIVETo study the influence of lipopolysaccharide (LPS)-induced inflammation on the testicular histology and reproductive endocrine function in male rats and investigate the possible mechanism of inflammation affecting male fertility.

METHODSThirty-six male SD rats were randomly divided into a control group (A) and three LPS intervention groups (B, C, and D) to receive saline and LPS (5 mg/kg i. p, once), respectively. The animals in groups B, C, and D were killed by anesthesia at 12, 24, and 72 hours after treatment. Histopathological changes in the left testis of the rats were observed by HE staining and the levels of the reproductive hormones T, FSH, and LH in the serum were determined by ELISA.

RESULTSCompared with group B, group A showed clear structure of seminiferous tubules, orderly arrangement of spermatogenic cells, a slightly decreased number of sperm in some seminiferous tubular lumens, and shed spermatogenic cells in the rat testis tissue; group C exhibited thinner seminiferous epithelia, disordered structure of seminiferous tubules, irregular arrangement of spermatogenic cells, decreased number of mature sperm and obvious shedding of spermatogenic cells in seminiferous tubular lumens; group D manifested similar findings to those of group C, with even more shed spermatogenic cells that blocked the tubular lumens. The levels of serum T, LH, and FSH were (0.490 +/- 0.028) ng/ml, (6.290 +/- 0.515) ng/L, and (1.837 +/- 0.127) IU/L in group A, (0.460 +/- 0.024) ng/ml, (5.881 +/- 0.124) ng/L, and (1.707 +/- 0.098) IU/L in group B, (0.417 +/- 0.021) ng/ml, (5.123 +/- 0.271) ng/L, and (1.620 +/- 0.115) IU/L in group C, and (0.378 +/- 0.021) ng/ml, (4.504 +/- 0.279) ng/L and (1.562 +/- 0.216) IU/L in group D, all decreased in group B as compared with A (P > 0.05). The decreases of T and LH were extremely significant (P < 0.01) and that of FSH was significant in groups C and D (P < 0.05) in comparison with A.

CONCLUSIONLPS-induced inflammation affects the testicular tissue and reproductive endocrine function of male rats, resulting in decreased levels of serum T, LH, and FSH.

Animals ; Endocrine System ; drug effects ; physiology ; Fertility ; drug effects ; physiology ; Follicle Stimulating Hormone ; blood ; Humans ; Lipopolysaccharides ; toxicity ; Luteinizing Hormone ; blood ; Male ; Random Allocation ; Rats ; Reproduction ; Seminiferous Tubules ; drug effects ; pathology ; Spermatocytes ; drug effects ; Testis ; drug effects ; pathology ; Testosterone ; blood

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 quantitatively evaluate the murine model of spermatogenesis regeneration induced by two-dose busulfan injection.

METHODSFifty-four male mice were randomly divided into a control and two model groups of equal number, the former treated by two-dose intraperitoneal injection of 50% DMSO solution at 10 ml/kg, and the latter by that of busulfan at 10 mg/kg and 15 mg/kg respectively to establish spermatogenesis regeneration models, both at the interval of 24 days between the two doses. Spermatogenesis in seminiferous epithelia was evaluated by Johnsen score, and the expressions of GATA-4 and GDNF mRNA in Sertoli cells were detected by real time quantitative PCR at 3, 4 and 8 weeks after the treatment.

RESULTSJohnsen score kept stable in the control group at all stages (P > 0.05), but higher than in the model groups at 3 and 4 weeks (P < 0.01). It was lower in the 15 mg/kg than in the 10 mg/kg model group at 4 and 8 weeks (P < 0.01) , and than in the control group at 8 weeks (P < 0.05), but had no significant difference between the 10 mg/kg and the control groups (P > 0.05). Nor did the expression of GATA-4 mRNA in Sertoli cells show any significant difference among the three groups at different stages after the treatment (P > 0.05), and that of GDNF mRNA at different stages in the control group (P > 0.05). Compared with the controls, the level of GDNF mRNA in Sertoli cells was significantly higher at 3 weeks but lower at 4 weeks in the model groups (P < 0.01), and lower in the 15 mg/kg group (P < 0.01) and comparable in the 10 mg/kg group at 8 weeks (P > 0.05); and it was lower in the 15 mg/kg than in the 10 mg/kg group at all stages (P < 0.01).

CONCLUSIONTwo-dose intraperitoneal injection of 10 mg/kg busulfan at the interval of 24 days is an optimal option for the establishment of a murine model of spermatogenesis regeneration. Higher dose of busulfan may induce deficient expression of GDNF in Sertoli cells and result in incomplete restoration of spermatogenesis.

Animals ; Busulfan ; adverse effects ; Glial Cell Line-Derived Neurotrophic Factor ; metabolism ; Male ; Mice ; Mice, Inbred Strains ; Models, Animal ; RNA, Messenger ; Regeneration ; drug effects ; Sertoli Cells ; drug effects ; Spermatogenesis ; drug effects ; Spermatozoa ; physiology ; Testis ; drug effects ; physiology

Both dimethyl methylphosphonate (DMMP) and trimethylphosphate (TMP) are organophosphorous compounds that can evoke sterility in male rodents. The following studies examined the pathology of reproductive organ, especially on the testis, by light microscopy after treatment with both agents. Adult male rats were treated per oral with DMMP, 1,750 mg/Kg, for up to 12 weeks and per oral with TMP, 400 mg/Kg for up to 5 weeks. After 5 weeks of treatment with DMMP there were occasional multinucleated giant cells composed of late spermatids in stages X, XI, XII as well as cytoplasmic vacuolation of Sertoli cell. Anachronistic spermiations were seldom, if ever, seen throughout the experiment. After 7 weeks of DMMP those were markedly diminished. The overall changes after treatment with TMP are somewhat similar to those treated with DMMP. The major changes were composed of aggregate of multinucleated giant cells and maturation arrest at spermatid level, which appear immediately after administration of TMP. The peak frequency in the emergence of multinucleated giant cells in treatment with TMP was noted just a week after treatment, but afterwards declined. Maturation arrest was prominent after 3 weeks in the cases treated with TMP.
Animal ; Comparative Study ; Male ; Organophosphorus Compounds/*toxicity ; Phosphoric Acid Esters/*toxicity ; Rats ; Rats, Sprague-Dawley ; Spermatogenesis/*drug effects ; Support, Non-U.S. Gov't ; Testis/*drug effects/physiology

OBJECTIVETo investigate the drag-reducing effect of polyethylene oxide (PEO) on the velocity of red blood cells in rat cremaster microcirculation.

METHODSBlood samples were collected from 6 Wistar male rats (100-110 g) via the post-orbital venous plexus. The red blood cells were separated by centrifugation and labeled by fluorescinisothiocyate (FITC). After successful establishment of cremaster model, the labeled red blood cells were injected into the jugular vein, and the microcirculation was observed and recorded under fluorescence microscope. The hemodynamic parameters and microcirculation video was recorded every 4 min since 4 min before PEO or normal saline injection. Both PEO (10 ppm) and normal saline was injected into the same rat in random sequence at a constant rate of 3.5 ml/h for 20 min followed by observation for another 20 min. The velocity of the labeled-red blood cells was determined by IPP 6.0 software.

RESULTSCompared with normal saline, PEO significantly increased the velocity of the red blood cells in the rat cremaster microcirculation (498.7-/+182.89 microm/s vs 773.54-/+308.27 microm/s, P=0.012). No significant changes in the heart rate and arterial blood pressure were observed during the experiment (P=0.836, P=0.420).

CONCLUSIONPEO at an extremely low concentration can significantly increase the velocity of the red blood cells in rat cremaster microcirculation and produces no significant impact on heart rate and arterial blood pressure.

Animals ; Blood Flow Velocity ; drug effects ; Male ; Microcirculation ; drug effects ; physiology ; Muscle, Smooth ; blood supply ; Polyethylene Glycols ; pharmacology ; Rats ; Rats, Wistar ; Testis

AIMTo assess proliferative and apoptotic potential of the seminiferous epithelium cells in relation to Sertoli cell maturation in newborn rats under the influence of estradiol, follicle stimulating hormone (FSH) or both agents given together.

METHODSFrom postnatal day (PND) 5 to 15 male rats were daily injected with 12.5 microg of 17beta-estradiol benzoate (EB) or 7.5 IU of human purified FSH (hFSH) or EB + hFSH or solvents (control). On postnatal day 16, autopsy was performed. Sertoli cell maturation/function was assessed by morphometry. Proliferation of the seminiferous epithelium cells was quantitatively evaluated using immunohistochemical labeling against proliferating cell nuclear antigen and apoptosis using the TUNEL method.

RESULTSAlthough EB inhibited Sertoli cell maturation and hFSH was not effective, a pronounced acceleration of Sertoli cell maturation occurred after EB + hFSH. Whereas hFSH stimulated Sertoli cell proliferation, EB or EB + hFSH inhibited Sertoli cell proliferation. All treatments significantly stimulated germ cell proliferation. Apoptosis of Sertoli cells increased 9-fold and germ cells 2-fold after EB, and was not affected by hFSH but was inhibited after EB + hFSH.

CONCLUSIONAt puberty, estradiol inhibits Sertoli cell maturation, increases Sertoli and germ cell apoptosis but stimulates germ cell proliferation. Estradiol in synergism with FSH, but neither of the hormones alone, accelerates Sertoli cell maturation associated with an increase in germ cell survival. Estradiol and FSH cooperate to induce seminal tubule maturation and trigger first spermatogenesis.

Animals ; Animals, Newborn ; Apoptosis ; drug effects ; Cell Differentiation ; drug effects ; Cell Proliferation ; drug effects ; Dose-Response Relationship, Drug ; Estradiol ; pharmacology ; Follicle Stimulating Hormone ; pharmacology ; Male ; Rats ; Rats, Wistar ; Seminiferous Tubules ; cytology ; drug effects ; Sexual Maturation ; drug effects ; physiology ; Spermatogenesis ; drug effects ; physiology ; Spermatozoa ; cytology ; drug effects ; Testis ; cytology ; drug effects