Proliferation Of Spermatogenic Cells Research Articles

Gandou Bushen Decoction improves spermatogenesis and promotes spermatogenic cell proliferation in Wilson disease TX mice by activating testicular ERK signaling pathway

To investigate the therapeutic mechanism of Gandou Bushen Decoction (GDBSD) for improving reproductive disorders in male mouse models of Wilson disease (WD). Sixty male homozygous TX mice were randomized equally into 4 groups and treated with daily gavage of saline (WD model group), penicillamine (0.09 g/kg), or GDBSD (0.2 mL/10 g), or with intraperitoneal injection of U0126 (20 mg/kg) in addition to GDBSD gavage, with 15 male DL mice as control. After 4 weeks of treatment, copper content in testicular tissue of the mice was detected, and histopathology of the testes and epididymis was examined using HE staining and electron microscopy. TUNEL staining was used to identify apoptotic cells in the testes. The protein expressions of Bcl-2, Cytc, caspase-3, ERK, and p-ERK in the testicular tissue were evaluated with Western blotting, and BrdU-positive cells were detected with immunohistochemical labeling. Sperm density, viability, malformation rate and fertility levels of male mice were studied. Treatment with penicillamine and GDBSD obviously improved pathological changes of the testis, increased sperm density and motility, lowered sperm abnormality rate, fertility levels and increased testicular JOHNSEN score of TK mice, but the therapeutic effect of GDBSD was blocked by U0126. GDBSD treatment significantly lowered Cytc and caspase-3 expressions and increased Bcl-2 expression in the testicular tissue of TX mice (P < 0.05), while U0126 treatment significantly lowered testicular Bcl-2 expression level. No significant differences were found in total protein expression levels of ERK1/2 among the 5 groups, but p-ERK protein expression was significantly reduced in WD and U0126 groups and increased in penicillamine and GDBSD groups. GDBSD can improve spermatogenesis and enhance fertility of male TX mice with WD possibly by activating the ERK signaling pathway to enhance proliferation and reduce apoptosis of the spermatogenic cells.

Guijiajiao-Lujiaojiao Synergistically Promote Spermatogenesis in Tripterygium Wilfordii Polyglycoside-Induced Oligoasthenozoospermia Rats via PI3K/AKT Signaling Pathway.

Guijiajiao-Lujiaojiao (GL) is a combination of Traditional Chinese Medicine (TCM) that can be used to treat oligoasthenozoospermia (OAS). However, its mechanistic role in OAS needs to be better understood and necessitates more studies. This study was planned to investigate GL's therapeutic effects and its mechanistic role in the tripterygium wilfordii polyglycoside (GTW)-induced OAS rat model. In total, 60 Sprague-Dawley (SD) rats at 8 weeks of age were assigned to six groups: blank (NC), model (GTW), GL low-dose (GL-L, 0.3 g/kg/day), GL medium-dose (GL-M, 0.6 g/kg/day), GL high-dose (GL-H, 1.2 g/kg/day), and GL high-dose + PI3K inhibitor LY294002 (GL-H 1.2 g/kg/day + LY 1.2 mg/kg/day) groups. The model was characterized after 8 weeks to examine sperm concentration and viability, serum hormone levels, testes histopathology, and specific protein markers. The treatment efficacy was evaluated by mRNA and protein expression levels, among other parameters. Compared with the GTW group, the viability and concentration of rat spermatozoa were significantly increased after GL intervention (p < .01). Meanwhile, the serum levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH), and T hormones in rats in the GL-M and GL-H groups were significantly higher than those in the GTW group (p < .05). Furthermore, GL enhanced the proliferation of spermatogenic cells by modulating the PI3K/AKT signaling pathway, increasing and decreasing the levels of Bcl-2 and Bax proteins, respectively. It is concluded that the mechanism by which GL effectively enhanced the spermatogenic function of the GTW-induced OAS model may be attributed to the PI3K/AKT signaling pathway activation and the elevation of serum LH, FSH, and T hormone levels.

Nicotinamide mononucleotide ameliorates ionizing radiation-induced spermatogenic dysfunction in mice by modulating the glycolytic pathway.

Radiotherapy, a common cancer treatment, leads to infertility in male cancer survivors, particularly young and middle-aged patients. Nicotinamide mononucleotide (NMN), a precursor of nicotinamide adenine dinucleotide (NAD +), plays crucial roles in energy metabolism, DNA repair, and gene expression. The purpose of this study is to investigate the protective effects and underlying mechanisms of NMN against ionizing radiation (IR)-induced testicular injury and spermatogenic dysfunction in an adult male mouse model. To assess the effects of NMN, single whole-body γ-ray irradiation is used to induce testicular injury and spermatogenic dysfunction in adult male mice. NMN is orally administered at 500 mg/kg before and after IR exposure. The structural and cellular damage to the testes caused by 5 Gy γ-ray irradiation, as well as the protective effect of NMN on testicular spermatogenic dysfunction, are evaluated. The serum hormone testosterone, LH, and FSH levels, as well as testicular NAD +, lactate, and pyruvate levels, are detected. Furthermore, the expressions of the apoptosis-related genes Bcl-2, Bax, and Caspase-3 and the rate-limiting enzymes HK2, PKM2, and LDHA, which are potentially associated with the mechanism of injury, are examined. The results demonstrate that 5 Gy γ-ray irradiation exposure causes a decrease in the serum testosterone, LH, and FSH levels in adult male mice, as well as in the testicular NAD +, lactate, and pyruvate levels, and causes damage to the testicular structure and cells. Morphometric analysis reveal a decrease in the testis mass, seminiferous tubule diameter, and height of the germinal epithelium. The sperm quantity, motility, and testicular volume are reduced in the 5 Gy group but are restored by NMN supplementation. NMN intervention downregulates the expressions of proapoptotic genes ( Bax and Caspase-3) and upregulates the expression of an antiapoptotic gene ( Bcl- 2). Sertoli cells marker genes ( WT-1, GATA-4, SOX9, and vimentin) and glycolysis rate-limiting enzyme-encoding genes ( HK2, PKM2, LDHA) are significantly upregulated. In summary, NMN has a positive regulatory effect on testicular spermatogenic dysfunction in male mice induced by ionizing radiation. This positive effect is likely achieved by promoting the proliferation of spermatogenic cells and activating glycolytic pathways. These findings suggest that NMN supplementation may be a potential protective strategy to prevent reproductive damage to male subjects from ionizing radiation.

Nicotinamide Mononucleotide Improves Spermatogenic Disorders in Aluminum-Exposed Rats by Modulating the Glycolytic Pathway.

This study aimed to investigate the protective effect of nicotinamide mononucleotide (NMN) on testicular spermatogenesis in aluminum chloride (AlCl3)-exposed rats and to elucidate the potential underlying mechanism. The results indicated that AlCl3-induced testicular damage, leading to reduced sperm quality, increased apoptosis, decreased cell proliferation, and impaired Sertoli cell function in rats. Additionally, glycolytic metabolism was observed to be hindered. However, after NMN treatment, there was a noticeable improvement in testicular damage among the rats, marked by increased sperm quality, reduced apoptosis, enhanced cell proliferation, improved Sertoli cell function, and an activated glycolytic metabolism. The findings of this study suggest that NMN alleviates testicular spermatogenesis impairment induced by AlCl3 exposure through the inhibition of spermatogenic cell apoptosis, promotion of spermatogenic cell proliferation, and activation of glycolytic pathways. The study contributes an experimental foundation for potential future clinical applications of NMN in cases of AlCl3-exposed spermatogenic dysfunction.

GRPR down-regulation inhibits spermatogenesis through Ca2+ mediated by PLCβ/IP3R signaling pathway in long-term formaldehyde-exposed rats.

Formaldehyde (FA), which is known as an air pollutant, has been proven to induce male infertility. However, the underlying mechanism of FA-induced male infertility remains elusive. In this study, 24 male SD rats were exposed to different levels of FA (0, 0.5, 2.46, and 5mg/m3) for eight consecutive weeks. Through HE staining and sperm smear, we observed that FA exposure resulted in spermatogenic injury and the sperm quality decreased in rats. The qRT-PCR and Western blot analysis further revealed that GRPR was down-regulated in testicular tissues of FA-exposed rats as well as primary spermatogenic cells. Meanwhile, ZDOCK uncovered an interaction between GRPR and PLCβ. In addition, the CCK8, Fluo 3-AM and Flow cytometry results showed that FA exposure suppressed the expression of GRPR, PLCβ and IP3R, consequently reducing the Ca2+ concentration in spermatogenic cells, inducing apoptosis and inhibiting proliferation of spermatogenic cells. Moreover, rescue experiments confirmed that promoting GRPR could improve intracellular Ca2+ concentration by upregulating PLCβ and IP3R, partially reducing the apoptosis and promoting the proliferation of FA-treated spermatogenic cells. These findings revealed that GRPR participates in spermatogenesis through Ca2+ mediated by the PLCβ/IP3R signaling pathway in FA-exposed rats.

Prominin-1 deletion results in spermatogenic impairment, sperm morphological defects, and infertility in mice.

Spermatogenesis is a complex process orchestrated by several essential genes. Prominin-1 (Prom1/PROM1) is a gene that is expressed in the testis but with a poorly understood role in spermatogenesis. We used Prom1 knockout (Prom1 KO) mice to assess the role of Prom1 in spermatogenesis. To this end, we performed immunohistochemistry, immunofluorescence, western blotting, β-galactosidase staining, and apoptosis assay. Additionally, we analyzed the morphology of sperm and assessed litter sizes. We observed that PROM1 is localized to the dividing spermatocytes in seminiferous epithelial cells, sperm, and columnar epithelium in the epididymis. In the Prom1 KO testis, an aberrant increase in apoptotic cells and a decrease in proliferating seminiferous epithelial cells were observed. Cellular FLICE-like inhibitory protein (c-FLIP) and extracellular signal-regulated kinase 1/2 (ERK1/2) expression were also significantly decreased in Prom1 KO testis. In addition, a significantly increased number of epididymal spermatozoa with abnormal morphology and less motility was found in Prom1 KO mice. PROM1 maintains spermatogenic cell proliferation and survival via c-FLIP expression in the testis. It is also involved in sperm motility and fertilization potential. The mechanism underlying the effect of Prom1 on sperm morphology and motility remains to be identified.

The potential for nanomaterial toxicity affecting the male reproductive system.

With the development of nanotechnology, nanomaterials offer great advantages in a wide variety of industrial and consumer products, and show promise for biomedical applications. However, with these new products, nanomaterial pollutants may enter the human body to cause adverse health effects, including hazards to the male reproductive system. Nanomaterials can enter the body through inhalation, oral exposure, or intravenous injection, and reach the testis via the blood, penetrate the Sertoli cell barrier, and directly or indirectly elicit toxicopathological changes to the testicles. These may then trigger hormone disorders, inhibit spermatogenic cell proliferation, and induce apoptosis, ultimately leading to a decrease in sperm motility and number, ultimately diminishing male reproductive capacity. This review will discuss the toxicological effects of nanomaterials on the male reproductive system, including inflammation, the impact on the hypothalamic-pituitary-gonadal axis (HPG axis), lipid peroxidation, and free ion release relevant to germ cells, Sertoli cell tight junctions, and the gonadal endocrine system. This article is categorized under: Toxicology and Regulatory Issues in Nanomedicine > Toxicology of Nanomaterials.

Coenzyme Q10 alleviates testicular endocrine and spermatogenic dysfunction induced by high-fat diet in male Wistar rats: Role of adipokines, oxidative stress and MAPK/ERK/JNK pathway.

The current study investigated the possible protective effects of Coenzyme Q10 (Co Q10 ) on rat model of high-fat diet (HFD) induced testicular dysfunction. Thirty male Wistar rats were allocated randomly into three groups: control, HFD, HFD + Co Q10 (75 mg/kg/day) groups. Animals were sacrificed after 3 months and epididymal sperm suspension, blood, and testes were collected for further analysis. In comparison to the untreated HFD group, the Co Q10 treated group revealed significantly increased serum testosterone, adiponectin levels, and decreased LH, FSH, and leptin levels. In addition, HFD resulted in significant increase in testicular oxidative stress (increased MDA, iNOS, NO, XO & decreased catalase, SOD, GSH) and inflammation (increased pJNK/JNK, pERK/ERK, and p-p38MAPK/MAPK), while Co Q10 was effective to ameliorate these changes. In addition, Co Q10 significantly increased sperm count, motility and viability that were markedly deteriorated by HFD. Regarding testicular ultrastructure, seminiferous tubular diameter and epithelium height were reduced in HFD group and Co Q10 significantly improved these testicular changes. Finally, a significant reduction in spermatogenic cell proliferation was detected by PCNA fluorescent expression and Co Q10 significantly reversed this change. In summary, our results indicated that Co Q10 could suppress testicular dysfunction produced by HFD. This protective effect could be attributed to its antioxidant, anti-inflammatory properties and to its effect on adipokines and spermatogenic cell proliferation. So, Co Q10 may be a promising food supplement to protect against testicular dysfunction induced by HFD.

Adipose Mesenchymal Stromal Cell-Derived Exosomes Prevent Testicular Torsion Injury via Activating PI3K/AKT and MAPK/ERK1/2 Pathways.

Adipose mesenchymal stromal cell-derived exosomes (ADSC-Exos) have shown great potential in the treatment of oxidative stress induced by ischemia-reperfusion injury. However, alleviation of testicular torsion injury by ADSC-Exos has not been reported. Therefore, we investigated the protective effect of ADSC-Exos against testicular torsion-detorsion injury. ADSC-Exos were isolated by ultracentrifugation and injected into torsion-detorsion-affected testes of rats. H&E staining and sperm quality were used to evaluate the therapeutic effects of ADSC-Exos, and tissue oxidative stress was measured by determining MDA and SOD levels. In addition, TUNEL staining and immunohistological analysis (Ki67, Cleaved Caspase-3, IL-6, IL-10, CCR7, and CD163) were used to clarify the effects of ADSC-Exos on spermatogenic cell proliferation, apoptosis, and the inflammatory microenvironment in vivo. Possible signaling pathways were predicted using sequencing technology and bioinformatics analysis. The predicted signaling pathways were validated in vitro by assessing the proliferation (EdU assay), migration (transwell assay and scratch test), and apoptosis (flow cytometry, TUNEL staining, and western blotting) of spermatogenic cells. The results showed that ADSC-Exos alleviated testicular torsion-detorsion injury by attenuating oxidative stress and the inflammatory response. In addition, ADSC-Exos promoted the proliferation and migration of spermatogenic cells and inhibited their apoptosis by activating the PI3K/AKT and MAPK/ERK1/2 signaling pathways.

Effect of spermidine on ameliorating spermatogenic disorders in diabetic mice via regulating glycolysis pathway

Diabetes mellitus (DM), a high incidence metabolic disease, is related to the impairment of male spermatogenic function. Spermidine (SPM), one of the biogenic amines, was identified from human seminal plasma and believed to have multiple pharmacological functions. However, there exists little evidence that reported SPM’s effects on moderating diabetic male spermatogenic function. Thus, the objective of this study was to investigate the SPM’s protective effects on testicular spermatogenic function in streptozotocin (STZ)-induced type 1 diabetic mice. Therefore, 40 mature male C57BL/6 J mice were divided into four main groups: the control group (n = 10), the diabetic group (n = 10), the 2.5 mg/kg SPM-treated diabetic group (n = 10) and the 5 mg/kg SPM-treated diabetic group (n = 10), which was given intraperitoneally for 8 weeks. The type 1 diabetic mice model was established by a single intraperitoneal injection of STZ 120 mg/kg. The results showed that, compare to the control group, the body and testis weight, as well the number of sperm were decreased, while the rate of sperm malformation was significantly increased in STZ-induced diabetic mice. Then the testicular morphology was observed, which showed that seminiferous tubule of testis were arranged in mess, the area and diameter of which was decreased, along with downregulated anti-apoptotic factor (Bcl-2) expression, and upregulated pro-apoptotic factor (Bax) expression in the testes. Furthermore, testicular genetic expression levels of Sertoli cells (SCs) markers (WT1, GATA4 and Vimentin) detected that the pathological changes aggravated observably, such as the severity of tubule degeneration increased. Compared to the saline-treated DM mice, SPM treatment markedly improved testicular function, with an increment in the body and testis weight as well as sperm count. Pro-apoptotic factor (Bax) was down-regulated expression with the up-regulated expression of Bcl-2 and suppression of apoptosis in the testes. What’s more, expression of WT1, GATA4, Vimentin and the expressions of glycolytic rate-limiting enzyme genes (HK2, PKM2, LDHA) in diabetic testes were also upregulated by SPM supplement. The evidence derived from this study indicated that the SMP’s positive effect on moderating spermatogenic disorder in T1DM mice’s testis. This positive effect is delivered via promoting spermatogenic cell proliferation and participating in the glycolytic pathway’s activation.

Epimedium protects against dyszoospermia in mice with Pex3 knockout by exerting antioxidant effects and regulating the expression level of P16

Oxidative stress (OS) is one of the primary factors leading to male infertility. Oral administration of antioxidants has thus far been found to significantly improve the quality of human sperm. Therefore, antioxidant treatment has become the consensus among international experts on male infertility. In this study, peroxisomal biogenesis factor 3 (Pex3)-knockout (KO, −/−) mice were used as a model to compare the efficacy of three types of traditional Chinese medicine (TCM) granules (Epimedium [YYH], Cuscuta [TSZ], and Rhodiola [HJT]) for male reproductive function rescue. YYH was revealed to be the best and exerted a rescue effect on Pex3−/− mice with spermatogenesis defects. In addition, YYH prominently reduced ROS levels in the testes, inhibited DNA oxidative damage in spermatogenic cells, promoted the proliferation of spermatogenic cells, and inhibited apoptosis in Pex3−/− male mice. Furthermore, the mechanism by which YYH ameliorated dyszoospermia was confirmed via the establishment of cyclin-dependent kinase inhibitor 2 A (P16Ink4a)-KO mice. Specifically, Pex3−/− mice produced elevated amounts of ROS, which damaged germ cell DNA and further activated the signaling pathway of the cell senescence regulatory protein P16-CDK6, resulting in cell cycle arrest and eventually contributing to spermatogenesis dysfunction. YYH supplementation partially corrected the associated phenotype in gene KO mice by affecting P16 expression levels, thus improving the reproductive outcome to a certain extent.

Expression of cell proliferation regulatory factors bricd5, tnfrsf21, cdk1 correlates with expression of clock gene cry1 in testes of Hu rams during puberty.

Cryptochrome 1 (cry1), the core regulator of the circadian clock, is essential for ontogeny and mammalian reproduction. Unlike in other tissues, the cry1 gene have noncircadian functions in spermatogenesis, which implies the unique role of cry1 gene in the development of testis. The role of cry1 during the puberty has not been described yet. This study aimed to explore the relationship between cry1 expression and spermatogenic cell numbers. We analyzed testicular tissues from Hu sheep aged 0-180days by hematoxylin and eosin staining, measured cry1 and cell proliferation regulatory factors (bricd5, tnfrsf21, cdk1) expression by quantitative real-time PCR and characterized the transcription factor in the 5' flanking region of cry1 gene. The data revealed that the number of spermatocytes and early spermatocytes increased rapidly from 90 to 120 dpp (day postpartum). Correspondingly, there was a marked variation in the cry1 and cell proliferation related genes (bricd5, tnfrsf21, cdk1) mRNA expression in the testes from the age of 90days to 180days (p < 0.05). We also identified some transcription factors (tcfl5) related to cell proliferation. There is a significant causal relationship between the transcription level of cry1 gene in Hu sheep testes and the number of spermatogenic cells. It is speculated that cry1 gene may regulate the proliferation of spermatogenic cells by regulating the expression of cell proliferation related genes such as bricd5, tnfrsf21 and cdk1.

Role of alpha lipoic acid in protecting testes of adult rats from lead toxicity

The current study was conducted to investigate the role of alpha lipoic acid (ALA) against testicular toxicity- induced by lead acetate (PbAc) in rats. Four groups of adult Wistar albino rats (8 for each) were intubated daily for 56 days as follows; control (C)received dislled water; lead acetate at dose of 5mg/kg b.w (T1); ALA at dose of 60mg/kg b.w (T2) and and group T3 received both of PbAc + ALA at the same doses of above. Blood samples were collected at 0, 28 and 56 day of the experiment, then the sera were collected for determination of testosterone(T) and follicular stimulating hormone (FSH). At the end of the experiment, body weight, testes weight and epididymal sperm parameters was studied. Furthermore, histo-morphometric and histopathological study changes were examined. The results revealed a significant decrease in testes weight to body weight ratio, serum testosterone, sperm concentration and motility, diameters of seminiferous tubules, height of seminiferous epithelia and number of Leydig cells, moreover the results showed a significant increase in serum FSH, dead sperm and abnormal sperm morphology in group T1 when compared with the other groups. Comparing to lead acetate treated rats, group T3 showed an improvement at the level of the studied parameters, accompanied with mild congestion in the interstitial tissue with a marked developing proliferation of spermatogenic cells, as well as presence of mature spermatozoa in the seminiferous tubules. In conclusion, subchronic exposure of rats to lead acetate showed an amelioration of all reproductive parameters near to normal values due to the antioxidant effects of ALA and the histological changes of the testes confirmed such change in serum parameters and the beneficial role of ALA.

The role of miR-128-3p through MAPK14 activation in the apoptosis of GC2 spermatocyte cell line following heat stress.

MicroRNAs play a crucial role in the regulation of spermatogenesis. For example, miR-128-3p expression is known to decrease significantly after testicular hyperthermia, but the regulatory effect of this change on the spermatogenesis damage caused by heat stress remains unclear. This study aimed to verify whether the target gene of miR-128-3p is MAPK14, which affects spermatogenic cell proliferation and apoptosis under testicular hyperthermia. Mouse testis and GC2 spermatocyte cell line heat stress models were established. miR-128-3p expression before and after heat stress was analyzed by reverse transcription polymerase chain reaction. MAPK14 and p-MAPK14 expression was detected by Western blot, and cell apoptosis was analyzed by Annexin V-FITC/PI. Subsequently, miR-128-3p inhibitors and mimics were used to interfere with spermatocytes before and after heat stress, respectively, for correlation detection. Compared with the control group, the heat stress group showed decreased miR-128-3p expression, increased p-MAPK14 expression, and decreased cell proliferation activity. In the GC2-spd cell line in vitro, miR-128-3p inhibitors were found to upregulate p-MAPK14 expression, reduce cell proliferation activity, and increase apoptosis, consistent with the results obtained in the heat treatment alone. Furthermore, miR-128-3p mimics transfected in the GC2 cells after heat stress reduced p-MAPK14 expression, alleviated the decrease in cell proliferation, and decreased the apoptosis level. The downregulation of miR-128-3p expression plays an important role in spermatogenesis damages after testicular hyperthermia, which is probably attributable to the activation of the MAPK signaling pathway. Downregulated miR-128-3p expression induces the apoptosis and inhibits the proliferation of spermatogenic cells by promoting MAPK14 phosphorylation.

Effects of Zuogui Wan on testis structure and expression of c-Kit and Oct4 in rats with impaired spermatogenesis

Context Zuogui Wan is a classic traditional Chinese prescription. Preliminary studies have confirmed that it could improve sperm quality significantly. Objective To investigate the effect of Zuogui Wan on testis structure and c-kitproto-oncogeneprotein (c-Kit) and octamer-binding transcription factor-4 (Oct4) expression in a rat model of impaired spermatogenesis. Material and methods Thirty-six Sprague-Dawley (SD) rats were divided into Blank control, Tripterygium glycosides (GTW) and Zuogui Wan groups (n = 12). GTW was used to generate models of impaired spermatogenesis. Then Zuogui Wan group was administered 6 g/kg/d of Zuogui Wan granules for 4 weeks. Changes in the pathological structure and ultrastructure were observed with optical microscope and transmission electron microscope. Expression of c-Kit and Oct4 were quantified by RT qPCR and Western blots. Results Both the pathological damage and the damages in the ultrastructure of spermatogenic epithelium had improved in Zuogui Wan group. Compared with the GTW model group (0.47 ± 0.19; 0.38 ± 0.14), c-Kit and Oct4 protein expression increased in the Zuogui Wan group (0.75 ± 0.27; 0.65 ± 0.23). C-Kit and Oct4 mRNA expression increased in Zuogui Wan group (1.06 ± 0.16; 1.85 ± 1.04) compared to the GTW model group (0.66 ± 0.23; 0.46 ± 0.29). Conclusions Zuogui Wan is capable of restoring the damage to the testis structure and ultrastructure and regulates the expression of c-Kit and Oct4 at protein and mRNA levels, inhibiting apoptosis and promoting proliferation of spermatogenic cells.

Resveratrol attenuates metabolic, sperm, and testicular changes in adult Wistar rats fed a diet rich in lipids and simple carbohydrates

High-fat diets affect male reproduction and sexual function. Therefore, we evaluated the effects of prolonged resveratrol administration on the metabolic, sperm, and testicular parameters of rats fed a cafeteria diet. Male Wistar rats were divided at weaning into control (C, n = 20) and cafeteria (CAF, n = 16) groups. At 3 months, half of them were given daily supplementations of resveratrol (C-R, n = 10; CAF-R, n = 8) at a dosage of 30 mg kg−1 body mass for 2 months. Animals were killed at 5 months of age, and blood, spermatozoa, and testes were collected for further analysis. Data were analyzed by one-way ANOVA, and P < 0.05 was considered statistically significant. The CAF diet promoted hyperglycemia (P < 0.0001), and treatment with resveratrol reversed this condition (P < 0.0001). The CAF diet reduced sperm viability and motility, while resveratrol improved these parameters (P < 0.05). Regarding testicular morphology, the height of the seminiferous epithelium was reduced in the CAF group compared with that of the C group (P = 0.0007). Spermatogenic cell proliferation was also reduced in the CAF group compared with that of the C group. However, the CAF-R showed an increase in cell proliferation rate compared with that of the untreated CAF group (P = 0.0024). Although it did not modify body mass, the consumption of a CAF diet promoted hyperglycemia, adverse testicular morphology remodeling, and abnormal sperm, which were attenuated by treatment with resveratrol, thus suggesting a protective effect of this antioxidant on spermatogenesis.

HISTOLOGICAL AND ENZYME HISTOCHEMICAL STUDIES ON THE TRANSITIONAL

The present work was carried out using twenty mature Epinephelus tauvina (Perciforms: Serranidae) collected from Arabian Gulf coast at Dammam City. Fishes of this species are known to undergo sex change during certain stage of their life cycle. Histological and enzyme histochemical studies were performed on gonads of the collected fishes. The examination of the gonads of E. tauvina revealed the presence of three developmental phases during the sex change process. These were: Female, early transition phase and late transition phase each one may subdivide into two stages. In female phase several developmental stages of the oocytes were recognized. At the beginning of early transition phase perinucleolar mature oocytes began degeneration while late transition phase characterized by rapid proliferation of spermatogenic cells. The histochemical studies demonstrated that alkaline phosphatase enzyme gave intense reaction in granulosa cells of mature oocytes while acid phosphatase gave an intense reaction in the interstitial cells and atretic follicles but ∆5 –3β hydroxysteroid dehydrogenase enzyme gave intense reaction to special cells in capsule of gonads.

HISTOLOGICAL AND ENZYME HISTOCHEMICAL STUDIES ON THE TRANSITIONAL

The present work was carried out using twenty mature Epinephelus tauvina (Perciforms: Serranidae) collected from Arabian Gulf coast at Dammam City. Fishes of this species are known to undergo sex change during certain stage of their life cycle. Histological and enzyme histochemical studies were performed on gonads of the collected fishes. The examination of the gonads of E. tauvina revealed the presence of three developmental phases during the sex change process. These were: Female, early transition phase and late transition phase each one may subdivide into two stages. In female phase several developmental stages of the oocytes were recognized. At the beginning of early transition phase perinucleolar mature oocytes began degeneration while late transition phase characterized by rapid proliferation of spermatogenic cells. The histochemical studies demonstrated that alkaline phosphatase enzyme gave intense reaction in granulosa cells of mature oocytes while acid phosphatase gave an intense reaction in the interstitial cells and atretic follicles but ∆5 –3β hydroxysteroid dehydrogenase enzyme gave intense reaction to special cells in capsule of gonads.

The effect of kisspeptin on spermatogenesis and apoptosis in rats.

To study the effect of kisspeptin, a gonadotropin release stimulator, on the testicular tissue of the rat. Four groups were formed as follows: control, Kiss-10 501397645907nmol administration for 1 day, Kiss-10 administration for 13 days, and one last group kept for 7 days following Kiss-10 applied for 13 days. Testicular tissues were stained with hematoxylin-eosin, periodic acid Schiff, Masson trichrome staining, terminal deoxynucleotidyl transferased UTP nick-end labeling, and Ki-67 immune staining. Serum testosterone levels were determined. Serum testosterone level increased following acute application, while it was reduced by chronic treatment. Spermatogenic cells as stained by Ki-67 and TUNEL increased in the treated groups compared to the controls. Following a 7-day rest after treatment, a decrease in testosterone levels and Ki-67-stained cell numbers and an increase in TUNEL-stained cells were observed. Leydig cells showed increased vacuolization in the Kiss-1 group. Leydig cell vacuolization continued in the Kiss (13) group and was reduced in the Kiss (13 + 7) group. Kiss-10 increased spermatogenic cell proliferation, while testosterone level and proliferation decreased and apoptosis increased during the waiting period.

Long-term imatinib treatment reduces spermatogenic cell proliferation in juvenile rat testes

Long-term imatinib treatment reduces spermatogenic cell proliferation in juvenile rat testes