Decreased Sperm Count Research Articles

Signs of ROS-Associated Autophagy in Testis and Sperm in a Rat Model of Varicocele.

Since autophagy was suspected to occur in the pathological situation of varicocele (VCL), we have attempted to confirm it here using a surgical model of varicocele-induced rats. Thirty Wistar rats were divided into three groups (varicocele/sham/control) and analyzed two months after the induction of varicocele. Testicular tissue sections and epididymal mature sperm were then monitored for classic features of varicocele, including disturbance of spermatogenesis, impaired testicular carbohydrate and lipid homeostasis, decreased sperm count, increased sperm nuclear immaturity and DNA damage, oxidative stress, and lipid peroxidation. At the same time, we evaluated the Atg7 protein content and LC3-II/LC3-1 protein ratio in testis and mature sperm cells, two typical markers of early and late cellular autophagy, respectively. We report here that testis and mature sperm show higher signs of autophagy in the varicocele group than in the control and sham groups, probably to try to mitigate the consequences of VCL on the testis and germ cells.

Resistin Changes Following Aerobic Exercise and its Relationship With Fertility in Male Rats With Type 2 Diabetes

Aims Resistin is secreted by adipose tissue and could be the link between diabetes and infertility. This study aimed to investigate the alteration of resistin following aerobic exercise training in diabetic rats and its possible interaction with sperm parameters. Methods & Materials In this experimental study, 30 male Wistar rats (age: 56 days, weight: 200-250g) were randomly divided equally into three groups of healthy control, diabetic control, and diabetic aerobic exercises. Diabetes was induced with a unique intraperitoneal injection (65 mg/kg body weight) of streptozotocin. Seven days after the injection and after 12 hours of fasting, the animals with blood glucose levels of ≥250 mg/dL were considered diabetic. Seven days after the induction of diabetes, the animals in the exercise group were subjected to progressive aerobic training (treadmill running for 1 h, 27 m/min, 5 d/wk). After 10 weeks of exercise, the sperm quality and resistin concentrations were measured. The obtained data were compared using Analysis of Variance (ANOVA) (P<0.05). Findings The induction of diabetes significantly decreased sperm count (P=0.001), motility (P=0.001), viability (P=0.001), and morphology (P=0.01). The sperm parameters, such as count (P=0.03) and viability (P=0.002) were significantly higher in the diabetic exercise group, compared to the diabetic sedentary group. No significant changes were found in resistin levels between diabetic exercise and diabetic sedentary groups (P=0.40). Conclusion The collected results indicated that the 10-week aerobic training regimen improved sperm quality, independent of changes in resistin levels, in type 2 diabetes mellitus rat models.

Protective effects of Equisetum arvense methanolic extract on sperm characteristics and in vitro fertilization potential in experimental diabetic mice: An experimental study.

BackgroundDiabetes mellitus is a metabolic disorder characterized by impaired insulin secretion or the inability of tissues to respond to insulin. This disease can damage the testis and reduce semen quality. Therefore, it can impair the potential for male fertility. Different herbal therapeutic treatments have been used to control diabetes and its complications.ObjectiveThis study aimed to evaluate the effects of streptozotocin-induced diabetes on sperm and in vitro fertilization (IVF) potential and investigate the protective effects of Equisetum arvense methanolic extract on diabetic mice.Materials and MethodsTwenty-four adult male mice were divided into four groups: control-sham, diabetic, diabetic + Equisetum extract (250 mg/kg), and diabetic + Equisetum extract (500 mg/kg). After 45 days, sperm samples were collected from the cauda epididymis to evaluate the characteristics of sperm (including viability, count, motility, morphology and chromatin/DNA integrity of sperm) and the IVF potential.ResultsSperm motility and viability were increased remarkably (p 0.001) in the treated groups compared with the non-treated diabetic group. The decrease in sperm count in the diabetic group compared with the treated groups was not significant. Moreover, the percentage of sperm with DNA damage, nuclear immaturity, and abnormal morphology was decreased significantly (p 0.001) in the treated groups compared with the diabetic group. The treated animals exhibited remarkably higher fertilization rates and a higher percentage of fertilized oocytes that developed toward the blastocyst stage compared with the non-treated diabetic group (p 0.001).ConclusionThe methanolic extract of the Equisetum arvense inhibited diabetes-induced detrimental effects on sperm quality and fertilization rate, which may have been associated with hypoglycemic and antioxidative activities in this plant.

Cytogenetic and Biochemical Changes Induced by Bisphenol A on Testis of Albino Rats and Possible Protection of Black Seed Oil.

Background: Bisphenol A (BPA), an estrogenic compound, is one of the world’s highest production volume chemicals used in polycarbonate plastics in many consumer products and epoxy resins lining food containers. BPA is known to have toxic effects on various systems in man and animals. The aim of this study was to evaluate the cytogenetic and biochemical changes induced by BPA on testis of albino rats and the possible protective effect of black seed oil. Materials and Methods: This study was carried out on (80 rats), divided into four groups (20 rats each). Group I: negative control Group II: received black seed oil (2ml/ kg b w), Group III: administered BPA (25mg/ kg b w), Group IV: administered BPA + black seed oil same as previous doses. Blood, testis and epididymis were collected for biochemical and cytogenetic evaluation. Results: BPA caused a significant decrease in sperm count, total content of DNA, RNA and Protein in the testis, while, significant increase of DNA damage of spermatocyte, head and tail abnormalities compared with control. Co-administration of BPA+ black seed oil resulted in significant improvement of sperm count, total content of DNA, RNA and Protein with significant decrease in DNA damage of spermatocyte and head and tail abnormalities compared to BPA group. Also, BPA group showed a significant decrease in serum testosterone and catalase levels, while, a significant increased super oxide dismutase (SOD) compared to control. However, BPA + black seed oil group showed significant improvement of serum testosterone, catalase and (SOD) levels compared to BPA group. Conclusion: Exposure of rats to BPA resulted in reproductive toxicity through inducing a significant DNA damage and impaired synthesis of DNA, RNA and protein in testicular tissue. Black seed oil attenuate oxidative damage in rat testis via upregulating the activities of enzymatic antioxidants Catalase and SOD.

Effects of particulate matter exposure on semen quality: A retrospective cohort study.

Particulate matter (PM) exposure is closely associated with male infertility. Even though an association between poor semen quality and PM exposure has been widely accepted, which and when the semen parameter could be affected are still controversial. The purpose of this study is to estimate the effects of PM exposure on semen quality in Huai'an, China. The study included 1955 men with 2073 semen samples between 2015 and 2017 with moderate to high exposure to air pollution in Huai'an, China. Three multivariable linear regression models were used to conduct exposure-response analyses for PM exposure and semen quality and to estimate the influence during different exposure periods by every 15 days period before ejaculation in all participants group and normal semen quality participants group. The average age of the observations was 28.9±5.4 old years and the average abstinence period was 4.2±1.5 days. The results showed high correlations between both PM2.5 and PM10 exposures throughout entire spermatogenesis and the declines of sperm count (β: -0.93, p<2×10-16 and β: -1.00, p<2×10-16), and sperm concentration (β: -1.00, p<2×10-16 and β: -1.06, p<2×10-16), and PM10 exposure decreased sperm total motility (β: -0.60, p=2.56×10-7), but not sperm progressive motility. Furthermore, PM2.5 exposure decreased sperm count and concentration during 15-75 lag days, and PM10 exposure showed significant association with sperm count and concentration during 0-75 lag days. PM2.5 and PM10 exposures during 45-59 lag days were both inversely associated with sperm total motility (all p value<0.05). The present study revealed that ambient PM exposure throughout spermatogenesis during a long period, especially at early and middle stage were adversely associated with semen quality, sperm count and sperm concentration in particular.

Risk Assessment of Cosmetics Using Triclosan on Future Generation's Germ Cell Maturation via Lactating Mother Rats.

Triclosan (TCS) is a widely used chemical in personal care and household products as an antimicrobial agent but some studies have reported it as being estrogenic. We investigated the influence of TCS on the male reproductive system of postnatal pups. Lactating mother rats (Rattus norvegicus) were given daily doses of 0 mg, 3 mg, and 5 mg/kg/day from the day of delivery until 28 days, equivalent to their natural breastfeeding duration. At 28 days, the male pups of all three groups were sacrificed and their biochemical parameters evaluated. TCS-treated pups had decreased mRNA levels for 3β hydro-hydroxysteroid dehydrogenases (3βHSD), OCT3/4, and androgen receptor (AR) (p < 0.05). The higher dose (5 mg/kg/day) male pups exhibited more significantly affected germ cell maturation and decreased body weight. In summary, TCS-treated lactating mothers passed the deleterious effects to their untreated male pups as exhibited by reduced androgens synthesis and subsequently decreased sperm count.

Investigation the Anti-Sterility Role of Ubiquinone-10 Against Procarbazine-Induced Infertility in Male Rats

Procarbazineis cytotoxic chemotherapy drug with obvious deleterious effects on male fertility. The present study aimed to investigate protective method via co-administration of Ubiquinone-10 with procarbazine to reduce harmful effects of procarbazine. Twenty- eight adult healthy male rats (3 months in age and weighing 250-300g) were randomly divided into four equal groups as following: animals of first group were received propylene glycol 20% orally and phosphate-buffered saline solution (PBS) intraperitoneally as control group while of second , third and fourth group were received procarbazine (30mg/ kg), Ubiqunone-10 (10 mg/kg) and combination of Ubiqunone-10 with procarbazine respectively, all treatments were lasted for 9 weeks. Results revealed that procarbazine induces significant increase in serum FSH and LH level while Testosterone level was significantly decreased .Similar decrease were also noticed in levels of glutathione (GSH)&nbsp;,as well as activity of catalase (CAT) and superoxide dismutase (SOD) in testis . Moreover, procarbazine caused significant decrease in sperm count, motility and viability and significant increase in sperm abnormality. On the other hand, Co-administration of Ubiqunone-10 with procarbazine lead to ameliorate levels of hormone as well as to improve testicular catalase activity in addition to glutathione and superoxide dismutase levels.

Ameliorating effects of agomelatine on testicular and epididymal damage induced by methotrexate in rats.

The aim of this study was to investigate the possible prophylactic effects of agomelatine (AGO) against testicular and epididymal damage induced by methotrexate (MTX) in rats. Twenty-four male Wistar albino rats were divided into three groups: Group I (control group), Group II (MTX group: 20 mg/kg MTX, i.p, single dose), and Group III (MTX+AGO group: 20 mg/kg MTX, i.p, single dose+40 mg/kg AGO; gavage, 7 days). The rats were killed under anesthesia 24 hours after the last AGO application. Testicular and epididymal tissues were bilaterally removed for morphometric, biochemical, pathological, and immunohistochemical analyses. Body, testicular, and epididymal weights were measured. Malondialdehyde (MDA), superoxide dismutase, catalase, and glutathione peroxidase levels were measured in testes. Sperm count, hyperemia, edema, inflammatory reaction, degenerated and necrotic cells were evaluated by histopathological analysis. In addition, inducible nitric oxide synthase (iNOS), granulocyte colony-stimulating factor (G-CSF), osteopontin (OPN), and heat shock protein-70 (HSP70) immune reactions were analyzed in testes and epididymides. Decreased epididymal weights, increased MDA levels, decreased sperm count, hyperemia, edema, inflammatory reaction, and degenerated and necrotic cells were observed in the MTX group. In addition, iNOS, HSP70, G-CSF, and OPN immune reactions were increased. AGO improved morphometric, biochemical, histopathological, and immunohistochemical findings. The present study confirms that MTX induces testicular and epididymal damage both biochemically and immunohistochemically. However, AGO demonstrated ameliorative effects on both biochemical and pathological findings of the current study.

Melatonin ameliorates some biochemical alterations following ketoconazole administration in rats.

Background Ketoconazole (Keto), an antifungal drug and a common therapeutic option in the treatment of advanced prostate cancer, is known to cause reproductive dysfunctions. Like Keto, melatonin has antifungal and anticarcinogenic actions. Moreover, the hormone has been used to reverse the damaging effects of different toxicants on the reproductive system. Therefore, this study investigated the effects of Keto with/without melatonin on selected biomarkers in rats. Methods Forty rats of 10 animals per group were used in this study, which lasted for 6 weeks. The control group was administered with saline (0.1 mL/day), while group 2 was administered with Keto during the last 3 weeks of experiment; however, in groups 3 and 4, Keto was administered during the first 3 weeks; thereafter, they were administered with saline and melatonin, respectively, during the subsequent 3 weeks. Keto and melatonin were administered at 100 and 10 mg/kg b.w./day (p.o.), respectively. Results The central effects of Keto are independent of the follicle stimulating hormone (FSH) and prolactin; however, relative to the control group, the drug significantly decreased the gonadotrophin releasing hormone (GNRH) and the luteinizing hormone (LH), substantiated by the corresponding significant decreases in sperm count and sperm morphology. Keto caused significant elevations in malondialdehyde (MDA) and lactate dehydrogenase (LDH) and a significant decrease in catalase (CAT) compared with the control group. Moreover, the drug triggered pro-inflammatory events. In group 3 (Keto recovery), MDA and uric acid levels were returned to the baseline (i.e. control), but not GNRH, LH, C-reactive protein (CRP), LDH, and CAT. Treatment with melatonin after Keto administration caused significant increases in FSH, LH, superoxide dismutase, total antioxidant capacity (TAC), sperm count, and sperm morphology but significant decreases in MDA and CRP, relative to groups 2 and 3. Conclusions Melatonin ameliorates some biochemical alterations following ketoconazole administration.

Codeine-induced sperm DNA damage is mediated predominantly by oxidative stress rather than apoptosis

ABSTRACT Background: Opioids have been implicated to induce infertility. Although codeine remains the most used opioid for recreational purpose, no study has documented its effect on sperm quality. Elucidating the effect of codeine on sperm cells and the associated mechanisms may provide an insight into preventing drug-induced sperm damage. Twenty-one New Zealand white rabbits were randomized into three groups; control and codeine-treated. The codeine-treated groups received either 4 or 10mg/kg b.w of codeine for six weeks. Results: Codeine treatment led to significant decrease in sperm count, motility, viability, normal morphology, and sperm membrane integrity. This was associated with significant rise in sperm DNA fragmentation, oxidative damage, and caspase 3 activity. The percentage of sperm DNA fragmentation correlates positively with 8-hydroxy-2'-deoxyguanosine, a biomarker of oxidative DNA damage, and caspase 3 activity, a biomarker of apoptosis. The observed correlation was stronger between sperm DNA fragmentation and oxidative DNA damage than sperm DNA fragmentation and caspase 3 activity. Conclusion: This study revealed that chronic codeine exposure causes sperm DNA fragmentation and poor sperm quality primarily via oxidative stress rather than activation of caspase 3-dependent apoptosis. Findings of the present study may explain drug-induced male factor infertility, particularly, those associated with opioid use.

Protective effect of vitamin E on sperm quality and in vitro fertilizing potential and testosterone concentration in polyvinyl chloride treated male rats.

Polyvinyl chloride (PVC) has toxic effects through the induction of oxidative stress in the body and testicles. Vitamin E (Vit E) is a dietary compound that functions as an antioxidant scavenging toxic free radicals. The present study aimed to probe the protective effect of Vit E against PVC-induced reprotoxicity in male rats. In this experimental study, 24 male rats were randomly divided into four groups (n=6) including control, Vit E (150 mg kg-1 per day; orally), PVC (1000 mg kg-1 per day; orally) and PVC + Vit E. After 40 days, rats were euthanized and epididymal sperms characteristics, embryo development and malondialdehyde (MDA) and testosterone levels were examined. The PVC decreased sperm count, motility and viability as well as testosterone level and increased sperms with damaged chromatin in comparison with controls. Also, the percentages of fertilization, two-cell embryos and blastocysts as well as MDA levels were decreased in PVC-treated rats. However, Vit E improved PVC-induced alterations in aforesaid parameters. The results indicated that PVC can reduce fertility potential in male rats probably through androgen and sperm quality and quantity reductions, while Vit E can exert protective effects in PVC-related reproductive toxicities.

Effect of Amlodipine and Captopril on Reproductive Capabilities of Male Laboratory Mice

Background: Hypertension is well confirmed as a major risk factor for cardiovascular disease. Researches in the treatment of hypertension has produced a multitude of drug classes with different efficacy profiles, which including β-blockers, diuretics, ACE inhibitors, angiotensin receptor blockers and calcium channel blockers. This study aimed to investigate the effects of captopril and amlodipine on some of reproductive abilities. Materials and Methods: The laboratory mice were 10-12 weeks and 23-25 g divided into three groups, six mice of each one. Group A served as control group; injected with 0.1 ml of normal saline, group B; injected with 0.1 ml of Captopril with 0.2 mg / kg, group C injected with 0.1 ml of amlodipine 0.08 mg / kg. Results: Decrease in sperm count and testis weights and testosterone hormone of Amlodipine treated mice. While the numbers of sperms and testis weight of captopril treated mice were comparable to that of control groups. But decrease normal sperms of captopril and Amlodipine treated mice comparable to that of control group. Conclusion: These results suggest that the treatment with amlodipine causes a significant testicular weight regression and reduction in sperm count.

Paternal activation of CB2 cannabinoid receptor impairs placental and embryonic growth via an epigenetic mechanism

The cannabinoid receptor type 2 (CB2) is the peripheral receptor for cannabinoids, involved in the homeostatic control of several physiological functions. Male mitotic germ cells express a high level of CB2, whose activation promotes their differentiation in both in vitro and in vivo experiments, controlling the correct progression of spermatogenesis. However, it remains elusive if CB2 activation in spermatogonia could affect reproductive success in terms of fertility and healthy pregnancy outcomes. In this study, we explored the effects of male CB2 activation on sperm number and quality and its influence on next generation health. We show that exposure of male mice to JWH-133, a selective CB2 agonist, decreased sperm count, impaired placental development and reduced offspring growth. These defects were associated with altered DNA methylation/hydroxymethylation levels at imprinted genes in sperm and conserved in placenta. Our findings reveal that paternal selective activation of CB2 alters the sperm epigenome and compromises offspring growth. This study demonstrates, for the first time, a new role of CB2 signaling in male gametes in causing epigenetic alterations that can be transmitted to the next generation by sperm, highlighting potential risks induced by recreational cannabinoid exposure.

Relationship Between Smoking Habit and Sperm Parameters Among Patients Attending an Infertility Clinic

BackgroundThis study aimed to estimate stress markers, oxidative stress (OS), reproductive hormones and sperm parameters in male smokers and non-smokers and observe the impact of oxidative stress markers and smoking on sperm count, motility and morphology in a selected population of Karachi, Pakistan.MethodsThis cross-sectional study was conducted from July 2017 to July 2018 at Aga Khan University (AKU), in Karachi, Pakistan. The subjects were recruited from the Sindh Institute of Reproductive Medicine (SIRM), Karachi based on defined inclusion criteria. The subjects were categorized into fertile and infertile based on cut off values of sperm parameters as recommended by the WHO i.e., sperm count/ejaculate of 39 × 106/ml, sperm motility 40% and normal morphology 4%. Two hundred eleven fertile and 165 infertile male subjects were included in the study. Serum cortisol, adrenaline, superoxide dismutase (SOD), and glutathione peroxidase (GPX) were analyzed by ELISA kits. Data was analyzed on SPSS-22. A p-value of <0.05 was considered statistically significant.ResultsAge, Body Mass Index (BMI), and body fat were similar among smokers and non-smokers. Age was significantly lower, while mean BMI and body fat were significantly higher among infertile smokers vs. fertile smokers (p-value < 0.05). The testosterone levels were significantly reduced among smokers as compared to non- smokers (p-value < 0.05). The median cortisol levels were increased as well as GPX, and steroid hormone-binding globulin (SHBG) were significantly reduced among smokers as compared to non-smokers. Additionally, the same findings with a significant difference have also been observed among infertile smokers as compared to fertile smokers (p-value < 0.05). This study has shown that the semen parameters (total count, motility, and morphology) are decreased in infertile smokers as compared to infertile non-smokers. Furthermore, the multivariate analysis showed that smoking causes a significant decrease in sperm count and morphology but it did not have any significant effect on motility.ConclusionSmoking has a significant effect on fertility, specifically sperm count and normal morphology of sperm. This might be due to OS produced by smoking, which has devastating effects on semen parameters, thus reducing male fertility. Infertility specialist should counsel their patients about the ill effects of smoking on their fertility status and should advise maintaining a healthy lifestyle, including normal weight and avoiding smoking, to prevent future health problems. Hence smokers should quit smoking for their next generation.

Prenatal Exposure to Bisphenol A, E, and S Induces Transgenerational Effects on Male Reproductive Functions in Mice.

This study was performed to examine the transgenerational effects of bisphenol (BP) A analogs, BPE, and BPS on male reproductive functions using mice as a model. CD-1 mice (F0) were orally exposed to control treatment (corn oil), BPA, BPE, or BPS (0.5 or 50 µg/kg/day) from gestational day 7 (the presence of vaginal plug = 1) to birth. Mice from F1 and F2 offspring were used to generate F3 males. Prenatal exposure to BPA, BPE, and BPS decreased sperm counts and/or motility and disrupted the progression of germ cell development as morphometric analyses exhibited an abnormal distribution of the stages of spermatogenesis in F3 males. Dysregulated serum levels of estradiol-17β and testosterone, as well as expression of steroidogenic enzymes in F3 adult testis were also observed. In the neonatal testis, although apoptosis and DNA damage were not affected, mRNA levels of DNA methyltransferases, histone methyltransferases, and their associated factors were increased by BP exposure. Furthermore, BP exposure induced immunoreactive expression of DNMT3A in Sertoli cells, strengthened DNMT3B, and weakened H3K9me2 and H3K9me3 in germ cells of the neonatal testis, whereas DNMT1, H3K4me3, and H3K27ac were not affected. In adult testis, stage-specific DNMT3B was altered by BP exposure, although DNMT3A, H3K9me2, and H3K9me3 expression remained stable. These results suggest that prenatal exposure to BPA, BPE, and BPS induces transgenerational effects on male reproductive functions probably due to altered epigenetic modification following disruption of DNMTs and histone marks in the neonatal and/or adult testis.

Heat shock sensitivity of adult male fertility in the parasitoid wasp Anisopteromalus calandrae (Hymenoptera, Pteromalidae).

In insects, decreased reproduction is a sublethal consequence of high temperatures, with males being more sensitive to this in many species. In hymenoptera, arrhenotokous parthenogenesis means that female offspring are produced using sperm and are thus diploid, while males are haploid. Consequently, sperm stocks in males and females (after copulation) are a key regulator of the sex ratio. Anisopteromalus calandrae is a parasitoid wasp in which males can suffer from subfertility due to a drastic decrease in sperm count after exposure to high temperatures during a critical early pupal stage. However, in this species spermatogenesis continues during adulthood, therefore the heat sensitivity of adult males remains to be studied. Laboratory studies were conducted on virgin and previously mated young adult males under control (30 °C) and heat shock (10 min at 48 °C) conditions to exhaust their initial sperm stock. After heat shock, in both virgin and already mated males, the individual sperm potential was half that of controls. Both groups continuously produced sperm, but sperm stock of heat shocked males' never reached that of the controls. Heat shock reduced survival at 10 days only in previously experienced males but had no impact on the mating ability in competition for a female compared to controls. Despite a reduced sperm count, heat shocked males had fully fertile spermatozoa. Such a physiological response to heat shock in a species with continuous sperm production could be of major interest for both wild populations in a context of temperature variations and parasitoid wasps introduced for agronomical purposes.

N-Butylparaben exposure through gestation and lactation impairs spermatogenesis and steroidogenesis causing reduced fertility in the F1 generation male rats

Parabens are class of preservatives used in vast majority of commercial products, and a potential Endocrine Disrupting Chemical (EDC). The present study was undertaken to delineate the effects of n-butylparaben on F1 male progeny exposed maternally through gestation and lactation via subcutaneous route. The F0 dams were given subcutaneous injections of n-butylparaben from gestation day (GD) 6 to postnatal day (PND) 21 with doses of 10, 100, 1000 mg/kg Bw/day in corn oil. The F1 male rats were monitored for pubertal development and sexual maturation; these were sacrificed on PND 30, 45 and 75. On PND 75, these F1 male rats were subjected for fertility assessment with unexposed female rats.A delayed testicular descent at 100 and 1000 mg/kg Bw dose and delayed preputial separation at 10 mg/kg Bw dose was observed in exposed F1 male rats. Decreased sperm count, motility and Daily Sperm Production was observed at 100 mg/kg Bw dose at PND 75. Interestingly, the sperm transit time in the epididymis was accelerated at this dose. Significant perturbed testicular expression of steroid receptors (ERα and β, AR), INSL3 and StAR genes with increased T and LH levels indicates direct effect on spermatogenesis and steroidogenesis. These F1 generation adult rats were sub-fertile with increased (%) pre- and post-implantation loss at 100 and 1000 mg/kg Bw/day dose. This is the first report on n-butylparaben highlighting the involvement of testicular leydig cells with accelerated sperm transit time leading to reduced fertility in the maternally exposed F1 male rats through estrogenic/anti-androgenic action.

Role of JNK and ERK1/2 MAPK signaling pathway in testicular injury of rats induced by di-N-butyl-phthalate (DBP)

BackgroundDi-N-butyl-phthalate (DBP) is an endocrine disrupting substance. We investigated the adverse effect of DBP on testis of male rat and reveal its potential mechanism of MAPK signaling pathway involved this effect in vivo and in vitro. Gonadal hormone, sperm quality, morphological change and the activation status of JNK, ERK1/2 and p38 was determined in vivo. Primary Sertoli cell was established and cultivated with JNK, ERK1/2 inhibitors, then determine the cell viability, apoptosis and the expression of p-JNK, p-ERK1/2. Data in this study were presented as mean ± SD and determined by one-way analysis of variance (ANOVA) followed by Bonferroni’s test. Difference was considered statistically significant at P < 0.05.ResultsIn vivo experiment, DBP impaired the normal structure of testicular tissue, reduced testosterone levels in blood serum, decreased sperm count and increased sperm abnormality, p-ERK1/2 and p-JNK in rat testicular tissue increased in a dose-dependent manner. In vitro studies, DBP could decrease the viability of Sertoli cells and increase p-ERK1/2 and p-JNK. Cell apoptosis in SP600125 + DBP group was significantly lower than in DBP group (P < 0.05). p-JNK was not significantly decreased in SP600125 + DBP group, while p-ERK1/2 was significantly decreased in U0126 + DBP group.ConclusionsThese results suggest that DBP can lead to testicular damage and the activation of ERK1/2 and JNK pathways, the JNK signaling pathway may be primarily associated with its effect.

Selenium protection against mercury toxicity on the male reproductive system of Clarias gariepinus

The present study aimed to evaluate the protective role of Selenium (Se) (0.1 ppm) on the male reproductive system of the catfish Clarias gariepinus exposed to sublethal doses of Mercury (Hg) (0.04 and 0.12 ppm) for 30 days. Indicators of seminal and gonadal hormone disruption (testosterone, estradiol and 11 keto testosterone), antioxidants (total antioxidant capacity (TAO), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx)), oxidative stress biomarkers (lipid peroxidation (LPO), percentage of DNA fragmentation, carbonylated proteins (CP) and nitric oxide (NO)) and histopathological alterations in testicles of Clarias gariepinus were determined. The exposure to Hg resulted in a high accumulation of residues of this metal in testicular tissues. The results showed a significant decrease in sperm count, activity and motility and in all gonadal hormones in Hg exposed groups. Hg exposure also induced a decline in TAO, SOD, CAT and GPx, whereas LPO, DNA fragmentation, CP and NO significantly increased in testicles of C. gariepinus respect to the control group. Although exposure to Se did not reduce the degree of mercury bioconcentration in the testicles, the sperm quality parameters were recovered. Moreover, TAO levels and GPx activity significantly increased after fish exposure to Se, whereas CP levels decreased. LPO, NO, CAT and SOD were also partially normalized when compared with the groups exposed to only Hg. In conclusion, the results showed that Hg, even in the small doses is capable to induce reproductive toxicity in the male catfish. Se exposure partially restored the values of biochemical parameters and sperm quality in Hg-treated fish suggesting protective effects against Hg reproductive toxicity.

FSH and estradiol benzoate administration recover spermatogenesis and sexual hormone levels in a busulfan-injured rat model

Busulfan induces azoospermia and testicular atrophy, while follicle stimulating hormone (FSH) and estradiol benzoate (EB) may improve spermatogenesis. Our objective was to determine the effects of FSH and EB on the recovery of spermatogenesis, histology, sexual hormones, and testicular gene expression in the testis of a busulfan-injured rat model. Forty adult rats were assigned into eight groups. Half received a single intraperitoneal saline or 30 mg/kg busulfan injection, and 42 days after, the animals received intramuscular injections for 10 days: 1 ml saline, 7.5 IU FSH, and 12 μg/kg EB or FSH+EB. One day after, blood plasma was obtained for hormone analysis, sperm was recovered from epididymis, and testes were processed for histology and RNA extraction. Busulfan decreased sperm count, motility, and viability; induced seminiferous tubular atrophy; and decreased blood testosterone, FSH, and luteinizing hormone. Hormonal treatments partially recovered spermatogenesis, decreasing tubular atrophy. They also decreased caspase 3 and iNOS expression while increasing Bcl-2 expression, compared with the busulfan treatment. FSH+EB was the most efficient treatment, also increasing the concentration of sexual hormones close to no-busulfan levels. Thus, busulfan has a clear negative effect in spermatogenesis in the rat model, and FSH and EB, especially combined, could help to reverse these effects.