Reproductive System Of Male Mice Research Articles

Oxidative stress, inflammatory reactions and apoptosis mediated the negative effect of chronic stress induced by maternal separation on the reproductive system in male mice

Exposure to severe and long-lasting stressors during early postnatal life negatively affects development of the brain and associated biological networks. Maternal separation (MS) is a valid stressful experience in early life that adversely affects neurobiological circuits. In the present study, we aimed to evaluate the effects of MS on sperm quality and histology of the testis in adult male mice. In this study, male mice were subjected to MS during post-natal days (PND) 2–14. Sperm parameters, histological alterations in the testicular tissue, ROS production (using DCFH-DA assay), gene expression of TLR4, NLRP3, TNFα, BAX, ASC, caspase-1 and BCL-2 (using RT-PCR), protein levels of caspase-3 and caspase-8 (using western blotting), and protein levels of IL-1β, IL-18, GPx and ATP (using ELISA) as well as protein expression of caspase-1 and NLRP3 (using immunocytochemistry) were evaluated. Findings showed that MS decreased count, morphology and viability of spermatozoa. MS decreased the diameter of seminiferous tubules and decreased the thickness of seminiferous epithelium. Furthermore, MS increased the level of ROS production and decreased the concentrations of GPx and ATP. MS led to increased expression of TLR4, NlRP3, TNFα, caspase-1, ASC, IL-1β and IL-18. In addition, MS induced apoptosis as evidenced by increased BAX, caspase-3 and caspase-8 as well as decreased BCL-2 expression. We concluded that early life stress induced by MS has detrimental effects on sperm parameters and testicular tissue. Our results suggest that these effects are mediated by activation of ROS production, and alterations in mitochondrial function, inflammatory processes and apoptosis pathways.

Transcriptomic analysis of reproductive damage in the epididymis of male Kunming mice induced by chronic infection of Toxoplasma gondii PRU strain

BackgroundSome researchers have reported that Toxoplasma gondii can cause serious reproductive impairment in male animals. Specifically, T. gondii destroy the quality of sperm in the epididymis, which affects their sexual ability. However, among such studies, none have investigated the male reproductive transcriptome. Therefore, to investigate the relationship between T. gondii and sperm maturation, we infected mice with T. gondii prugniaud (PRU) strain and performed transcriptome sequencing of the epididymis.ResultsCompared with the control group, 431 upregulated and 229 downregulated differentially expressed genes (DEGs) were found (P-value < 0.05, false discovery rate (FDR) < 0.05 and |log2 (fold change)| ≥ 1). According to results of a bioinformatics analysis, Gene Ontology (GO) function is divided into three categories: cellular component, molecular function and biological process. Upon performing GO analysis, we found that some DEGs correlated with an integral part of membrane, protein complex, cell surface, ATP binding, immune system process, signal transduction and metabolic process which are responsible for the epididymal injury. DEGs were mapped to 101 unique KEGG pathways. Pathways such as cytokine-cytokine receptor interaction, glycolysis/gluconeogenesis and apoptosis are closely related to sperm quality. Moreover, Tnfsf10 and spata18 can damage the mitochondria in sperm, which decreases sperm motility and morphology.ConclusionsWe sequenced the reproductive system of male mice chronically infected with T. gondii, which provides a new direction for research into male sterility caused by Toxoplasma infection. This work provides valuable information and a comprehensive database for future studies of the interaction between T. gondii infection and the male reproductive system.

Sulforaphane Protects the Male Reproductive System of Mice from Obesity-Induced Damage: Involvement of Oxidative Stress and Autophagy.

(1) Background: In recent decades, the prevalence of obesity has grown rapidly worldwide, thus causing many diseases, including male hypogonadism. Sulforaphane (SFN), an isothiocyanate compound, has been reported to protect the reproductive system. This research investigated the protective effect of SFN against obesity-induced impairment in the male reproductive system and explored the potential mechanism involved in mice. (2) Methods: One hundred thirty mice were divided into 5 groups (Control, DIO (diet-induced obesity), DIO + SFN 5 mg/kg, DIO + SFN 10 mg/kg, and DIO + SFN 20 mg/kg). The effects of SFN on the male reproductive system were determined based on the sperm count and motility, relative testes and epididymis weights, hormone levels, and pathological analyses. Oxidative stress was determined by measuring malondialdehyde (MDA), total antioxidant capacity (T-AOC), superoxide dismutase (SOD), glutathione (GSH), H2O2, catalase (CAT), and glutathione peroxidase (GSH-PX) levels. Protein expression of nuclear factor erythroid-2 related factor 2 (Nrf2), Kelch-like ECH-associated protein-1 (Keap1), Microtubule-associated protein light chain 3 (LC3), Beclin1, and P62 were determined by western blotting. (3) Results: High-fat diet (HFD)-induced obesity significantly decreased relative testes and epididymis weights, sperm count and motility, and testosterone levels but increased leptin and estradiol levels. SFN supplementation ameliorated these effects. Additionally, SFN administration inhibited the obesity-induced MDA accumulation and increased the SOD level. Western blot indicated that SFN had an important role in the downregulation of Keap1. Moreover, SFN treatment attenuated obesity-induced autophagy, as detected by LC3 and Beclin1. (4) Conclusions: SFN ameliorated the reproductive toxicity associated with obesity by inhibiting oxidative stress mediated by the nuclear factor erythroid-2 related factor 2/ antioxidant response element (Nrf2/ARE) signaling pathway and recovery of normal autophagy.

Multigenerational analysis of the functional status of male reproductive system in mice after exposure to realistic doses of manganese

The present study aimed to analyze the effect of multigenerational exposure to Mn at realistic doses on the functional quality of the male reproductive system of mice. Females and males (generation F0) were treated for 60 days with MnCl2, via gavage, at the doses of 0, 0.013, 0.13, and 1.3 mg/kg/day. Treatment of F0 dams continued throughout gestation and lactation periods. At the time of weaning, the offspring (F1 generation) was divided into: animals that were not exposed after weaning – parental exposure (PE); and those exposed via parental generation and directly (PDE) for additional 60 days, at the same dose of F0 generation. F0 and F1 males were euthanized for assessment of sperm parameters and redox changes in the reproductive system. There was a decrease in the sperm concentration of the F0 generation. In addition, the sperm parameters of F1 generation were drastically affected. The activity of antioxidant enzymes was significantly reduced in PE animals. It was possible to verify that the biochemical damages were higher in the PE individuals, as demonstrated by the integrated biomarker response index. Our results show that Mn, even at low doses, is able to promote a reduction in sperm quality over a generation.

Protective effects of hydro-alcoholic extract of Quercus brantii against lead-induced oxidative stress in the reproductive system of male mice.

Exposure to heavy metals such as lead (Pb) results in oxidative stress induction in the male reproductive system. Herbal medicine can be utilized as antioxidant agents against oxidative stress. Quercus brantii (QB) has shown antioxidant activity in previous studies. The aim of the present study was to evaluate effects of QB hydro-alcoholic extract against Pb-induced oxidative stress in the male mice reproductive system. Forty-two NMRI adult male mice were randomly divided into 7 groups of 6 animals each. Group I was the control group that received no treatment. Group II was the sham group and received 0.2 ml distilled water. Groups III and IV received QB hydro-alcoholic extract 500 and 1000 mg/kg bw, respectively. Group V received Pb 1000 ppm/kg bw. Group VI and VII received Pb 1000 ppm/kg bw and QB extract 500 and 1000 mg/kg bw, respectively. All groups received treatment via oral gavage. After 35 days, sperm parameters (i.e. sperm motility, count and morphology) were evaluated. Levels of sex hormones including LH, FSH, and testosterone, total antioxidant capacity (TAC), superoxide dismutase (SOD) and malondialdehyde (MDA) were measured in animals' serum. Exposure to Pb negatively affected sperm parameters (i.e. sperm motility, count and morphology), decreased serum concentrations of sex hormones (i.e. LH, FSH, and testosterone), TAC and SOD activity but increased MDA levels. However, co-administration of 500 and 1000 mg/kg bw QB hydro-alcoholic extract and Pb considerably improved sperm parameters (i.e. sperm motility, count and morphology), increased sex hormones (i.e.LH, FSH, and testosterone), TAC, and SOD activity while decreased MDA levels in animals' serum. Administration of QB extracts (Low dose and high dose) is able to protect the male reproductive system of mice against Pb-induced oxidative stress.

Trypanosoma brucei triggers a marked immune response in male reproductive organs.

African trypanosomiasis is caused by the protozoan parasite Trypanosoma brucei, transmitted between mammals by the bite of a tsetse. It has been recently shown that parasites accumulate in large numbers in various organs and tissues, including the mouse testis. Whether parasites are protected from the immune system in the male reproductive organ or can be transmitted through sexual route remains unknown. Here we show that parasites can be detected by fine needle aspiration cytology of the male reproductive system in mice, and histopathological analysis revealed that T. brucei accumulates in the stroma of the epididymis, epididymal adipose tissue and fibrous tunics of the testis. No parasites were found in the lumen of intact epididymal ducts or seminiferous tubules of the testis, indicating that the large majority of the parasites are not located in immune-privileged sites. In fact, these parasites are associated with marked inflammatory cell infiltration, parasite degeneration, and severe tissue damage and rupture of epididymal ducts, which may be related with reduced fertility. Overall, we show that just like in the bloodstream and most other tissues, in the male reproductive organs, T. brucei are exposed to a strong immune response. The detection of a very high number of parasites in this organ and its accessibility opens the possibility of using fine needle aspiration cytology as a complementary diagnostic tool in Animal African Trypanosomiasis.

Di-(2-Ethylhexyl) Phthalate Increases Obesity-Induced Damage to the Male Reproductive System in Mice.

Objective This study evaluated the effects of di-(2-ethylhexyl) phthalate (DEHP) and obesity on male reproductive organ function in male mice and the potential mechanism of male secondary hypogonadism (SH) in such mice. Methods 140 mice were assigned to six groups for 12 weeks: normal, DEHP, DIO, DIO + DEHP low, DIO + DEHP middle, and DIO + DEHP high. The effects of DEHP and obesity upon the reproductive organs were determined by measuring sperm count and motility, relative testis and epididymis weight, hormone level, and pathological changes. Oxidative stress was evaluated by determining malondialdehyde, T-AOC, SOD, GSH, H2O2, CAT, and GSH-PX in testicular tissues. Nrf2 and Keap1 protein were measured by Western blotting. Results DEHP and obesity reduced sperm count and motility, relative testis and epididymis weight, and testosterone level but increased the levels of MDA, H2O2, leptin, and estradiol. Pathological injury was observed in the testicular Leydig cells. Moreover, the activity of CAT, SOD, and GSH-Px enzymes was inhibited. Nrf2 protein expression was reduced but that of Keap1 was increased. Conclusions DEHP and obesity jointly caused damage to male productive function. Oxidative stress in testicular tissue, and a high level of leptin, may provide some evidence to clarify the mechanisms of male SH with DEHP and obesity.

Reproductive toxicity of melamine against male mice and the related mechanism

Melamine is a nitrogen-containing heterocyclic organic compound with a triazine skeleton, which has been widely applied in industrial and chemical fields. Previous toxicity studies of melamine mainly focused on renal toxicity and hepatic pathological changes, but its toxicity against the reproductive system has seldom been assessed. We investigated the effects of melamine on the reproductive system of male mice. Forty healthy male Kunming mice were randomly divided into a normal saline negative control group, a low-dose melamine group, a medium-dose melamine group and a high-dose melamine group (n = 10). The mice were administered for five consecutive days and killed on the 35th day after first administration. In melamine administration groups, seminiferous tubules had disordered, loose arrangement, and spermatogenic cells at all levels obviously decreased. The sperm count and motility decreased significantly, and the sperm deformity rate increased significantly. Melamine induced apoptosis of testicular spermatogenic cells. To further explore the mechanism, we detected metabolism-related enzymes sorbitol dehydrogenase (SDH) and lactate dehydrogenase (LDH) as well as oxidative stress indices superoxide dismutase (SOD) and malondialdehyde (MDA). The activities of SDH, LDH and SOD in melamine treatment groups decreased significantly, and the MDA level increased obviously. The expressions of apoptosis-related proteins Bcl-2, Bax and caspase-3 were detected by immunohistochemistry. The expression of Bcl-2 significantly increased, but those of Bax and caspase-3 significantly reduced (p < 0.05). In conclusion, melamine damaged the reproductive system of mice via the oxidative stress pathway and by inducing cell apoptosis.

The effect of aqueous extract of Rosa damascena on formaldehyde-induced toxicity in mice testes

Context: Rosa damascena L. (Rosaceae) (RD) essential oil and extracts are commonly used as a flavour in herbal medicine which increase libido. Previous studies have shown inhalation of RD flower’s oil increases libido and causes protective effects in formaldehyde (FA)-induced testicular damage.Objective: The protective effects of aqueous extract of RD on the male reproductive system of mice were examined following FA-induced damage.Materials and methods: Forty-eight adult NMRI male mice were randomly assigned to six groups (n = 8): control (normal saline, 10 mg/kg); RD40 (40 mg/kg, p.o.); FA treated (10 mg/kg of 10%, i.p.) and FA + RD treated at 10, 20 and 40 mg/kg (FA + RD10), (FA + RD20) and (FA + RD40), respectively, for 40 days. At the end of treatment regimes, serum testosterone (T) level and the reproductive activity, viz. body/organ weights, testicular structure and sperm characteristics were studied.Results: Formaldehyde administration significantly decreased serum T level (p < 0.001), testicular weight/volume, tubular diameter and sperm characteristics compared to the control group (p < 0.05). RD (40 mg/kg) administration in FA-treated mice significantly improved serum T level, testicular weight/histological structure, tubular diameter, Leydig cell number and epididymal sperm characteristics in comparison to its lower doses and the control group (p < 0.05).Discussion and conclusions: We may conclude that RD flower extract can withstand effects of FA in the male reproductive system of mice possibly due to its antioxidative properties.

Therapeutic Effect of Resveratrol on Morphine-Induced Damage in Male Reproductive System of Mice by Reducing Nitric Oxide Serum Level

Therapeutic Effect of Resveratrol on Morphine-Induced Damage in Male Reproductive System of Mice by Reducing Nitric Oxide Serum Level

From the Cover: Roles of mmu_piR_003399 in Microcystin-Leucine Arginine-Induced Reproductive Toxicity in the Spermatogonial Cells and Testis.

Our previous work has demonstrated that microcystin-leucine arginine (MC-LR) is a potent toxin for the reproductive system of male mice and it exerts cytotoxicity in spermatogonial cells, resulting in the constitutional and functional changes of the mouse testis. The present study was designed to investigate the functions of P-element-induced wimpy (piwi)-interacting RNAs (piRNAs) in MC-LR-induced reproductive toxicity in male mice. We observed an increase in the mmu_piR_003399 level in spermatogonial cells and mouse testicular tissues following treatment with MC-LR. Moreover, our data confirmed that cyclin-dependent kinase 6 (CDK6) was the target gene of mmu_piR_003399. Increases in the concentration of mmu_piR_003399 were correlated with the reduced expression of CDK6 both in vitro and in vivo. mmu_piR_003399 induced cell cycle arrest at the G1-phase, down-regulated sperm counts and sperm motility, and compromised sperm morphology. On the contrary, suppressing the expression of mmu_piR_003399 could substantially attenuate MC-LR-induced pathology in mice including cell cycle arrest, reduced mature sperm counts, sperm viability loss and abnormal sperm morphology. Furthermore, our data supported that mmu_piR_003399 existed in mouse serum and plasma, and its level was increased in MC-LR-treated mice. In conclusion, we demonstrate that mmu_piR_003399 plays a crucial role in regulating MC-LR-induced reproductive toxicity.

Prenatal and postnatal exposure to low levels of permethrin exerts reproductive effects in male mice

Permethrin, a pyrethroid chemical, is widely used as a pesticide because of its rapid insecticidal activity. Although permethrin is considered to exert very low toxicity on mammalian reproductive organs, the effects of early low-level and chronic exposure on adult spermatogenesis are unclear. We exposed mice to environmentally relevant concentrations of permethrin (0, 0.3, and 30ppm) in drinking water during prenatal and postnatal period and examined the effects on the testis in mice offspring when they reached maturity (12 weeks of age). Using methyl green-pyronin staining, we found an abnormal accumulation of RNA in the seminiferous epithelia of mice treated with permethrin; this accumulation may be derived from an enlargement of the residual body. Additionally, permethrin may cause a decline of Sertoli cell functions. Our findings demonstrate that low-level and chronic permethrin exposure during prenatal and postnatal period has distinct effects on male reproductive system in mice.

RIPK1-RIPK3-MLKL-dependent necrosis promotes the aging of mouse male reproductive system.

A pair of kinases, RIPK1 and RIPK3, as well as the RIPK3 substrate MLKL cause a form of programmed necrotic cell death in mammals termed necroptosis. We report here that male reproductive organs of both Ripk3- and Mlkl-knockout mice retain 'youthful' morphology and function into advanced age, while those of age-matched wild-type mice deteriorate. The RIPK3 phosphorylation of MLKL, the activation marker of necroptosis, is detected in spermatogonial stem cells in the testes of old but not in young wild-type mice. When the testes of young wild-type mice are given a local necroptotic stimulus, their reproductive organs showed accelerated aging. Feeding of wild-type mice with an RIPK1 inhibitor prior to the normal onset of age-related changes in their reproductive organs blocked the appearance of signs of aging. Thus, necroptosis in testes promotes the aging-associated deterioration of the male reproductive system in mice.

Chronic Water-Pipe Smoke Exposure Induces Injurious Effects to Reproductive System in Male Mice

There is a global increase in the popularity of water-pipe tobacco smoking including in Europe and North America. Nevertheless, little is known about the male reproductive effects of water-pipe smoke (WPS), especially after long-term exposure. Here, we assessed effects of WPS exposure (30 min/day) in male mice for 6 months. Control mice were exposed to air-only for the same period of time. Twenty-four hours after the last exposure, testicular histopathology, and markers of inflammation and oxidative stress, and the tyrosine–protein kinase vascular endothelial growth factor receptor 1 (VEGFR1) were assessed in testicular homogenates. Moreover, plasma testosterone, estradiol, and luteinizing hormone (LH) concentrations were also measured. Chronic WPS exposure induced a significant decrease of testosterone and estradiol, and a slight but significant increase of LH. Glutathione reductase, catalase, and ascorbic acid were significantly decreased following WPS exposure. Plasma concentration of leptin was significantly decreased by WPS exposure, whereas that of tumor necrosis factor α and interleukin 6 was significantly increased. Histopathological analysis of the testes revealed the presence of a marked reduction in the diameter of the seminiferous tubules with reduced spermatogenesis. Transmission electron microscopy examination showed irregular thickening and wrinkling of the basement membranes with abnormal shapes and structures of the spermatozoa. VEGFR1 was overexpressed in the testis of the mice exposed to WPS and was not detected in the control. The urine concentration of cotinine, the predominant metabolite of nicotine, was significantly increased in the WPS-exposed group compared with the control group. We conclude that chronic exposure to WPS induces damaging effects to the reproductive system in male mice. If this can be confirmed in humans, it would be an additional concern to an already serious public health problem, especially with the increased use of WPS use all over the world, especially in young adults.

The toxic effect of nickel chloride (II) and potassium dichromate (VI) on the activity of reproductive system in male mice

Increase distribution of heavy metal and its compound in the environment, especially through anthropogenic and natural activity, raises increasing concern for toxicological effects. The present study was based on the fact that Ni and Cr elements are important as the environmental factor produce the male genital system abnormalities. 35 male mice (10 weeks old) were randomly divided into seven groups 5 animals for each group, group 1 served as control received tap water, group 2,3 and 4 received (20, 40, and 60 mg/kg of Nicl2 respectively), while group 5,6 and 7 received (20, 60, and 100 mg/kg of K2Cr2O7 respectively). The results showed a high significant decrease (P≤0.0001) in the sperm count of male mice for intermediate and high dose treated with Nicl2 (II) as compared with control group, while no any significant differences between the lowest doses as compared with control group. The result showed a high significant difference (P≤0.0001) in the percentage of sperm abnormalities for intermediate and high dose treated with Nicl2 (II) as compared with control group. Also the result showed a high significant difference (P≤0.0001) in the sperm count for all groups treated with different doses of K2Cr2O7 (VI) as compared with control group. About percentage of sperm abnormalities the result showed a high significant difference (P≤0.0001) in the percentage of sperm abnormalities for intermediate and high dose treated as compared with control group.

96 IN VITRO FERTILIZATION IN MOUSE AS A REPROTOXICITY MODEL FOR XENOBIOTICS

To assess reprotoxicity of pesticides and other xenobiotics, rodents are often used with natural mating and litter size as end-points. However, because a male mouse can produce normal-size litters even with &gt;50% reduced sperm count (Ecotox. Env. Saf. 73, 1092), this model could approve some chemical substances despite their reprotoxic effect. Thus, we aimed to establish a mouse IVF system to evaluate reprotoxicity of xenobiotics, illustrated by 2 pesticides [vinclozolin (vin), chlormequat (ccc)]. Experimental mice were given 2 pesticide doses by mixing into the feed: low (L) or high (H), equivalent to no or lowest observed adverse effect level, respectively (Env. Health Perspect. 117, 1272). To produce experimental males, mated NMRI females were fed low dose (vinL, cccL), high dose (vinH, cccH), or no pesticide from 1-cell stage through birth and until weaning, from where experimental males continued pesticide feeding. Each experimental male at 8 to 10 weeks old was naturally mated with 2 females having normal feed for 5 days, then continued with pesticide or control feed for at least 35 days before use for IVF. Naturally mated females had normal feed until birth to evaluate litter size. For IVF, oocytes were collected after superovulation of 3- to 4-week-old C57BL/6J females (2–5/male). Based on our previous experiment (Anim. Reprod. 13, in press), 25,000 sperm/mL was within the responsive range and selected for IVF (Theriog. 65, 1716). The IVF embryos were in vitro cultured for 4 days. Pronuclei were evaluated 9 h after IVF start (Day 0), and 2-cell/blastocyst were evaluated on Day 1/4. Mean litter size was estimated by normal linear mixed-effects model, and mean pronuclei, 2-cell, and blastocyst rates were estimated by binomial generalized linear mixed-effects models with identity link function, included a male-subject random intercept accounting for correlation between multiple fertilizations by same male, and a factor defining groups as fixed effect. Preliminary results (Table 1) are based on current data from half of our full experiment. No signs of different litter sizes after natural mating were observed between pesticide groups and control. Compared with control, rates of pronuclei, 2-cell, and blastocyst tended to decrease in vinH and increase in vinL group. No clear differences between cccL, cccH, and control groups were found. These results could indicate a pesticide effect (vinH) on mouse male reproductive system that can be detected in an IVF system but not by natural mating. Our data show a large variation in IVF results between individual males and females, so our full dataset is required before conclusions are made. Table 1. Preliminary results

Pulmonary exposure to cellulose nanocrystals caused deleterious effects to reproductive system in male mice

ABSTRACTOver the past several years there has been an increased number of applications of cellulosic materials in many sectors, including the food industry, cosmetics, and pharmaceuticals. However, to date, there are few studies investigating the potential adverse effects of cellulose nanocrystals (CNC). The objective of this study was to determine long-term outcomes on the male reproductive system of mice upon repeated pharyngeal aspiration exposure to CNC. To achieve this, cauda epididymal sperm samples were analyzed for sperm concentration, motility, morphological abnormalities, and DNA damage. Testicular and epididymal oxidative damage was evaluated, as well as histopathology examination of testes. In addition, changes in levels of testosterone in testes and serum and of luteinizing hormone (LH) in serum were determined. Three months after the last administration, CNC exposure significantly altered sperm concentration, motility, cell morphology, and sperm DNA integrity. These parameters correlated with elevated proinflammatory cytokines levels and myeloperoxidase (MPO) activity in testes, as well as oxidative stress in both testes and epididymis. Exposure to CNC also produced damage to testicular structure, as evidenced by presence of interstitial edema, frequent dystrophic seminiferous tubules with arrested spermatogenesis and degenerating spermatocytes, and imbalance in levels of testosterone and LH. Taken together, these results demonstrate that pulmonary exposure to CNC induces sustained adverse effects in spermatocytes/spermatozoa, suggesting male reproductive toxicity.

Endocrine disrupting potential and reproductive dysfunction in male mice exposed to deltamethrin.

Pesticide exposure may affect semen quality and male fertility in humans. The aim of the present work was to elucidate the adverse effects of deltamethrin (Delta), a synthetic pyrethroid, on exposed male mice and their offspring. Adult male Albino/Swiss mice received deltamethrin (5 mg/kg) daily for 35 days and mated with untreated females to produce offspring. Classical measurements of ejaculate and sperm quality and testicular histopathological changes were assessed. Deltamethrin treatment affects sperm quality and quantity in the ejaculated semen of mice that had also markedly impaired libido as measured by indices of mating and fertility and number of pregnant females housed with male mice exposed to this pesticide. Exposure mice to deltamethrin significantly decreased their testosterone and inhibin B levels and affected reproductive performance. Testes of exposed mice showed marked histopathological alterations as compared to the control group. The mice exposed to 5 mg/kg body weight/day of deltamethrin showed severe alterations of the seminiferous tubules, sloughing of the germ cells, the vacuolization of germ cell cytoplasm, and the disruption of spermatogenic cells compared to the control group. Altered pregnancy outcomes were directly attributed to damage of sperm of male mice exposed to deltamethrin compared to the control group. We concluded that exposure to deltamethrin affected the reproductive system of male mice explored by altered total sperm density, motility, and morphology in mice spermatozoa.

The synergy effect of daidzein and genistein isolated from Butea superba Roxb. on the reproductive system of male mice

Butea superba Roxb. (BS) has been used in Thai men as an aphrodisiac, and prevent erectile dysfunction. Nevertheless, the active ingredients, dosages, have not been cleared. Hence, this study was to investigate the effect of compounds from the BS on the reproductive parameters of male mice. The results revealed that BS was extracted to afford biochanin A and genistein, which were first reported on BS, and daidzein. The mice were treated by daidzein and genistein alone and in combination. The results showed that the sperm number and motility, cholesterol and testosterone level of all isoflavones-treated groups were significantly higher than controls (p < 0.01). Obviously, daidzein plus genistein exhibited a synergistic effect, which is also the first report, and resulted in significantly displayed higher levels of these parameters compared to others. So, the synergistic activity of these isoflavones may be useful in improving libido, erectile capacity and assist infertility of poor spermatozoa in men.

Evaluation of toxic effects of CdTe quantum dots on the reproductive system in adult male mice

Fluorescent quantum dots (QDs) are highly promising nanomaterials for various biological and biomedical applications because of their unique optical properties, such as robust photostability, strong photoluminescence, and size-tunable fluorescence. Several studies have reported the in vivo toxicity of QDs, but their effects on the male reproduction system have not been examined. In this study, we investigated the reproductive toxicity of cadmium telluride (CdTe) QDs at a high dose of 2.0 nmol per mouse and a low dose of 0.2 nmol per mouse. Body weight measurements demonstrated there was no overt toxicity for both dose at day 90 after exposure, but the high dose CdTe affected body weight up to 15 days after exposure. CdTe QDs accumulated in the testes and damaged the tissue structure for both doses on day 90. Meanwhile, either of two CdTe QDs treatments did not significantly affect the quantity of sperm, but the high dose CdTe significantly decreased the quality of sperm on day 60. The serum levels of three major sex hormones were also perturbed by CdTe QDs treatment. However, the pregnancy rate and delivery success of female mice that mated with the treated male mice did not differ from those mated with untreated male mice. These results suggest that CdTe QDs can cause testes toxicity in a dose-dependent manner. The low dose of CdTe QDs is relatively safe for the reproductive system of male mice. Our preliminary result enables better understanding of the reproductive toxicity induced by cadmium-containing QDs and provides insight into the safe use of these nanoparticles in biological and environmental systems.