Reproductive Function Of Male Mice Research Articles

Low-dose polystyrene microplastics exposure impairs fertility in male mice with high-fat diet-induced obesity by affecting prostate function

The harmful effects of microplastics (MPs) on male fertility are receiving more and more attention. However, the impact of low-dose MPs exposure on the reproductive function of male mice is still unclear. In this study, we exposed male mice to low-dose MPs (25–30 μg/kg body weight/day) or low-dose MPs combined with high-fat diet (HFD) feeding. Our results showed that low-dose MPs exposure or HFD feeding significantly reduced sperm quality and the number of offspring born, while low-dose MPs exposure combined with HFD feeding further enhanced the above effects. The combination of low-dose MPs exposure and HFD feeding resulted in a notable elevation of inflammatory level within the prostate of mice and induced apoptosis of prostate epithelium and a decrease in nutrients (zinc, citrate) in seminal plasma fluid. Our findings in this study could provide valuable clues for better understanding the influence of low-dose MPs exposure on the reproductive system under metabolic disorders and facilitate the development of the prevention of reproductive toxicity caused by MPs exposure.

Protective effects of L-theanine and dihydromyricetin on reproductive function in male mice under heat stress

Protective effects of L-theanine and dihydromyricetin on reproductive function in male mice under heat stress

Melatonin or vitamin C attenuates lead acetate-induced testicular oxidative and inflammatory damage in mice by inhibiting oxidative stress mediated NF-κB signaling

Lead (Pb) acts as an environmental endocrine disruptor and has negative effects in animals; excessive accumulation of lead causes reproductive dysfunction in male animals. Oxidative stress plays a vital role in Pb-induced injury. However, the mechanisms underlying chronic testicular toxicity of Pb remain unclear. In this study, we aimed to determine the effects of lead acetate on reproductive function in male mice, identify the underlying mechanisms, and test counter measures to alleviate the toxic effects. Male mice were dosed with lead acetate (500 mg/L) in free drinking water for 12 weeks, and administered melatonin (5 mg/kg) or vitamin C (500 mg/kg) by intraperitoneal injection. Blood from the eyeball, testicles, and sperm from the caudal epididymis were collected after 12 weeks and analyzed. Pb exposure reduced sperm count and motility, increased sperm malformation (P < 0.01), disrupted testicular morphology and structure, and decreased the expression of steroid hormone synthesis-related enzymes and serum testosterone concentration (P < 0.01). Pb also increased the number of inflammatory cells and the levels of the pro-inflammatory cytokines TNF-α and IL-6 (P < 0.01), and activated NF-κB signaling. Furthermore, the ROS yield and oxidation indicators LPO and MDA were significantly increased (P < 0.01), and the antioxidant indicators T-AOC, SOD, and GSH were significantly reduced (P < 0.01). Treatment with melatonin or vitamin C reversed the effects of lead acetate; vitamin C was more effective in restoring SOD activity (P < 0.01) and enhancing ZO-1 protein levels (P < 0.01). Thus, long-term exposure to lead acetate at low concentrations could adversely affect sperm quality and induce inflammatory damage by oxidative stress mediated NF-κB signaling. Vitamin C could act as a protective agent and improve reproductive dysfunction in male animals after lead accumulation.

Polystyrene nanoplastics aggravate reproductive system damage in obese male mice by perturbation of the testis redox homeostasis.

The potential impact of the combination of a high-fat diet (HFD) and polystyrene nanoplastics (PS-NPs) on fertility cannot be ignored, especially when the fertility rate is declining. However, it has not attracted considerable attention. In this study, an obese mouse model was established using an HFD, and the reproductive function of male mice was evaluated after intragastric administration of 100 μL of a 10 mg/mL PS-NP suspension for 4 weeks. By determining the morphology and vitality of sperm and related indicators of testosterone production, it was found that PS-NPs aggravated the destruction of sperm mitochondrial structure, decrease sperm activity, and testosterone production in HFD-fed mice. To comprehensively analyze the injury mechanism, the integrity of the blood testicular barrier (BTB) and the function of Leydig and Sertoli cells were further analyzed. It was found that PS-NPs could destroy BTB, promote the degeneration of Leydig cells, reduce the number of Sertoli cells, and decrease lactate secretion in HFD-fed mice. PS-NPs further interfered with redox homeostasis in the testicular tissues of HFD-fed mice. This study found that PS-NPs could aggravate the damage to the reproductive system of obese male mice by further perturbing its redox homeostasis and revealed the potential health risk of PS-NPs exposure under an HFD.

Sevoflurane inhibited reproductive function in male mice by reducing oxidative phosphorylation through inducing iron deficiency.

Sevoflurane (Sev) is one of the commonly used inhalation anesthetic chemicals in clinics. It has great impact on spermatogenesis and fertilization in male animals. The underlying mechanism remains largely unexplored. Based on our previous research, we hypothesized that Sev induced iron metabolism disturbance in the testis and epididymis and inhibited the spermatogenesis. In this study, two-month-old C57BL/6 male mice were treated with 3% Sev for 6h, and their fertility (including sperm concentration, sperm mobility, and the number of offspring) was evaluated. Mice testis, epididymis, and sperm were harvested and subjected to Western blot analysis and immunofluorescence analysis. Iron levels were reflected by the gene expression of iron metabolism-related proteins (including ferritin, TfR1, and FpN1) and ICP-MS and Perl's iron staining. Electron transport and oxidative phosphorylation levels were measured by Oxygraph-2k and ATP contents. The activity of ribonucleotide reductase was evaluated by assay kit. DNA synthesis status in testis and/or epididymis was marked with BrdU. Cell proliferation was evaluated by double immunofluorescence staining of specific protein marker expression. Our results revealed that the mice exposed to Sev showed damaged testicular and epididymis structure and significantly reduced the sperm concentration, sperm motility, and fertility. Sev decreases the iron levels through down-regulating the expression of H-ferritin, L-ferritin, and FpN1, and up-regulating the expression of TfR1 in the testis and epididymis. Iron levels also significantly reduced in germ cells which decrease the number of germ cells, including sperm, Sertoli cells, and primary spermatocyte. Iron deficiency not only decreases electron transport, oxidative phosphorylation level, and ATP production but also suppresses the activity of ribonucleotide reductase and the expression of Ki67, DDX4, GATA1, and SCP3, indicating that Sev affects the spermatogenesis and development. Meanwhile, Sev impaired the blood-testis barrier by decreasing the ZO1 expression in the testis and epididymis. The damage effect induced by Sev can be significantly ameliorated by iron supplementation. In conclusion, our study illustrates a new mechanism by which Sev inhibits spermatogenesis and fertility through an oxidative phosphorylation pathway due to iron deficiency of epididymis and testis or sperm. Furthermore, the damaging effects could be ameliorated by iron supplementation.

Toxicological effects of micro/nano-plastics on mouse/rat models: a systematic review and meta-analysis.

Micro/nano-plastics (MNPs) are considered a heterogeneous class of environmental contaminants that cause multiple toxic effects on biological species. As the commonly used mammalian models to study the effects of MNPs with regard to their toxic effects, the mouse and rat models are making a great contribution to the disciplines of environmental toxicology and medical health. However, the toxic effects of MNPs have not been systematically summarized. Therefore, a systematic review and a meta-analysis of the toxic effects of MNPs on mouse/rat models were conducted. A total of seven main categories were established in this systematic review, and 24 subcategories were further divided according to the specific physiological significance of the endpoint or the classification of the physiological system, which covered all the selected pieces of literature. A total of 1,762 biological endpoints were found, and 52.78% of them were significantly affected. This fact indicates that there are relative factors, including the size, polymer type, concentration, and exposure time of MNPs and different sexes of mouse/rat models that could significantly affect the biological endpoints. These biological endpoints can be classified into various factors, such as the dose-response relationships between MNP concentration and physiological categories of the nervous system, growth, reproduction, digestive tract histopathology, and inflammatory cytokine level, among others. MNPs negatively affected the blood glucose metabolism, lipid metabolism, and reproductive function in mice. The reproductive function in male mice is more sensitive to the toxic effects of MNPs. These findings also provide insights into and directions for exploring the evidence and mechanisms of the toxic effects of MNPs on human health. It is clear that more research is required on the pathological mechanisms at the molecular level and the long-term effects of tissue accumulation.

Construction of a testis Elovl4 gene knockout mouse model based on Cre/loxP system

Very long chain polyunsaturated fatty acids (VLC-PUFAs) are unique fatty acids in tissues of mammals such as retina and testis, and the key enzyme of its biosynthesis is very long chain fatty acid elongase 4 (Elovl4). Development of an animal model of tissue-specific knockout of Elovl4 gene is conducive to the in-depth study of the biological function of VLC-PUFAs. Therefore, we constructed Stra8-Cre mice and Elovl4 floxed mice based on Cre/loxP system, and obtained the (Elovl4[flox/+], Stra8-Cre) heterozygous knockout mice by hybridization. Subsequently, female mice were selected to cross with male mice with homozygous Elovl4[flox/flox] to gain homozygous mice (Elovl4[flox/flox], Stra8-Cre) through genotype identification and screening. RT-PCR, qRT-PCR, Western blotting, immunohistochemistry and immunofluorescence techniques were used to detect the knock-out efficiency of Elovl4 in testis. The expression of Elovl4 in testis of both heterozygous and homozygous knockout mice were significantly down-regulated at mRNA and protein levels, but were not affected in other tissues. In summary, we constructed a mouse model with specific knockout of Elovl4 gene in testis, which provides a reliable animal model for studying the effect of VLC-PUFAs on the reproductive function of male mice and the underpinning molecular mechanisms.

Effects of the Ethanol Extracts of Ficus deltoidea leaves on the Reproductive Parameters in Male Mice

BACKGROUND: Indonesia, and in particular East Kalimantan, has a very high diversity of flora that has the potential to be used as traditional medicine. One type of flora is the leaves of Ficus deltoidea Jack. At present, there are no available data about the impact of F. deltoidea leaf ethanol extract on the male reproductive system. AIM: The present study aims to investigate the effect of F. deltoidea leaf ethanol extract on several parameters of reproductive function in male mice, including changes in testicular biochemistry, reproductive hormones profile, and histopathology of the testes after subchronic exposure. METHODS: In total, 25 male mice were divided into five groups: The control group and four treatment groups that received extract doses of 125, 250, 500, and 1000 mg/kgbw for 28 days, respectively. At the end of the treatment, surgery was performed, weight of body and reproductive organs (testis, epididymis, and seminal vesicles) were measured, and testicular biochemistry, reproductive hormone profile, antioxidant activity, and testes histopathology were analyzed. RESULTS: In the subchronic toxicity test, there were no significant changes in body weight or in weight and relative weight of reproductive organs. Levels of testosterone, luteinizing hormone and follicle-stimulating hormone, protein, cholesterol, and activity of enzymes in the testes (alkaline phosphatase, lactate dehydrogenase, and glutamyltransferase) and activity of the enzyme superoxide dismutase increased significantly in the treated mice when compared to control mice (p &lt; 0.05). Glycogen levels were not significantly different, but lipid peroxide (MDA) decreased significantly, though it did not change the histological structure of the testes. CONCLUSION: Ethanolic extract of the leaves of F. deltoidea Jack does not cause toxic effects and even has a beneficial effect on the reproduction of male mice by increasing fertility, reproductive hormones, and antioxidant activity, and it does not change the histological structure of the testes.

Effect of gold nanocomposite treatment on male reproductive function

Recently, it has been proved that polymers with a dextran core and grafted polyacrylamide chains dextran–polyacrylamide are effective in photodynamic chemotherapy, which gives confidence in the prospect of drug nanosystem. However, further research is needed to determine the effect of the treatment on male reproductive function. Experiments have been conducted on 50 male and 50 females Albino white laboratory mice (25–30 g). Copolymer dextran-graft-polyacrylamide in nonionic (D-g-PAA) and anionic forms (D-g-PAA(PE) was used as a polymer matrix for in situ synthesis of gold nanoparticles (AuNPs). D-g-PAA consists of dextran core and five grafted PAA chains. The copolymer in anionic form was prepared by alkaline hydrolysis. Polymer/AuNP systems contain AuNPs of 2–11 nm in size and have spherical shape. The treatment of substances was carried out in the following way: D-g-PAA and D-g-PAA(PE) (10,00 mg/kg), D-g-PAA/AuNPs and D-g-PAA(PE)/AuNPs (9.78 mg/kg), saline solution was introduced intravenously (in the tail vein, in 0.3 mL) once a day, five times. For the first time, it has been shown that treatment with D-g-PAA, D-g-PAA(PE), and D-g-PAA/AuNPs did not affect reproductive function in male mice. Disorder of the male reproductive function occurs under conditions of treatment with D-g-PAA(PE)/AuNPs. Significant changes in the values of were established in: (1) pre- and post-implantation mortality of embryos; (2) the number of live newborns (pups); (3) sperm and abnormal sperm forms (%); (4) spermatocytes (primary) and spermatids (%); (5) living, apoptotic and necrotic cells in the testis (spermatocytes (primary)) and in the epididymis (spermatozoa).

Joint effects of nano-selenium and nano-cerium on the male reproductive function of mice exposed to microwave radiation

To study effect of nano-selenium and nano-cerium(nano cerium oxide) on the spermatogenic ability of mice irradiated by 1800 MHz microwave radiation(MR). Forty-two ICR mice were randomly divided into groups: blank control group, solvent control group, microwave radiation model group, low, medium and high dose groups of nano-selenium+nano-cerium. In joint effects groups of nano-selenium and nano-cerium, the nano-selenium solution(60, 120 and 240 μg/kg) and the nano-cerium oxide solution(15, 30, 60 μg/kg) were administered to the stomach at 7:30 in the morning and 18:30 in the evening, respectively. The blank control group was orally administered with an equal volume of distilled water, and the solvent control group and the MR group were orally administered with an equal volume of carboxymethylcellulose sodium solution. During the second week of gastric administration, the mice were exposed to microwave radiation(1800 MHz) for 2 h every day(specific absorption ratio: 0. 2986 W/kg). After MR treatment, the daily sperm production of testis, sperm motility and sperm deformity rate in epididymis were measured, and the testicular marker enzymes [G6 PDH(6-phosphatedehydrogenase), ACP(acid phosphatase), LDH(lactate dehydrogenase)], antioxidant indexes [CAT(catalase), MDA(malondialdehyde) and T-AOC(total antioxidant capacity)] in testicular tissue were analyzed. Compared with the solvent control group, MR led to the decrease of sperm motility and the increase of sperm deformity rate, decreased the enzymes activities of G6 PDH, ACP and CAT, increased LDH activity and MDA content, and decreased the T-AOC level in testicular tissue, and the differences were statistically significant(P&lt;0. 05). Compared with the MR group, the joint action of nano-selenium and nano-cerium with medium dose increased the daily sperm production of testis((18. 98±1. 27) ×10~6/g) vs. (15. 53±1. 24) ×10~6/g), decreased the sperm deformity rate(11. 74%±0. 91% vs. 16. 84%±2. 05%), and the joint action of nano-selenium and nano-cerium with medium and high dose increased the sperm motility in epididymis(61. 98%±6. 33%, 54. 17±4. 38 vs. 45. 16%±5. 01%), and the differences were statistically significant(P&lt;0. 05). Compared with the MR group, the joint action of nano-selenium and nano-cerium with low and medium dose increased the activity of ACP(11. 07±0. 98, 14. 85±1. 39 vs. 8. 72±0. 91 nmol/(min·mg prot), P&lt;0. 05). The joint action of nano-selenium and nano-cerium with medium and high dose increased the activity of G6 PDH(24. 12±2. 06, 21. 36±3. 65 vs. 15. 11±1. 73 nmol/(min·mg prot), P&lt;0. 05) and decreased the activity of LDH(15. 52±1. 17, 13. 51±1. 68 vs. 22. 46±2. 01 nmol/(min·mg prot), P&lt;0. 05). The joint action of nano-selenium and nano-cerium with medium dose increased the activity of CAT(17. 92±2. 03 vs. 11. 69±0. 87 nmol/(min·mg prot), P&lt;0. 05) and decreased the content of MDA(5. 17 ±0. 62 vs. 9. 03 ±0. 63 nmol/mg prot, P&lt;0. 05). The joint action of nano-selenium and nano-cerium with low, medium and high dose increased the level of T-AOC(22. 06±1. 54, 29. 36±2. 39, 21. 01±2. 47 vs. 12. 88±1. 82 U/mg prot, P&lt;0. 05). The joint addition of nano-selenium and nano-cerium can improve the reproductive function of male mice exposed to MR, and can effectively alleviate the changes of mouse testicular marker enzyme activity and the decline of antioxidant capacity caused by MR.

Effect of molybdenum on reproductive function of male mice treated with busulfan

Infertility is a serious public health problem worldwide. Molybdenum (Mo) plays an important role in maintaining normal metabolism. To explore the therapeutic efficacy of molybdenum (Mo) on male infertility, 90 mice were randomly divided into control, busulfan and busulfan + Mo groups. The male mice in the busulfan and busulfan + Mo groups were exposed to busulfan (20 mg/kg body weight) with a single intraperitoneal injection to establish the infertility model. The sterile mice were successfully obtained 30 days after busulfan exposure. Then, the male mice in the busulfan + Mo group were given drinking water containing 20 mg/L Mo continuously for 42 days. At 72 Day after treatment, 30 mice in the three groups were tested for various indices, and 60 mice were mated with females in spontaneous estrus. Mo significantly reversed the thinner seminiferous tubules and disappeared tubule and germ cells. Mo also normalized previously abnormal levels of testosterone, estradiol, luteinizing hormone, superoxide dismutase, lactate dehydrogenase, malondialdehyde. Furthermore, expression levels expression of Bax, Bcl-2, caspase-3 and caspase-9 returned to control levels; and finally, Mo-treated sterile mice obtained offspring with normal number and gender ratio. These results suggested that Mo at 20 mg/L had a significant therapeutic effect on reproductive dysfunction in sterile mice. Its mechanism could via repair of damaged testicular structures, regulation of abnormal reproductive hormone levels, decreased oxidative stress or and resistance to cell apoptosis. Mo may be a new candidate medicine for treatment of male infertility.

Bupropion promotes alterations in the spermatogenesis of mice and congenital malformations in the offspring.

Bupropion hydrochloride (BUP) has been associated with male sexual dysfunction. The aim of this study was to evaluate the effects of BUP on the reproductive function of male mice and to evaluate offspring development. The mice were distributed into BUP group (40mgkg-1) and control group (saline). On Day 35 of treatment the males were placed to mate with females and then killed on Day 46 for evaluation of reproductive function. On Day 18 of pregnancy, pregnant females were killed for evaluation of congenital malformations in the offspring. The BUP group showed a decrease in the Johnsen score (Control, 9.354±0.092; BUP, 7.615±0.147), Sertoli (Control, 5.623±0.184; BUP, 4.215±0.097) and Leydig (Control, 11.430±0.817; BUP, 7.531±0.213) cell counts, testosterone levels (Control, 783.5±154.2ngdL-1; BUP, 201.4±54.8ngdL-1) and sperm production (Control, 2.852±0.211; BUP, 1.988±0.116) and increased morphological alterations of the sperm head (Control, 8.134%; BUP, 10.423%) and tail (Control, 4.96%; BUP, 16.211%). The congenital malformations observed in BUP-derived offspring were: kyphosis (Control, 0.00%; BUP, 5.26%), retroverted rear legs (Control, 14.43%; BUP, 53.68%), incomplete ossification of the supraoccipital and exoccipital (Control, 21.82%; BUP, 86.00%) and sternum (Control, 25.45%; BUP, 82.00%). BUP had toxic effects on testicular function and teratogenic potential.

The Antioxidative Action of Dehydroepandrosterone (DHEA) on the Testicular Histology in adult mice treated with two doses of Nitrofu-rantoin

The antioxidant role of Dehydroepiandrosterone(DHEA) was investigated against two dose of Nitrofurantoin (NFT). Seventy-two adult albino mice were divided in to six equal groups. (G1) control, (G2) received 2 mg/kg B.w of DHEA, (G3) received oral dose of 1.5 mg/kg B.W NFT, (G4) received oral dose of 3 mg/kg B.W of NFT,(G5) received DHEA and 1.5 mg kg/B.w NFT and (G6) received DHEA and 3 mg/kg B.w NFT. Histopathological examination of testes was studied after 30 and 60 day of the experiment and revealed a great number of testicular damage including interstitial hemorrhage and vacuoles, abnormal immature spermatozoa, atrophy in germ cells with severe damage and necrosis of tubules in Nitrofuantoin treated mice. In conclusion, this study showed that NFT has deleterious effect on the reproductive function of male mice and DHEA can protect this system against this harmful effect induced by NFT through its antioxidative activity.

Study efficacy of new model of derivative clonazepam on hypnotic, sedative, blood hematology and evaluation reproductive function in male mice

Study efficacy of new model of derivative clonazepam on hypnotic, sedative, blood hematology and evaluation reproductive function in male mice

Overexpression of PRL7D1 in Leydig Cells Causes Male Reproductive Dysfunction in Mice.

Prolactin family 7, subfamily d, member 1 (PRL7D1) is found in mouse placenta. Our recent work showed that PRL7D1 is also present in mouse testis Leydig cells, and the expression of PRL7D1 in the testis exhibits an age-related increase. In the present study, we generated transgenic mice with Leydig cell-specific PRL7D1 overexpression to explore its function during male reproduction. Prl7d1 male mice exhibited subfertility as reflected by reduced sperm counts and litter sizes. The testes from Prl7d1 transgenic mice appeared histologically normal, but the frequency of apoptotic germ cells was increased. Prl7d1 transgenic mice also had lower testosterone concentrations than wild-type mice. Mechanistic studies revealed that Prl7d1 transgenic mice have defects in the testicular expression of steroidogenic acute regulatory protein (STAR) and hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase cluster (HSD3B). Further studies revealed that PRL7D1 overexpression affected the expression of transferrin (TF) in Sertoli cells. These results suggest that PRL7D1 overexpression could lead to increased germ cell apoptosis and exert an inhibitory effect on testosterone production in Leydig cells by reducing the expression of certain steroidogenic-related genes. In addition, PRL7D1 appears to have important roles in the function of Sertoli cells, which, in turn, affects male fertility. We conclude that the expression level of PRL7D1 is associated with the reproductive function of male mice.

The combined effect of clothianidin and environmental stress on the behavioral and reproductive function in male mice.

Neonicotinoids, some of the most widely used pesticides in the world, act as agonists to the nicotinic acetylcholine receptors (nAChRs) of insects, resulting in death from abnormal excitability. Neonicotinoids unexpectedly became a major topic as a compelling cause of honeybee colony collapse disorder, which is damaging crop production that requires pollination worldwide. Mammal nAChRs appear to have a certain affinity for neonicotinoids with lower levels than those of insects; there is thus rising concern about unpredictable adverse effects of neonicotinoids on vertebrates. We hypothesized that the effects of neonicotinoids would be enhanced under a chronic stressed condition, which is known to alter the expression of targets of neonicotinoids, i.e., neuronal nAChRs. We performed immunohistochemical and behavioral analyses in male mice actively administered a neonicotinoid, clothianidin (CTD; 0, 10, 50 and 250 mg/kg/day), for 4 weeks under an unpredictable chronic stress procedure. Vacuolated seminiferous epithelia and a decrease in the immunoreactivity of the antioxidant enzyme glutathione peroxidase 4 were observed in the testes of the CTD+stress mice. In an open field test, although the locomotor activities were not affected, the anxiety-like behaviors of the mice were elevated by both CTD and stress. The present study demonstrates that the behavioral and reproductive effects of CTD become more serious in combination with environmental stress, which may reflect our actual situation of multiple exposure.

Disrupting Immune Regulation Incurs Transient Costs in Male Reproductive Function

BackgroundImmune protection against pathogenic organisms has been shown to incur costs. Previous studies investigating the cost of immunity have mostly focused on the metabolic requirements of immune maintenance and activation. In addition to these metabolic costs, the immune system can induce damage to the host if the immune response is mis-targeted or over-expressed. Given its non-specific nature, an over-expressed inflammatory response is often associated with substantial damage for the host. Here, we investigated the cost of an over-expressed inflammatory response in the reproductive function of male mice.Methodology/Principal FindingsWe experimentally blocked the receptors of an anti-inflammatory cytokine (IL-10) in male mice exposed to a mild inflammatory challenge, with each treatment having an appropriate control group. The experiment was conducted on two age classes, young (3 month old) and old (15 month old) mice, to assess any age-related difference in the cost of a disrupted immune regulation. We found that the concomitant exposure to an inflammatory insult and the blockade of IL-10 induced a reduction in testis mass, compared to the three other groups. The frequency of abnormal sperm morphology was also higher in the group of mice exposed to the inflammatory challenge but did not depend on the blockade of the IL-10.ConclusionsOur results provide evidence that immune regulation confers protection against the risk of inflammation-induced infertility during infection. They also suggest that disruption of the effectors involved in the regulation of the inflammatory response can have serious fitness consequences even under mild inflammatory insult and benign environmental conditions.

Oxidative Stress: Role in Acetamiprid-Induced Impairment of the Male Mice Reproductive System

Acetamiprid has a wide range of influence on physiological functions in mammals. The objective of this study was to examine the effect of acetamiprid on the reproductive function of male mice, and to study the role of oxidative stress in acetamiprid-induced damage to the testes. Fifty adult Kunmin male mice (25–30 g) were divided into five groups (n=10 per group), i.e., control, blank, acetamiprid alone, acetamiprid and vitamin E, and vitamin E alone. All groups were treated for 35 d. The results showed that acetamiprid significantly decreased the body weight and the weight of testosteroneresponsive organs, such as the testis, epididymis, seminal vesicle, and prostate. Furthermore, acetamiprid also significantly reduced the serum testosterone concentration, and decreased sperm count, viability, motility, and the intactness of the acrosome ( P<0.05 for each parameter). The mice treated with acetamiprid had damaged seminiferous tubules and Leydig cells based on the histological structure of testes; there was degeneration of the mitochondria and endoplasmic reticulum of Leydig cells. These deleterious effects of acetamiprid may be mediated by increasing oxidative stress, as acetamiprid increased malondialdehyde and nitric oxide in the testes, reduced the activity of catalase, glutathione peroxidase, superoxide dismutase, and activated p38. The concentration of acetamiprid in the testes was lower than that in liver, so did the concentrations of liver function tests, including aspartate transaminase (AST), alanine transaminase (ALT) and alkaline phosphatase (ALP), which suggest that male reproductive function may be affected through the indirect action of its metabolites. Vitamin E significantly ameliorated the effects of acetamiprid. We conclude that acetamiprid damages male reproductive function through inducing oxidative stress in the testes.

Beta-cypermethrin impairs reproductive function in male mice by inducing oxidative stress

Cypermethrin (CYP), an insecticide, has deleterious effects on male reproductive function. The objective was to identify whether the effects of beta-CYP on male reproductive organs were associated with oxidative stress. Three doses of beta-CYP (1, 10, and 20 mg/kg) were administered to male mice for 35 d, with or without vitamin E (20 mg/kg). The moderate (10 mg/kg) and high (20 mg/kg) doses of beta-CYP not only decreased body weight and the weight of the testes, epididymides, seminal vesicles, and prostate (P < 0.05) but also reduced serum testosterone concentration and the expression of steroidogenic acute regulatory protein (P < 0.05), in addition to damaging the seminiferous tubules and sperm development. Furthermore, moderate and high doses of beta-CYP administration decreased sperm number, sperm motility, and intact acrosome rate (P < 0.05). Based on ultrastructural analyses, high doses of beta-CYP produced swelling and degeneration of mitochondria and the smooth endoplasmic reticulum of Leydig cells and caused the formation of concentric circles. These toxic effects of beta-CYP may be mediated by increasing oxidative stress, as the moderate and high doses of this compound increased malondialdehyde and nitric oxide in testes (P < 0.05); reduced the activity of catalase, glutathione peroxidase (GSH-Px), and superoxide dismutase (P < 0.05); and activated ERK1/2 (P < 0.05). Vitamin E reversed the effects of beta-CYP on testosterone production and testis damage (P < 0.05 vs. the high-dose group). Therefore, we inferred that beta-CYP damaged the structure of testes and decreased sperm output by inducing oxidative stress.

Effects of fetal exposure to carbon nanoparticles on reproductive function in male offspring

To investigate the effects of fetal nanoparticle exposure on reproductive function in male mice offspring. Animal study. Academic research laboratory. Forty pregnant ICR mice and 120 male offspring. Two hundred microg of 14-nm carbon nanoparticles was administered intratracheally on days 7 and 14 of gestation, and reproductive function of male offspring was determined at ages 5, 10, and 15 weeks after birth. Maternal and fetal growth, histologic changes in the testes, and daily sperm production (DSP). Histologic examination showed partial vacuolation of seminiferous tubules. and cellular adhesion of seminiferous epithelia was reduced at all three ages. In addition, DSP was significantly decreased in fetal carbon nanoparticle-exposed mice. The DSP in the fetal carbon nanoparticle-exposed mice decreased by 47% at the age of 5 weeks, by 34% at the age of 10 weeks, and by 32% at the age of 15 weeks. On the other hand, nanoparticle administration had no marked effect on body weight, testicle weight, epididymis weight, or serum testosterone concentration. These findings suggest that fetal nanoparticle exposure affects the reproductive function of male offspring. In the future, it would be necessary to clarify the onset mechanisms of nanoparticle-induced male reproductive disorders.