Damage To Reproductive System Research Articles

Arginine Biosynthesis Mediates Wulingzhi Extract Resistance to Busulfan-Induced Male Reproductive Toxicity.

Busulfan, an indispensable medicine in cancer treatment, can cause serious reproductive system damage to males as a side effect of its otherwise excellent therapeutic results. Its widespread use has also caused its accumulation in the environment and subsequent ecotoxicology effects. As a Chinese medicine, Wulingzhi (WLZ) has the effects of promoting blood circulation and improving female reproductive function. However, the potential effects of WLZ in male reproduction and in counteracting busulfan-induced testis damage, as well as its probable mechanisms, are still ambiguous. In this study, busulfan was introduced in a mouse model to evaluate its production of the testicular damage. The components of different WLZ extracts were compared using an untargeted metabolome to select extracts with greater efficacy, which were further confirmed in vivo. Here, we demonstrate abnormal spermatogenesis and low sperm quality in busulfan-injured testes. The WLZ extracts showed a strong potential to rehabilitate the male reproductive system; this effect was more prominent in room-temperature extracts. Additionally, both water and ethanol WLZ extracts at room temperature alleviated various busulfan-induced adverse effects. In particular, WLZ recovered spermatogenesis, re-activated arginine biosynthesis, and alleviated the increased oxidative stress and inflammation in the testis, ultimately reversing the busulfan-induced testicular injury. Collectively, these results suggest a promising approach to protecting the male reproductive system from busulfan-induced adverse side effects, as well as those of other similar anti-cancer drugs.

Effect of quercetin and mirtazapine on spermatogenesis and testis structure in phenylhydrazine-induced hemolytic anemia mice: An experimental study

Anemia poses a significant healthcare challenge across different socioeconomic groups and can result in reproductive system damage through the generation of free radicals and lipid peroxidation. This study examines the protective effects of quercetin (QUE) and mirtazapine (MIR) against the reproductive damage caused by phenylhydrazine (PHZ) in mice. Fifty NMRI mice, aged 8–10 weeks with an average weight of 27.0 ± 2.0 g, were randomly divided into five groups. The control group (Group 1) received oral administration of 10 mL/kg/day of normal saline. Group 2 (PHZ group) received an initial intraperitoneal dose of 8 mg/100 g body weight of PHZ, followed by subsequent doses of 6 mg/100 g every 48 h. Group 3 received PHZ along with oral QUE at a dosage of 50 mg/kg/day. Group 4 received PHZ along with oral MIR at a dosage of 30 mg/kg/day. Group 5 received PHZ along with oral QUE at a dosage of 50 mg/kg/day and MIR at a dosage of 30 mg/kg/day. The treatment duration was 35 days. Sperm samples were collected from the caudal region of the epididymis post-euthanasia to assess the total mean sperm count, sperm viability, motility, DNA damage, and morphology. Testicular tissue was employed to quantify total antioxidant capacity (TAC), superoxide dismutase (SOD), glutathione peroxidase (GPx), and malondialdehyde (MDA) concentrations, while serum levels of testosterone, luteinizing hormone (LH), and follicle-stimulating hormone (FSH) were analyzed. Additionally, various aspects, including testicular histopathology, oxidative enzyme levels, gene expression related to apoptosis and antiapoptotic pathways, and in vivo fertility index, were evaluated after 35 days. The QUE, MIR, and QUE + MIR groups showed less abnormal morphology and DNA damage, as well as better total and progressive sperm motility, motility characteristics, viability, and plasma membrane function compared to the PHZ group. QUE, MIR, and QUE + MIR administration increased TAC, SOD, and GPx activities in testicular tissue, while reducing MDA levels compared to the PHZ group. Furthermore, QUE, MIR, and QUE + MIR significantly reduced Bax, and caspase-3 expression levels, and increased Bcl-2 expression levels, compared to the PHZ group. Mice treated with QUE, MIR, and QUE + MIR exhibited an increased in vivo fertility index and plasma sex hormone levels compared to the PHZ group. These results show that QUE, MIR, and QUE + MIR might be able to improve the fertility index, boost the testicular antioxidant defense system, and control the death of germ cells. This could mean that they could be used to treat mice with PHZ-induced testicular damage.

Efficacy of a novel affitoxin targeting MOMP against Chlamydia trachomatis in vitro and in vivo

Abstract Targeted therapy is an attractive approach for treating infectious diseases. Affibody molecules have similar capability to antibodies that facilitate molecular recognition in both diagnostic and therapeutic applications. Targeting major outer membrane protein (MOMP) for treating infection of Chlamydia trachomatis, one of the most common sexually transmitted pathogens, is a promising therapeutic approach. Previously, we have reported a MOMP-specific affibody (ZMOMP:461) from phage display library. Here, we first fused it with modified Pseudomonas Exotoxin (PE38KDEL) and a cell-penetrating peptide (CPP) to develop an affitoxin, Z461X-CPP. We then verified the addition of both toxin and CPPs that did not affect the affinitive capability of ZMOMP:461 to MOMP. Upon uptake by C.trachomatis-infected cells, Z461X-CPP induced cell apoptosis in vitro. In animal model, Z461X significantly shortened the duration of C. trachomatis infection and prevented pathological damage in mouse reproductive system. These findings provide compelling evidence that the MOMP-specific affitoxin has great potential for targeting therapy of C. trachomatis infection.

Hyperuricemia Induces Reproductive Damage in Male Rats through Zinc Homeostasis Imbalance and Oxidative Stress

Studies have reported the adverse effects of hyperuricemia on male reproduction, but the mechanism is still unclear. The purpose of this study is to explore the mechanism of hyperuricemia on reproductive system damage in male rats. The rats were divided into a control group and a model group. Rats were given hypoxanthine and potassium oxonate dissolved in 0.5% (w/v) sodium carboxymethyl cellulose solution to induce the hyperuricemia (HUA) model. After 6 weeks, the blood, testis, and epididymis tissues of the anesthetized rats were collected for further experiments and analysis. Compared with the control rats, the serum uric acid of HUA rats was significantly increased, and the serum testosterone, sperm count, and motility were significantly decreased. The protein expression of testosterone-related molecules CYP11A1, 3β-HSD, and StAR was downregulated in the testis of HUA rats. The protein expression of blood–testis barrier (BTB) related molecules ZO-1 and Connexin43 was downregulated in the testis of HUA rats. Compared with the control group, the zinc content and zinc-containing enzymes (ALP and LDH) were decreased, and the mRNA and protein expression of zinc transporters (ZnT4 and ZIP7) were downregulated in the testis of HUA rats. Furthermore, the level of MDA increased and the activities of CAT, GSH-PX, and SOD decreased in the testicular tissue of HUA rats. The PI3K/AKT/mTOR pathway in the testis of HUA rats was activated. However, there was no significant change in the protein expression of autophagy associated molecules LC3, Beclin1, and ATG5 in the testis of HUA rats. Thus, the conclusion is that hyperuricemia can lead to the destruction of BTB, impaired testosterone synthesis, and decreased sperm count and motility in male rats, mainly by inducing zinc homeostasis imbalance and oxidative stress, rather than autophagy.

Research progress on reproductive system damage caused by high altitude hypoxia.

The high altitude area is characterized by low pressure and hypoxia, and rapidly entering the high altitude area will cause a series of damage to the body. Some studies have shown that hypoxia can cause damage to the reproductive system. In recent years, researchers have been paying attention to the effects of hypoxia on hormone level, ovarian reserve, embryonic development, testicular development, sperm motility level, and have begun to explore its injury mechanism, but its mechanism is not clear. In this paper, the mechanism of hypoxia on the reproductive system is reviewed, which is expected to provide a new idea for solving the problem of the low fertility rate of humans and animals at high altitudes. A comprehensive PubMed search was conducted, selecting all relevant peer-reviewed English papers published before January 2022. Other relevant papers were selected from the list of references. Studies have shown that the complete fertility rate of people living at low altitudes is 7.7, and the complete fertility rate of people living at high altitudes is 4.77, and the hypoxic environment at high altitudes reduces fertility. At the same time, high-altitude, low-oxygen environments are associated with increased infant mortality and post-neonatal mortality. To date, most studies seem to point to a correlation between anoxic exposure at high altitudes and low fertility in humans and animals. Although the molecular mechanisms are not fully understood, the effects of hypoxia at high altitude on hormonal level, ovarian reserve, embryonic development, testicular development, and sperm motility and levels require further research to investigate this complex topic.

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.

Di(2-ethylhexyl) phthalate induces reproductive toxicity and transgenerational reproductive aging in Caenorhabditis elegans

With the large-scale production and use of plastic products, the global plastic pollution problem is becoming more and more serious. The plasticizer di (2-ethylhexyl) phthalate (DEHP), which is widely used in the production of plastics, has caused great concern for the health of the population. Exposure of organisms to DEHP can cause a variety of health damage, of which reproductive system damage is an important part. At present, there are still few studies on DEHP in reproductive aging, and it is of great significance to explore the role of DEHP in promoting reproductive aging and its underlying mechanism. In this study, the model organism Caenorhabditis elegans (C. elegans) was used to preliminarily explore the mechanism of DEHP-induced female reproductive senescence. The results showed that DEHP reduced the number of offspring and gonad area of C. elegans, resulting in shortened reproductive and life span, abnormal phenotypes in somatic gonad structure including the Emo phenotype, the BOW phenotype, a twisted gonad arm, and atrophied oocytes. Biochemical studies showed that DEHP promoted oxidative stress and autophagy in C. elegans. Further, we found the decreased number of offspring, malformed somatic gonad structure, oxidative damage and autophagy induced by DEHP in parental worms can be inheritance to the not directly exposed offspring.

Testicular toxicity induced by T-2 toxin and protective effect of vitamin E in Wistar rats

Background and purpose: Mycotoxicosis is a very common problem in stored feed and fodder. Ingestion of T-2 toxin through feedstuff leads to serious consequences and production losses in exposed populations. That may lead to reproductive organ system damage resulting in the reproductive problem. The study was planned to investigate the effect of T-2 toxin and vitamin E on testicular function in Wistar rats. Material and methods: Male Wistar rats were fed with standard rat feed. T-2 toxin treatment groups received T-2 toxin (2.5 ppm and 5.0 ppm) mixed feed, while vitamin E (100 mg/kg) was given by oral gavage alone and in T-2 toxin fed groups. After completion of 28 days of oral feeding of text compounds reproductive toxicity parameters were evaluated. Results: Total live sperm counts, sperm motility, and serum testosterone levels were reduced in T-2 toxin-treated groups. Antioxidant enzymes/nonenzymes and oxidative stress indicators were altered significantly and cellular damage to testis and epididymis in T-2 toxin groups was in a dosedependent manner. However, vitamin E intervention caused a marked reversal effect in T-2 toxin-fed rats on testicular damage and male reproductive parameters. Oxidative stress and related events appear to be a potential mechanism involved in T-2 toxin-mediated testicular damage. Conclusion: This study validated that the use of an optimum dose of vitamin E has the potential to protect against the testicular damage caused by the T-2 toxin.

Nanoparticles Induced Oxidative Damage in Reproductive System and Role of Antioxidants on the Induced Toxicity.

Nanotechnology is used in a variety of scientific, medical, and research domains. It is significant to mention that there are negative and severe repercussions of nanotechnology on both individuals and the environment. The toxic effect of nanoparticles exerted on living beings is termed as nanotoxicity. Nanoparticles are synthesized by various methods such as chemical, biological, physical, etc. These nanoparticles' nanotoxicity has been observed to vary depending on the synthesis process, precursors, size of the particles, etc. Nanoparticles can enter the cell in different ways and can cause cytotoxic effects. In this review, the toxicity caused in the reproductive system and the role of the antioxidants against the nanotoxicity are briefly explained.

The role of taurine in male reproduction: Physiology, pathology and toxicology.

Taurine, a sulfur-containing amino acid, has a wide range of biological effects, such as bile salt formation, osmotic regulation, oxidative stress inhibition, immunomodulation and neuromodulation. Taurine has been proved to be synthesized and abundant in male reproductive organs. Recently, accumulating data showed that taurine has a potential protective effect on reproductive function of male animals. In physiology, taurine can promote the endocrine function of the hypothalamus-pituitary-testis (HPT) axis, testicular tissue development, spermatogenesis and maturation, delay the aging of testicular structure and function, maintain the homeostasis of the testicular environment, and enhance sexual ability. In pathology, taurine supplement may be beneficial to alleviate pathological damage of male reproductive system, including oxidative damage of sperm preservation in vitro, testicular reperfusion injury and diabetes -induced reproductive complications. In addition, taurine acts as a protective agent against toxic damage to the male reproductive system by exogenous substances (e.g., therapeutic drugs, environmental pollutants, radiation). Related mechanisms include reduced oxidative stress, increased antioxidant capacity, inhibited inflammation and apoptosis, restored the secretory activity of the HPT axis, reduced chromosomal variation, enhanced sperm mitochondrial energy metabolism, cell membrane stabilization effect, etc. Therefore, this article reviewed the protective effect of taurine on male reproductive function and its detailed mechanism, in order to provide reference for further research and clinical application.

Chronic oral exposure to short chain chlorinated paraffins induced testicular toxicity by promoting NRF2-mediated oxidative stress

As a widespread environmental contaminant, short chain chlorinated paraffins (SCCPs) has attracted great attention. However, the toxicity of SCCPs on male reproductive system remains ambiguous. In this study, we treated mice with SCCPs by gavage and investigated the toxic effects of SCCPs on testis. According to the results, the sperm parameters of mice were significantly reduced after exposure to 1, 10, 100 mg/kg body mass per day SCCPs for 35 days. SCCPs resulted in disorderly arranged seminiferous epithelium and increased apoptotic cells in testes. Both in vivo and in vitro experiments indicated that the oxidative stress was induced after SCCPs exposure, and dysfunction of nuclear factor erythroid-related factor (NRF2) signaling pathway played a role in this process. Moreover, resveratrol, an NRF2 activator, could alleviate the damage of SCCPs onmale reproductive system. Our study indicated that oxidative stress is the key point for explaining the testicular toxicity caused by SCCPs, and NRF2 could be used as a potential target for clinical treatment to alleviate the reproductive toxicity induced by SCCPs.

BDE-209 induced spermatogenesis disorder by inhibiting SETD8/H4K20me1 related histone methylation in mice

Past studies have observed that decabromodiphenyl ether (BDE-209) induces reproductive and developmental toxicity, but the specific mechanism remains unclear. Based on our previous work, male mice were orally given BDE-209 at 75 mg/kg/d via continuous exposure for one spermatozoon development period (50 days) and then stopping exposure for another 50 days. The mouse spermatocyte line GC-2spd was used to examine the toxic effects of BDE-209 on histone methylation and spermatogenesis. The findings indicated that BDE-209 damaged testis and epididymis structure, induced spermatogenic cell apoptosis, and decreased sperm quantity and quality after the 50-day exposure. Furthermore, BDE-209 lowered the levels of SETD8/H4K20me1 and activated the upstream signaling of DNA damage response (Mre11/Rad50/NBS1), thereby causing spermatogenic cell cycle arrest and apoptosis. Downregulation of meiotic promoter Stra8 was associated with a decrease in SETD8 after BDE-209 exposure. After stopping the exposure for 50 days, reproductive system damage and meiosis and cell cycle inhibition due to histone methylation did not improve. In vitro experiments revealed that Setd8 overexpression upregulated the histone methylation and Stra8 expression but did not promote the cell cycle in GC-2 cells. Therefore, BDE-209 exposure impaired spermatogenesis by affecting SETD8/H4K20me1-linked histone methylation and inhibiting meiosis initiation and cell cycle progression, thereby resulting in long-term male reproductive toxicity.

Alleviating effects of selenium on fluoride-induced testosterone synthesis disorder and reproduction toxicity in rats

Fluoride (F) exists widely in food, water and other natural resources, and can cause damage to the reproductive system of human and animals. Studies have shown that selenium (Se) is a necessary trace element to maintain the normal male reproductive system. However, it is not clear whether it can alleviate the damage of reproductive system induced by F. Hence, sodium fluoride (NaF) was administered singly in drinking water at 100 mg L−1 alone and co-administered by drinking with sodium selenite (Na2SeO3) at 0.5, 1.0, 2.0 mg L−1 for 10 consecutive weeks. The results demonstrated that the sperm deformity rate were increased significantly by F, however, it was improved significantly after the addition of 2.0 mg L−1 Na2SeO3. The contents of glutathione peroxidase 4 (GPX-4), selenoprotein P (SePP), pregnenolone (PREG), androstenedione (ASD), and testosterone (T) were reduced obviously in the F group, however, it was increased significantly after adding 0.5, 1.0 and 2.0 mg L−1 Na2SeO3. F decreased noticeably the mRNA and protein expression levels of steroidogenic acute regulatory protein (StAR), cytochrome P450 cholesterol side chain lyase (P450scc), 3β-hydroxysteroid dehydrogenase (3β-HSD), cytochrome P450 17α-hydroxylase (P450c17) and 17β-hydroxysteroid dehydrogenase (17β-HSD), which was increased obviously after the addition of 1.0 and 2.0 mg L−1 Na2SeO3. In summary, 2.0 mg L−1 Na2SeO3 can alleviate testosterone synthesis disorder induced by F via reducing oxidative stress, increasing the level of selenoprotein in testis and regulating the content of related hormones and enzyme activity during testosterone synthesis pathway.

SCANNING ELECTRONIC MICROSCOPY OF MUCOUS MEMBRANE OF THE UTERINE TUBE UNDER THE CONDITIONS OF PHYSIOLOGICAL NORM AND SIX-WEEK ADMINISTRATION OF OPIOID

The toxic effects of opioids on the female reproductive system are important for theoretical and practical medicine, because excessive use of narcotic drugs causes pathological changes in organs and tissues and can predict the negative effects of "nalbuphine" on the female genitals. The excessive use of narcotic drugs, the prevalence of drug addiction, the use of opioids by modern medicine for therapeutic purposes, creates the need to carefully study the effects of opioids on the body of women, primarily the organs of the reproductive system, because despite the successes achieved in diagnosis and treatment, female infertility is an urgent problem.
 Aim of the research: to establish and describe the features of the structural organization of the mucous membrane of the uterine tube of a female laboratory rat in normal and under conditions of prolonged exposure to «nalbuphine» according to the results of scanning electron microscopy.
 Materials and methods. The material of the research was the mucous membrane of the uterine tubes of 20 mature white female rats, aged 4.5–6.0 months with body weight 180–220, which were kept in standard conditions at the vivarium of the Danylo Halytskyi Lviv National Medical University. The structural organization of the mucous membrane of the uterine tubes was normally studied in 5 animals. Experimental animals were divided into 2 groups. The first group of experimental animals (10 rats) was administered «nalbuphine» intramuscularly once daily, in one period of time for 6 weeks. The second group - control animals - 5 white female rats, which were injected with saline. The method of scanning electron microscopy of the mucous membrane of the uterine tube of the rat was used in the research.
 Results. Lesions of the reproductive system damage is an integral part of clinic both opiate addiction and intoxication of pharmaceutical remedies in particular the group of opioids. The connection between duration of «nalbuphine» administration and depth of changes of structural organization of mucous membrane of the uterine tube was established in the experiment. The obtained data show that the six-week administration of «nalbuphine» causes destructive changes in the mucous membrane of the uterine tube wall similar to long-term inflammatory processes, in particular, an increase in the lumen of the uterine tube, a decrease or absence of folds in certain areas of the uterine tube, a decrease in the number of microvilli of tubal exocrinocytes, and the occurrence of adenomatous proliferation of the tubal epithelium.
 The damage that has occurred indicates the ability of the opioid to cause irreversible changes with prolonged use.
 Conclusions. The connection between duration of «nalbuphine» administration and depth of changes of structural organization of the mucous membrane of the uterine tube was established in the experiment. Prolonged administration of opioids causes irreversible destructive changes in the mucous membrane of the uterine tube of the female rat, which is manifested by the phenomena of disorganization of both endothelial cells. The damage that has occurred proves the ability of opioid in long-term use to cause irreversible changes and structure and function damages on all levels starting with structural. The results of the work can serve as a basis for the further search for optimal methods of correcting changes in the structure of organs caused by the long-term use of opioids.

Molecular Hydrogen Reduces Electromagnetic Pulse-Induced Male Rat Reproductive System Damage in a Rodent Model.

Infertility has got to be a broadly concerned social issue these days, in which the malefactor cannot be overlooked. Numerous studies have shown that electromagnetic pulse (EMP) radiation may have seriously damaging effects on reproductive health, through nonthermal effects and oxidative stress. Molecular hydrogen, a selective hydroxyl radical scavenger, explains the protective effects against many diseases closely associated with oxidative damage, such as ionizing radiation (IR). We sought to characterize the beneficial effects of molecular hydrogen on the male reproductive system in a rodent EMP exposure model. The 8-week-old male Sprague-Dawley rats were exposed to EMP (peak intensity 1000 kV/m, pulse edge 20 ns, pulse width 200 ns, 1 Hz, and 200 pulses), with or without hydrogen-rich water. The pathological structure of the testis, the rate of apoptosis of the testis, the serum testosterone level, the sperm parameters, and the activity of the antioxidant enzymes of the testis were measured. Then, transcriptomic and untargeted metabolomic analyses were applied to uncover the underlying mechanism. Exposure to EMP increased testicular apoptosis rate and apoptosis protein level, decreased sperm viability and motility, decreased serum testosterone levels, and diminished testicular antioxidant capacity. Molecular hydrogen-alleviated damage decreased the testicular apoptosis rate and apoptosis protein level, increased sperm motility, increased serum testosterone levels, and improved antioxidative capacity. Omics results showed that molecular hydrogen has a strong influence on metabolic pathways, and EMP affects mainly oxidative phosphorylation, TNF signaling pathways, and cytokine-receptor interactions. The mechanism of molecular hydrogen's effect may be related to the reversal of some metabolite levels. These observations warrant molecular hydrogen as an innovative approach for potential protection against EMP.

Mechanism of 2,4-Dichlorophenoxyacetic acid-induced damage to rat testis via Fas/FasL pathway and the protective effect of Lycium barbarum polysaccharides.

The herbicide 2,4-Dichlorophenoxyacetic acid (2,4-D) is widely used to control broadleaved weeds and has been associated with male infertility. We studied the molecular mechanisms of 2,4-D induced male reproductive system damage and the protective effects of Lycium barbarum polysaccharides (LBP) using Sprague Dawley rats and TM4 cells. Treatment with 2,4-D caused architectural and functional changes in the testis, including collapsed and atrophied seminiferous tubules with reduced number of spermatozoa, scarce sperm in the epididymal duct, low levels of serum testosterone, decreased superoxide dismutase and glutathione peroxidase activity, high malondialdehyde content, and increased apoptosis in the testis and epididymis. The expression of Fas, FasL, FADD, Pro-caspase-8, Cleaved-Caspase-8, Pro-Caspase-3, and Cleaved-Caspase-3 were significantly increased in the testicular tissue of 2,4-D-treated rats. The proliferative activity of TM4 cells decreased with an increase in dose and time of 2,4-D exposure, along with enhanced Fas/Fas ligand expression and a decreased concentration of inhibin B in TM4 cell culture medium. Depletion of Fas by specific shRNA transfection reversed the effects of 2,4-D in TM4 cells, further confirming the involvement of death receptor pathway in 2,4-D-mediated apoptosis of sertoli cells. Treatment with LBP also reversed the effects of 2,4-D in testicular cells, resulting in improved cell architecture along with enhanced proliferative capacity. Moreover, in response to LBP treatment of Sertoli cells, the content of inhibin B increased, the level of reactive oxygen species and malondialdehyde decreased, the activities of superoxide dismutase and glutathione peroxidase increased, and the rate of apoptosis as well as the expression of Fas/Fas ligand signaling pathway proteins decreased.

Youjing granules ameliorate spermatogenesis in rats through regulating the prolifereation of spermatogonial stem cells.

Male infertility has evolved from a common reproductive system disease to a major social issue. Youjing granule (YG) is a Chinese medicinal material used as a therapy method for tonifying the kidneys and removing dampness due to its pathogenic characteristics. YG has been shown to regulate sperm quality in clinical trials, but the underlying mechanism is not fully understood. The present study was aimed to explore the protective effects and mechanism of action of YG on male reproductive system damage caused by methyl methane sulfonate (MMS). We first established an infertility model of rats through oral administration of MMS and then treated with YG. To determine the effect of YG, spermatogenesis, microvascular density, and secretory function of Leydig cells and Sertoli cells in rats were assessed. Spermatogonial stem cells (SSCs) were co-cultured with mouse embryo fibroblast (MEF) cells as an in vitro cell model before exposure to serum containing YG. Furthermore, the proliferation and apoptosis of SSCs were measured. Results indicated that YG increased the expression of self-renewal and proliferation-related molecules such as glial cell line derived neurotrophic factor (GDNF) and fibroblast growth factor-2 (FGF2), and improved the quality of sperm and the proliferation of SSCs. In conclusion, YG may protect spermatogenetic function of rats through regulating the proliferation and self-renewal of SSCs.

Infecciones abdominales y del tracto reproductor femenino por anaerobios

Anaerobic bacteria play an important role in abdominal cavity and female pelvic infections. Abdominal infections are generally severe diseases associated with variable mortality rates depending on various factors, including the patient's prior diseases and clinical condition, localization of the infection, bacteria involved in the infection, and type of treatment and time that passed until it was given. Infections of the female reproductive system damage the endometrium, fallopian tubes, ovaries, and pelvic peritoneum. Their late diagnosis contributes to the onset of infertility, ectopic pregnancy, and chronic pelvic pain in women. This work addresses the main clinical syndromes caused by anaerobic microorganisms located in the abdominal cavity and female genital tract.

Recent advances in toxicological research and potential health impact of microplastics and nanoplastics in vivo.

As emerging pollutants, direct and indirect adverse impacts of micro(nano)plastics (MPs/NPs) are raising an increasing environmental concern in recent years due to their poor biodegradability and difficulty in recycling. MPs/NPs can act as carriers of bacteria, viruses, or pollutants (such as heavy metals and toxic organic compounds), and may potentially change the toxicity and bioavailability of pollutants. Ingested or attached MPs/NPs can also be transferred from low-trophic level organisms to high-nutrient organisms or even the human body through the food chain transfer process. This article reviews the emerging field of micro- and nanoplastics on organisms, including the separate toxicity and toxicity of compound after the adsorption of organic pollutants or heavy metals, as well as possible mechanism of toxicological effects and evaluate the nano- and microplastics potential adverse effects on human health. The inherent toxic effects MPs/NPs mainly include the following: physical injury, growth performance decrease and behavioral alteration, lipid metabolic disorder, induced gut microbiota dysbiosis and disruption of the gut's epithelial permeability, neurotoxicity, damage of reproductive system and offspring, oxidative stress, immunotoxicity, etc. Additionally, MPs/NPs may release harmful plastic additives and toxic monomers such as bisphenol A, phthalates, and toluene diisocyanate. The vectors' effect also points out the potential interaction of MPs/NPs with pollutants such as heavy metals, polycyclic aromatic hydrocarbons, organochlorine pesticides, polychlorinated biphenyls, perfluorinated compounds, pharmaceuticals, and polybrominated diphenyl ethers. Nevertheless, these potential consequences of MPs/NPs being vectors for contaminants are controversial.

Predominance of Antioxidants in Some Edible Plant Oils in Ameliorating Oxidative Stress and Testicular Toxicity Induced by Malathion.

Malathion (MAL) is an insecticide that has been linked to reproductive system damage in both humans and animals. In the present investigation, the antitoxic effects of coffee and olive oils on MAL-induced testicular dysfunctions were evaluated. MAL-intoxicated rats were supplemented with coffee and olive oils (400 mg/kg) for 7 weeks. Exposure to MAL resulted in statistically altered antioxidant enzymes and histopathological findings of necrotic seminiferous tubules and spermatogenetic arrest in rats after seven weeks of treatment. The effects of MAL intoxication on physiological and histopathological changes were improved by the use of these oils. Murine double minute 2 (MDM2) was found to interact well with chlorogenic acid and oleuropein, two compounds from coffee and olive oils, respectively. Coffee oil and olive oil were found to be promising therapeutic agents for MAL-induced testicular toxicity and oxidative damage.