Decabromodiphenyl ether induces the chromosome association disorders of spermatocytes and deformation failures of spermatids in mice.

The environmental presence of decabromodiphenyl ether (BDE-209), which is toxic to the male reproductive system, is widespread. The current study investigated its mechanism of toxicity in mice. The results showed, that BDE-209 induced DNA damage, decreased the expression of the promoter of meiosis spermatogenesis- and oogenesis-specific basic helix-loop-helix 1 (Sohlh1), meiosis related-factors Lethal (3) malignant brain tumor like 2 (L3MBTL2), PIWI-like protein 2 (MILI), Cyclin-dependent kinase 2 (CDK2), Cyclin A, synaptonemal complex protein 1 (SYCP1) and synaptonemal complex protein 3 (SYCP3), and caused spermatogenic cell apoptosis, resulting in a decrease in sperm quantity and quality.

Effects of exposure to PM during pregnancy on the multigenerational reproductive outcomes of male mouse offspring and the role of Sertoli cells.

There is a paucity of studies on the multigenerational reproductive toxicity of fine particle matter (PM) exposure during pregnancy on male offspring and the underlying mechanisms. This study explored the effects of PM exposure during pregnancy on the spermatogenesis of three consecutive generations of male mouse offspring. We randomized pregnant C57BL/6 mice into the control group, the Quartz Fiber Membrane control group, and two experimental groups exposed to different concentrations of PM (4.

Decabromodiphenyl ethane induces male reproductive toxicity by glycolipid metabolism imbalance and meiotic failure.

Decabromodiphenyl ethane (DBDPE) is a typical flame retardant found in various electrical and textile items. DBDPE is abundantly available in the surrounding environment and wild animals based on its persistence and bioaccumulation. DBDPE has been shown to cause apoptosis in rat spermatogenic cells, resulting in reproductive toxicity.

Fat mass and obesity-associated gene (FTO) hypermethylation induced by decabromodiphenyl ethane causing cardiac dysfunction via glucolipid metabolism disorder.

Decabromodiphenyl ethane (DBDPE) is a major alternative to BDE-209 owing to its lower toxicity. However, the mass production and increased consumption of DBDPE in recent years have raised concerns related to its adverse health effects. However, the effect and mechanism of DBDPE on cardiotoxicity have rarely been studied.

Maternal exposure to PM2.5 induces the testicular cell apoptosis in offspring triggered by the UPR-mediated JNK pathway.

Contemporary exposure to PM has been reported to disrupt spermatogenesis. However, the subsequent toxicological responses and the mechanisms of male reproductive damage in offspring induced by maternal exposure to PM remain largely unknown. For the first time, this study aimed to explore the apoptotic response in spermatogenesis of male offspring following maternal exposure to PM and its mechanisms.

The impact of polystyrene microplastics on cardiomyocytes pyroptosis through NLRP3/Caspase-1 signaling pathway and oxidative stress in Wistar rats.

The extensive existing of microplastics (MPs) in the ecosystem have increased considerable attention concerning their potential adverse effects, the toxicities and the underlying mechanism of MPs are still scarce. To explore the effect of MPs on cardiac tissue in Wistar rats and unravel the mechanism of pyroptosis and oxidative stress in the process of cardiomyocytes injury, 32 male Wister rats were divided into control group and three model groups, which were exposed to 0.5 mm PS MPs at 0.

Silica nanoparticles induce unfolded protein reaction mediated apoptosis in spermatocyte cells.

With increasing air pollution, silica nanoparticles (SiNPs), as a main inorganic member of PM, have gained increasing attention to its reproductive toxicity. Most existing studies focused on the acute exposure, while data regarding the chronic effect of SiNPs on reproduction is limited. Therefore, this study was designed to evaluate the chronic toxicity of SiNPs on spermatocyte cells.

miR-205/IRAK2 signaling pathway is associated with urban airborne PM-induced myocardial toxicity.

Exposure to fine particulate matter (PM) is closely linked with cardiovascular diseases. However, the underlying mechanism of PM on cardiac function remains unknown. This study was aimed to investigate the role of microRNA-205 (miR-205) on PM-induced myocardial inflammation and cardiac dysfunction.

Polystyrene microplastics cause cardiac fibrosis by activating Wnt/β-catenin signaling pathway and promoting cardiomyocyte apoptosis in rats.

Microplastics (MPs) are new persistent organic pollutants derived from the degradation of plastics. They can accumulate along the food chain and enter the human body through oral administration, inhalation and dermal exposure. To identify the impact of Polystyrene (PS) MPs on the cardiovascular system and the underlying toxicological mechanism, 32 male Wister rats were divided into control group and three model groups, which were exposed to 0.

Low-Dose Exposure of Silica Nanoparticles Induces Neurotoxicity via Neuroactive Ligand-Receptor Interaction Signaling Pathway in Zebrafish Embryos.

Objective: Silica nanoparticles (SiO NPs) have been extensively employed in biomedical field. SiO NPs are primarily designed to enter the circulatory system; however, little information is available on potential adverse effects of SiO NPs on the nervous system.

Methods: The neurotoxicity of SiO NPs at different concentrations (3, 6, 12 ng/nL) on zebrafish embryos was determined using immunofluorescence and microarray techniques, and subsequently confirmed by qRT-PCR.

Endosulfan induces cardiotoxicity through apoptosis via unbalance of pro-survival and mitochondrial-mediated apoptotic pathways.

Although the associations between endosulfan and adverse cardiovascular health have been reported, the toxic effects and underlying mechanism of endosulfan on the heart are not well understood. In this study, we examined the cardiotoxicity induced by endosulfan using Wistar rats and human cardiomyocytes (AC16) cells. Wistar rats were divided into control group (received corn oil alone) and three concentrations of endosulfan groups (1, 5 and 10 mg/kg·bw) by gavage.

Maternal exposure to fine particle matters cause autophagy via UPR-mediated PI3K-mTOR pathway in testicular tissue of adult male mice in offspring.

Epidemiological studies have shown that particulate matters are closely related to human infertility. However, the long-term risk of particulate matters exposure in early life is rarely considered. For the first time this study is designed to explore and elucidate the mechanism of maternal exposure to fine particle matters (PM) on autophagy in spermatogenic cells of adult offspring.

Silica nanoparticles exacerbates reproductive toxicity development in high-fat diet-treated Wistar rats.

To demonstrate the combined adverse effect and the mechanism of silica nanoparticles (SiNPs) with 57.66 ± 7.30 nm average diameter and high-fat diet (HFD) on Wistar rats, 60 male Wistar rats were randomly divided into six groups (n = 10): Control group, SiNPs group, HFD group, 2 mg kg SiNPs + HFD group, 5 mg kg SiNPs + HFD group and 10 mg kg SiNPs + HFD group.

Silica nanoparticles induce spermatocyte cell autophagy through microRNA-494 targeting AKT in GC-2spd cells.

Researches had shown that silica nanoparticles (SiNPs) could reduce the quantity and quality of sperms. However, chronic effects of SiNPs have not been well addressed. In this study, mice spermatocyte cells (GC-2spd cells) were continuously exposed to SiNPs (5 μg/mL) for 30 passages and then the changes of microRNA (miRNA) profile and mRNA profile were detected.

Fine particulate matters induce apoptosis via the ATM/P53/CDK2 and mitochondria apoptosis pathway triggered by oxidative stress in rat and GC-2spd cell.

Fine particulate matters (PM) have been associated with male reproductive toxicity because it can penetrate into the lung's gas-exchange region, and spread to the whole body via circulatory system. Previous studies have shown that PM could induce DNA damage and apoptosis by reactive oxygen species (ROS). The aim of the present study is to determine the exact mechanism and role of apoptosis induced by PM in spermatocyte cells.

Silica nanoparticles induce spermatocyte cell apoptosis through microRNA-2861 targeting death receptor pathway.

Silica nanoparticles (SiNPs) are found in the environmental particulate matter and have been proved to pose an adverse effect on fertility. However, the relationship between miRNA and apoptosis induced by SiNPs in spermatogenesis and its underlying mechanism remains confusing. Therefore, the present study was designed to investigate the toxic effects of SiNPs on spermatogenic cells mediated through miRNAs.

Silica nanoparticles induce abnormal mitosis and apoptosis via PKC-δ mediated negative signaling pathway in GC-2 cells of mice.

The potential health hazards of silica nanoparticles (SiNPs) have attracted more and more attentions. Researches had shown that SiNPs could damage seminiferous epithelium and reduce the quantity and quality of sperms, however the specific mechanism of male reproductive toxicity induced by SiNPs still unclear. So we designed to investigate the mechanism of SiNPs on male mice using spermatocyte lines (GC-2spd cells) after exposure to SiNPs (6.

PM induces male reproductive toxicity via mitochondrial dysfunction, DNA damage and RIPK1 mediated apoptotic signaling pathway.

Recent years, air pollution has been a serious problem, and PM is the main air particulate pollutant. Studies have investigated that PM is a risky factor to the deterioration of semen quality in males. But, the related mechanism is still unclear.

Fine particle matter disrupts the blood-testis barrier by activating TGF-β3/p38 MAPK pathway and decreasing testosterone secretion in rat.

Fine particle matter (PM) is correlated with male reproductive dysfunction in animals and humans, but the underlying mechanisms remain unknown. To investigate the toxic mechanism of PM, 32 male Sprague-Dawley (SD) rats were exposed to saline or PM with the doses of 1.8, 5.

Silica nanoparticle exposure inducing granulosa cell apoptosis and follicular atresia in female Balb/c mice.

Given that the effects of ultrafine fractions (< 0.1 μm) on reproductive diseases are gaining attention, this study aimed to explore the influence of silica nanoparticle (SiNP)-induced female reproductive dysfunction. In this study, 80 female mice were randomly divided into four groups including a control group and three concentrations of SiNP groups (7, 21, 35 mg/kg).

Endosulfan induces cell dysfunction through cycle arrest resulting from DNA damage and DNA damage response signaling pathways.

Our previous study showed that endosulfan increases the risk of cardiovascular disease. To identify toxic mechanism of endosulfan, we conducted an animal study for which 32 male Wistar rats were randomly and equally divided into four groups: Control group (corn oil only) and three treatment groups (1, 5 and 10mgkg·d). The results showed that exposure to endosulfan resulted in injury of cardiac tissue with impaired mitochondria integrity and elevated 8-OHdG expression in myocardial cells.

Endosulfan inhibits proliferation through the Notch signaling pathway in human umbilical vein endothelial cells.

Our previous research showed that endosulfan triggers the extrinsic coagulation pathway by damaging endothelial cells and causes hypercoagulation of blood. To identify the mechanism of endosulfan-impaired endothelial cells, we treated human umbilical vein endothelial cells (HUVECs) with different concentrations of endosulfan, with and without an inhibitor for Notch, N-[N-(3, 5-difluorophenacetyl)-1-alanyl]S-Phenylglycinet-butylester (DAPT, 20 μM), or a reactive oxygen species (ROS) scavenger, N-Acetyl-l-cysteine (NAC, 3 mM), for 24 h. The results showed that endosulfan could inhibit cell viability/proliferation by increasing the release of lactate dehydrogenase (LDH), arresting the cell cycle in both S and G2/M phases, and inducing apoptosis in HUVECs.

Endosulfan induces autophagy and endothelial dysfunction via the AMPK/mTOR signaling pathway triggered by oxidative stress.

Cardiovascular diseases is related to environmental pollution. Endosulfan is an organochlorine pesticide and its toxicity has been reported. However, the relationship between oxidative stress and autophagy induced by endosulfan and its underlying mechanism remain confusing.