Polystyrene nanoplastics induce apoptosis, autophagy, and steroidogenesis disruption in granulosa cells to reduce oocyte quality and fertility by inhibiting the PI3K/AKT pathway in female mice.

BACKGROUND: Nanoplastics (NPs) are emerging pollutants that pose risks to living organisms. Recent findings have unveiled the reproductive harm caused by polystyrene nanoparticles (PS-NPs) in female animals, yet the intricate mechanism remains incompletely understood. Under this research, we investigated whether sustained exposure to PS-NPs at certain concentrations in vivo can enter oocytes through the zona pellucida or through other routes that affect female reproduction. RESULTS: We show that PS-NPs disrupted ovarian functions and decreased oocyte quality, which may be a contributing factor to lower female fertility in mice. RNA sequencing of mouse ovaries illustrated that the PI3K-AKT signaling pathway emerged as the predominant environmental information processing pathway responding to PS-NPs. Western blotting results of ovaries in vivo and cells in vitro showed that PS-NPs deactivated PI3K-AKT signaling pathway by down-regulating the expression of PI3K and reducing AKT phosphorylation at the protein level, PI3K-AKT signaling pathway which was accompanied by the activation of autophagy and apoptosis and the disruption of steroidogenesis in granulosa cells. Since PS-NPs penetrate granulosa cells but not oocytes, we examined whether PS-NPs indirectly affect oocyte quality through granulosa cells using a granulosa cell-oocyte coculture system. Preincubation of granulosa cells with PS-NPs causes granulosa cell dysfunction, resulting in a decrease in the quality of the cocultured oocytes that can be reversed by the addition of 17ß-estradiol. CONCLUSIONS: This study provides findings on how PS-NPs impact ovarian function and include transcriptome sequencing analysis of ovarian tissue. The study demonstrates that PS-NPs impair oocyte quality by altering the functioning of ovarian granulosa cells. Therefore, it is necessary to focus on the research on the effects of PS-NPs on female reproduction and the related methods that may mitigate their toxicity.

Environmental pollutants and male infertility: Effects on CatSper.

Infertility is a growing health concern among many couples worldwide. Men account for half of infertility cases. CatSper, a sperm-specific Ca2+ channel, is expressed on the cell membrane of mammalian sperm. CatSper plays an important role in male fertility because it facilitates the entry of Ca2+ necessary for the rapid change in sperm motility, thereby allowing it to navigate the hurdles of the female reproductive tract and successfully locate the egg. Many pollutants present in the environment have been shown to affect the functions of CatSper and sperm, which is a matter of capital importance to understanding and solving male infertility issues. Environmental pollutants can act as partial agonists or inhibitors of CatSper or exhibit a synergistic effect. In this article, we briefly describe the structure, functions, and regulatory mechanisms of CatSper, and discuss the body of literature covering the effects of environmental pollutants on CatSper.

Exposure to polystyrene nanoplastics induces hepatotoxicity involving NRF2-NLRP3 signaling pathway in mice.

Nanoplastic contamination has been of intense concern by virtue of the potential threat to human and ecosystem health. Animal experiments have indicated that exposure to nanoplastics (NPs) can deposit in the liver and contribute to hepatic injury. To explore the mechanisms of hepatotoxicity induced by polystyrene-NPs (PS-NPs), mice and AML-12 hepatocytes were exposed to different dosages of 20 nm PS-NPs in this study. The results illustrated that in vitro and in vivo exposure to PS-NPs triggered excessive production of reactive oxygen species and repressed nuclear factor erythroid-derived 2-like 2 (NRF2) antioxidant pathway and its downstream antioxidase expression, thus leading to hepatic oxidative stress. Moreover, PS-NPs elevated the levels of NLRP3, IL-1ß and caspase-1 expression, along with an activation of NF-κB, suggesting that PS-NPs induced hepatocellular inflammatory injury. Nevertheless, the activaton of NRF2 signaling by tert-butylhydroquinone mitigated PS-NPs-caused oxidative stress and inflammation, and inbihited NLRP3 and caspase-1 expression. Conversely, the rescuing effect of NRF2 signal activation was dramatically supressed by treatment with NRF2 inhibitor brusatol. In summary, our results demonstrated that NRF2-NLRP3 pathway is involved in PS-NPs-aroused hepatotoxicity, and the activation of NRF2 signaling can protect against PS-NPs-evoked liver injury. These results provide novel insights into the hepatotoxicity elicited by NPs exposure.

The emerging role of lysine succinylation in ovarian aging.

BACKGROUND: Ovarian aging is a process of decline in its reserve leading to ovary dysfunction and even reduced health quality in offspring. However, aging-related molecular pathways in the ovary remain obscure. Lysine succinylation (Ksuc), a newly post-translational modification (PTM), has been found to be broadly conserved in both eukaryotic and prokaryotic cells, and associated with multiple pathophysiological processes. There are no relevant reports revealing a link between the molecular mechanisms of ovarian aging and Ksuc. METHODS: The level of Ksuc in ovaries of aged and premature ovarian insufficiency (POI) mice were detected by immunoblotting and immunohistochemical. To further explore the role of Ksuc in ovarian aging, using in vitro mouse ovary tissue culture and an in vivo mouse model with changed Ksuc level. RESULTS: Increased Ksuc in ovaries of aged and POI mice and distribution of Ksuc in various types of mice ovarian cells and the high level of Ksuc in granulosa cells (GCs) were revealed. Histological assessments and hormone levels analyses showed that the high Ksuc level down-regulated the ovarian index and the anti-Müllerian hormone (AMH) and estrogen levels, and increased follicular atresia. Moreover, in the high Ksuc groups, the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) intensities and the expression of Cleaved-caspase-3 increased and the expression of B-cell lymphoma-2 (Bcl-2) decreased together with positively-expressed P21, an aging-related marker. These results suggest that ovarian aging is likely associated with alteration in Ksuc. CONCLUSION: The present study has identified Ksuc in mouse ovary and found that high Ksuc level most likely contributes to ovarian aging which is expected further investigation to provide new information for delaying physiological ovarian aging and treating pathological ovarian aging.

Exposure to nanoplastics induces mitochondrial impairment and cytomembrane destruction in Leydig cells.

Plastic particle pollution poses an emerging threat to ecological and human health. Laboratory animal studies have illustrated that nano-sized plastics can accumulate in the testis and cause testosterone deficiency and spermatogenic impairment. In this study, TM3 mouse Leydig cells were in vitro exposed to polystyrene nanoparticles (PS-NPs, size 20 nm) at dosages of 50, 100 and 150 µg/mL to investigate their cytotoxicity. Our results demonstrated that PS-NPs can be internalized into TM3 Leydig cells and led to a concentration-dependent decline in cell viability. Furthermore, PS-NPs stimulation amplified ROS generation and initiated cellular oxidative stress and apoptosis. Moreover, PS-NPs treatment affected the mitochondrial DNA copy number and collapsed the mitochondrial membrane potential, accompanied by a disrupted energy metabolism. The cells exposed to PS-NPs also displayed a down-regulated expression of steroidogenesis-related genes StAR, P450scc and 17ß-HSD, along with a decrease in testosterone secretion. In addition, treatment with PS-NPs destructed plasma membrane integrity, as presented by increase in lactate dehydrogenase release and depolarization of cell membrane potential. In summary, these data indicated that exposure to PS-NPs in vitro produced cytotoxic effect on Leydig cells by inducing oxidative injury, mitochondrial impairment, apoptosis, and cytomembrane destruction. Our results provide new insights into male reproductive toxicity caused by NPs.

Tri-ortho-cresyl phosphate (TOCP)-induced reproductive toxicity involved in placental apoptosis, autophagy and oxidative stress in pregnant mice.

Tri-ortho-cresyl phosphate (TOCP) has been widely used as plasticizers, and reported causing reproductive toxicity in mammals. However, little is known about the toxic effect on the placenta. In this study, dams were orally administered different doses of TOCP to explore the effect of TOCP on placental development. Results showed that TOCP exposure significantly reduced numbers of implanted embryo, caused atrophy and collapse of ectoplacental cone, and decreased total areas of placenta and numbers of PCNA-positive cells. Expression levels of placental development genes were prominently downregulated in the TOCP-treated groups. Moreover, TOCP administration induced placental apoptosis and autophagy by upregulating P53, Bax, Beclin-1, ratio of LC3 II/LC3 I and Atg5 and downregulating Bcl-2 protein. In addition, TOCP exposure markedly inhibited activities of catalase and superoxide dismutase and increased the production of H2 O2 and malondialdehyde. Collectively, these findings suggest that apoptosis, autophagy and oxidative stress may be involved in the TOCP-induced reproductive toxicity.

Abiraterone and MDV3100 inhibits the proliferation and promotes the apoptosis of prostate cancer cells through mitophagy.

BACKGROUND: Abiraterone and MDV3100 are two effective anticancer agents for prostate cancer, however, the mechanism of their downstream action remains undefined. METHODS: A dual fluorescent biosensor plasmid was transfected in LNCaP cells to measure mitophagy. The DNA of LNCaP cells was extracted and performed with quantitative real-time PCR to detect mitochondrial DNA copy number. JC-1 staining was utilized to detect the mitochondrial membrane potential and electron microscope was performed to analyze mitochondrial morphology. Moreover, the protein levels of mitochondrial markers and apoptotic markers were detected by western blot. At last, the proliferation and apoptosis of LNCaP cells were analyzed with CCK-8 assay and flow cytometry after abiraterone or MDV3100 treatment. RESULTS: Mitophagy was induced by abiraterone and MDV3100 in LNCaP cells. The low expression level of mitochondrial DNA copy number and mitochondrial depolarization were further identified in the abiraterone or MDV3100 treatment groups compared with the control group. Besides, severe mitochondria swelling and substantial autophagy-lysosomes were observed in abiraterone- and MDV3100-treated LNCaP cells. The expression of mitochondria-related proteins, frataxin, ACO2 and Tom20 were significantly downregulated in abiraterone and MDV3100 treated LNCaP cells, whereas the expression level of inner membrane protein of mitochondria (Tim23) was significantly upregulated in the same condition. Moreover, the proliferation of LNCaP cells were drastically inhibited, and the apoptosis of LNCaP cells was increased in abiraterone or MDV3100 treatment groups. Meanwhile, the addition of mitophagy inhibitor Mdivi-1 (mitochondrial division inhibitor 1) could conversely elevate proliferation and constrain apoptosis of LNCaP cells. CONCLUSIONS: Our results prove that both abiraterone and MDV3100 inhibit the proliferation, promote the apoptosis of prostate cancer cells through regulating mitophagy. The promotion of mitophagy might enhance the efficacy of abiraterone and MDV3100, which could be a potential strategy to improve chemotherapy with these two reagents.

Impact of different color fiber sleeves on beam hazards of 532-nm laser and vaporization efficiency.

The 532-nm laser has become increasingly popular for the treatment of urologic diseases. However, laser beam will pose significant hazards for the health of surgeons. In order to reduce beam hazards during surgery, we compared the beam hazards of laser fiber with black sleeves to the traditional fiber with transparent sleeves, and the vaporization efficiency. A total of 18 porcine kidney specimens were vaporized in normal saline at a room temperature under 532-nm laser delivered through a 760-µm core diameter side firing fiber. Two groups were divided according to the color of fiber sleeves: the transparent and the black. Each group was then divided into another three subgroups by laser power: the 80 W group, the 120 W group, and the 160 W group. The beam hazard was evaluated by light intensity measured in a sector area at a distance of 0 m, 0.5 m, and 1 m from the irradiation center. The vaporization efficiency was measured by the vaporization groove depth under the working power of 80 W, 120 W, and 160 W with a working distance of 5 mm and irradiation time of 10 s. The light intensity measured in the black fiber sleeve group is significantly lower than that in the transparent one (P < 0.01), regardless of the measuring distance (0 m, 0.5 m, and 1.0 m) and laser power (80 W, 120 W, and 160 W). No statistical difference was found on the vaporization efficiency between the groups protected by fiber sleeves of different colors (transparent/black, p > 0.05). Compared to the traditional transparent fiber sleeves, more beam hazards will be reduced in the operative region with the protection of black fiber sleeves, especially those from the irradiation center. The vaporization efficiency is not affected by the color of fiber sleeves. Such findings may offer a completely new idea for the protection of surgeons in surgeries with 532-nm lasers.

Down-Regulation of Neuropathy Target Esterase in Preeclampsia Placenta Inhibits Human Trophoblast Cell Invasion via Modulating MMP-9 Levels.

BACKGROUND/AIMS: Neuropathy target esterase (NTE, also known as neurotoxic esterase) is proven to deacylate phosphatidylcholine (PC) to glycerophosphocholine as a phospholipase B. Recently; studies showed that artificial phosphatidylserine/PC microvesicles can induce preeclampsia (PE)-like changes in pregnant mice. However, it is unclear whether NTE plays a key role in the pathology of PE, a pregnancy-related disease, which was characterized by deficient trophoblast invasion and reduced trophoblast-mediated remodeling of spiral arteries. The aim of this study was to investigate the expression pattern of NTE in the placenta from women with PE and normal pregnancy, and the molecular mechanism of NTE involved in the development of PE. METHODS: NTE expression levels in placentas from 20 pregnant women with PE and 20 healthy pregnant women were detected using quantitative PCR and immunohistochemistry staining. The effect of NTE on trophoblast migration and invasion and the underlying mechanisms were examined in HTR-8/SVneo cell lines by transfection method. RESULTS: NTE mRNA and protein expression levels were significantly decreased in preeclamptic placentas than normal control. Over-expression of NTE in HTR-8/SVneo cells significantly promoted trophoblast cells migration and invasion and was associated with increased MMP-9 levels. Conversely, shRNA-mediated down-regulation of NTE markedly inhibited the cell migration and invasion. In addition, silencing NTE reduced the MMP-9 activity and phosphorylated Erk1/2 and AKT levels. CONCLUSIONS: Our results suggest that the decreased NTE may contribute to the development of PE through impairing trophoblast invasion by down-regulating MMP-9 via the Erk1/2 and AKT signaling pathway.

The Urinary Sarcosine/Creatinine Ratio is a Potential Diagnostic and Prognostic Marker in Prostate Cancer.

BACKGROUND The aim of this study was to evaluate the role of the urinary sarcosine/creatinine ratio in the diagnosis and prognosis of prostate cancer, using a sarcosine oxidase assay. MATERIAL AND METHODS Urine samples were obtained from 203 patients with benign prostate hyperplasia (BPH) and 209 patients with prostate cancer. Levels of urinary sarcosine were measured using the sarcosine oxidase method. The urinary sarcosine/creatinine ratios were compared between the group of patients with BPH and the patients with prostate cancer. In the two patients groups, the urinary sarcosine/creatinine ratio was compared with the measurement of serum prostate-specific antigen (PSA) and the free/total (F/T) PSA ratio. Correlations between of the urinary sarcosine/creatinine ratio and the Gleason grade and stage of prostate cancer were analyzed. RESULTS There was a significant difference between the urinary sarcosine/creatinine ratio in the BPH group and prostate cancer group (P<0.01), which was independent of serum PSA. The receiver-operating characteristic (ROC) curve, and area under the curve (AUC) for the urinary sarcosine/creatinine ratio was significantly higher compared with the serum PSA and the F/T PSA ratio. There was a significant difference in the urinary sarcosine/creatinine ratio in patients with prostate cancer with Gleason score ≤6, 7, and ≥8, and between patients with metastatic and non-metastatic prostate cancer. CONCLUSIONS The urinary sarcosine/creatinine ratio was a diagnostic indicator of prostate cancer, for patients with a serum PSA level <10 ng/ml, and correlated with the Gleason score and with the presence of metastases (stage) of prostate cancer.

Exposure to 2,4-dichlorophenoxyacetic acid induces oxidative stress and apoptosis in mouse testis.

The herbicide 2,4-dichlorophenoxyacetic acid (2,4-D) is used worldwide. It has been associated with a variety of toxicities in rodents. In this study, male mice were orally administered 2,4-D at 50, 100 or 200mg/kg/day to investigate testicular toxicity and the possible mechanisms of action. Exposure to 2,4-D at high concentrations (100 and 200mg/kg/day) for 14 consecutive days caused spermatogenic disruption and seminiferous epithelial destruction. Furthermore, 2,4-D administration (100 and 200mg/kg/day) increased the formation of the lipid peroxidation product malondialdehyde and decreased activities of the antioxidant enzymes superoxide dismutase and catalase in the testis. Moreover, 2,4-D exposure up-regulated the expression of p53 and Bax protein and down-regulated the expression of Bcl-2 protein in the testis. These results demonstrate that oxidative stress and apoptosis may be involved in testicular toxicity induced by high concentrations of 2,4-D in mice.

Pyrolysis Treatment of Chromite Ore Processing Residue by Biomass: Cellulose Pyrolysis and Cr(VI) Reduction Behavior.

The pyrolysis treatment with biomass is a promising technology for the remediation of chromite-ore-processing residue (COPR). However, the mechanism of this process is still unclear. In this study, the behavior of pyrolysis reduction of Cr(VI) by cellulose, the main component of biomass, was elucidated. The results showed that the volatile fraction (VF) of cellulose, ie. gas and tar, was responsible for Cr(VI) reduction. All organic compounds, as well as CO and H2 in VF, potentially reduced Cr(VI). X-ray absorption near-edge structure (XANES) spectroscopy and extended X-ray absorption fine-structure (EXAFS) spectroscopy confirmed the reduction of Cr(VI) to Cr(III) and the formation of amorphous Cr2O3. The remnant Cr(VI) content in COPR can be reduced below the detection limit (2 mg/kg) by the reduction of COPR particle and extension of reaction time between VF and COPR. This study provided a deep insight on the co-pyrolysis of cellulose with Cr(VI) in COPR and an ideal approach by which to characterize and optimize the pyrolysis treatment for COPR by other organics.

Involvement of NRF2 in Perfluorooctanoic Acid-Induced Testicular Damage in Male Mice.

Perfluorooctane acid (PFOA) is a hazardous environmental pollutant that has been reported to exert adverse effects on animal and human health. In this study, male mice were orally administered different concentrations of PFOA (2.5, 5, or 10 mg/kg/day) to evaluate the reproductive toxicity. Exposure to PFOA for 14 consecutive days obviously disrupted seminiferous tubules and reduced sperm count. The highest concentration of PFOA (10 mg/kg/day) caused growth retardation and diminished absolute testis weight. Furthermore, PFOA treatment significantly increased the generation of oxidative stress indicators malondialdehyde and hydrogen peroxide, decreased the expression of transcription factor NRF2, and inhibited the activities of antioxidant enzymes superoxide dismutase and catalase in the testis. Moreover, PFOA exposure up-regulated p-p53 and BAX expression and down-regulated BCL-2 expression in the testis. These results indicated that PFOA-induced male reproductive disorders might be involved in developmental impairment and inhibition of NRF2-mediated antioxidant response in the testis of mice.

Expression and regulation of androgen receptor in the mouse uterus during early pregnancy and decidualization.

The androgen receptor (AR) is a ligand-activated transcription factor that is important for both the male and female reproductive systems. The expression and regulation of AR in the uterine endometrium during early pregnancy and decidualization remain relatively under-investigated, so we sought to immunohistochemically examine the spatiotemporal expression of AR in mouse uteri during the peri-implantation period as well as in response to specific steroid hormones. AR protein was found in the nuclei of uterine stromal cells starting on pregnancy Days 1 and 2, with its abundance increasing on Days 3 and 4. From pregnancy Days 5 to 9, however, the expression of AR markedly declined in stromal zones of uteri. No signal was detected in the decidualized cells surrounding the site of embryo implantation; moreover, no AR immunostaining was observed in decidualized uterine cells in an artificial oil-induced model of decidualization. Progesterone significantly inhibited AR protein expression, whereas estrogen dramatically elevated AR abundance in the stroma of ovariectomized mouse uteri. Taken together, our results are the first to demonstrate that decidualization and progesterone significantly inhibited the AR protein expression in vivo, whereas estrogen increased AR protein levels in the stromal cells of mouse uteri. These responses might be advantageous for the proliferation and differentiation of uterine stroma and for embryo implantation during early pregnancy.

DCM2Net: an improved face recognition model for panoramic stereoscopic videos.

The panoramic stereo video has brought a new visual experience for the audience with its immersion and stereo effect. In panoramic stereo video, the face is an important element. However, the face image in panoramic stereo video has varying degrees of deformation. This brings new challenges to face recognition. Therefore, this paper proposes a face recognition model DCM2Net (Deformable Convolution MobileFaceNet) for panoramic stereo video. The model mainly integrates the feature information between channels during feature fusion, redistributes the information between channels in the deeper part of the network, and fully uses the information between different channels for feature extraction. This paper also built a panoramic stereo video live system, using the DCM2Net model to recognize the face in panoramic stereo video, and the recognition results are displayed in the video. After experiments on different datasets, the results show that our model has better results on popular datasets and panoramic datasets.

Innovative overview of the occurrence, aging characteristics, and ecological toxicity of microplastics in environmental media.

Microplastics (MPs), pollutants detected at high frequency in the environment, can be served as carriers of many kinds of pollutants and have typical characteristics of environmental persistence and bioaccumulation. The potential risks of MPs ecological environment and health have been widely concerned by scholars and engineering practitioners. Previous reviews mostly focused on the pollution characteristics and ecological toxicity of MPs, but there were few reviews on MPs analysis methods, aging mechanisms and removal strategies. To address this issue, this review first summarizes the contamination characteristics of MPs in different environmental media, and then focuses on analyzing the detection methods and analyzing the aging mechanisms of MPs, which include physical aging and chemical aging. Further, the ecotoxicity of MPs to different organisms and the associated enhanced removal strategies are outlined. Finally, some unresolved research questions related to MPs are prospected. This review focuses on the ageing and ecotoxic behaviour of MPs and provides some theoretical references for the potential environmental risks of MPs and their deep control.

Aerobic granulation in a sequencing batch reactor for the treatment of piggery wastewater.

This study investigated the formation of aerobic granules fed with digested piggery wastewater. After 42 days of cultivation, small yellow granules with mean diameter of 0.4 mm were first observed in the reactor. Scanning electron microscope pictures showed the granules were compact, round structures with clear outer shapes and mainly composed of filamentous bacteria. Maximum chemical oxygen demand and ammonia removal ratios were 90.1 and 91.7%, respectively. The Monod equation, which was used to describe ammonium utilization, yielded a maximum rate of 6.25 mg (g volatile suspended solids)(-1) h(-1). The measurement of extracellular polymeric substances (EPS) content and three-dimensional excitation and emission matrix results showed that the EPS concentration increased during the granulation process. Fluorescence in situ hybridization analysis showed significant amounts of nitrifying bacteria in the aerobic granules. Results in this study provide insights to the treatment of piggery wastewater using aerobic granular sludge.

Impact of emerging pollutant florfenicol on enhanced biological phosphorus removal process: Focus on reactor performance and related mechanisms.

Florfenicol (FF), an emerging pollutant antibiotic that is difficult to biodegrade, inevitably enters sewage treatment facilities with high level. To date, however, the performance and related mechanism of FF on enhanced biological phosphorus removal (EBPR) have not been reported. In order to fill this gap, this work investigated the potential impacts of FF on EBPR and revealed the relevant mechanisms. The effect of FF on EBPR was dose-dependent, that was, low dose had no effect on EBPR, while high FF concentration inhibited EBPR. Mechanism investigation showed that FF had no effect on anaerobic phosphate release, but reduced oxic phosphorus uptake. Three-dimensional Excitation-emission Matrix fluorescence spectroscopy and X-ray photoelectron spectroscopy analysis showed that FF affected the structure and components of activated sludge extracellular polymers (EPS). High content of FF stimulated sludge to secrete more EPS. High level of FF reduced the relative abundance of microorganisms responsible for biological phosphorus removal. Microbiological community structure analysis indicated 2.0 mg FF/L increased the relative abundance of Candidatus_Competibacter and Terrimonas from 9.22 % and 12.49 % to 19.00 % and 16.28 %, respectively, but significantly reduced the relative abundance of Chinophagaceae from 11.32 % to 0.38 %, compared with the blank.

Toxic effects of per- and polyfluoroalkyl substances on sperm: Epidemiological and experimental evidence.

As emerging organic contaminants, per- and polyfluoroalkyl substances (PFASs) have aroused worldwide concern due to their environmental persistence, ubiquitous presence, bioaccumulation, and potential toxicity. It has been demonstrated that PFASs can accumulate in human body and cause multiple adverse health outcomes. Notably, PFASs have been detected in the semen of human, posing a potential hazard to male fecundity. This article reviews the evidence about the toxic effects of exposure to PFASs on male reproduction, focusing on the sperm quality. Epidemiological studies showed that PFASs, such as perfluorooctanoic acid (PFOA) and perfluorooctane sulfonic acid (PFOS), were adversely associated with the semen parameters in humans, including sperm count, morphology and motility. Experimental results also confirmed that PFAS exposure led to testicular and epididymal damage, therefore impairing spermatogenesis and sperm quality. The mechanisms of reproductive toxicity of PFASs may be involved in blood-testosterone barrier destruction, testicular apoptosis, testosterone synthesis disorder, and membrane lipid composition alteration, oxidative stress and Ca2+ influx in sperm. In conclusion, this review highlighted the potential threat of exposure to PFASs to human spermatozoa.

Maternal exposure to a glyphosate-based herbicide impairs placental development through endoplasmic reticulum stress in mice.

Glyphosate-based herbicides (GBHs) are the most widely used agrochemicals worldwide, increasing the risk of their occurrence in the environment. This study aimed to explore effects and mechanisms of GBH exposure on placental development in vivo during pregnancy in mice. Pregnant mice received GBH by gavage at 0, 5, and 50 mg⋅kg-1⋅day-1 doses from gestational day (GD) 1 to GD 13 and were sacrificed on GD 13 or GD19. Our data indicated that GBH administration significantly increased the number of resorbed fetuses, reduced the weight of fetuses and placentas, and inhibited placental growth, as evident from decreased placental total area and spongiotrophoblast area on GD 19. GBH treatment also inhibited proliferation and induced apoptosis of placenta via upregulation of Bax, cleaved caspase-3 and -12 expression, and downregulation of B cell lymphoma (Bcl)-2 expression. Further study showed that GBH exposure significantly increased expression levels of glucose-regulated protein 78 (GRP78), protein kinase RNA-like endoplasmic reticulum kinase (PERK), and C/EBP homologous protein (CHOP) mRNAs and proteins and triggered oxidative stress in placenta on GD 13 and GD 19. In conclusion, our findings suggest that maternal exposure to GBH can impair placental development through the endoplasmic reticulum stress-mediated activation of GRP78/PERK/CHOP signaling pathway in mice.