The blood–follicle barrier (BFB) between the blood and follicular fluid (FF) can maintain the microenvironment balance of oocyte. Boron, an exogenous environmental trace element, has been found to possibly play an important role in oocyte maturation. This study aimed to examine the distribution characteristics of boron across the BFB and find the potential effect of boron on FF microenvironment. We analyzed the concentration of boron in paired FF and serum collected from 168 women undergoing in vitro fertilization and embryo transfer in Beijing City and Shandong Province, China. To explore the potential health impact of boron enrichment in oocyte maturation, a global proteomics analysis was conducted to tentatively correlate the protein levels with the boron enrichment. Interestingly, the results showed that the concentration of boron in FF (34.5 ng/mL) was significantly higher than that in serum (22.0 ng/mL), with a median concentration ratio of 1.52. Likewise, the concentrations of boron in FF and serum were positively correlated (r = 0.446), suggesting that boron concentration in serum can represent its concentration in follicular fluid to a large extent.. This is the first time to observe the enrichment of boron in the FF to our knowledge. It is interesting to observe a total of 13 proteins, which mainly belong to immunoglobulin class, were positively correlated with boron concentration in FF. We concluded that boron, as one environmental trace element, was enriched in FF from blood validated by two area in north china, which may be involved in an increased level of immune processes of immunoglobulins.

Monobutyl phthalate (MBP) is the main metabolite of dibutyl phthalate (DBP) in vivo. MBP has a stable structure, can continuously accumulate in living organisms, and has the potentially to harm animal and human reproductive function. In the ovarian follicle microenvironment, MBP may lead to defects in follicular development and steroid production, abnormal meiotic maturation, impaired ovarian function and other reproductive deficits. In this study, SMART-seq was used to investigate the effects of MBP exposure on the in vitro maturation (IVM) and development of porcine oocytes. The results showed that differentially expressed genes after MBP exposure were enriched in the biological processes cytoskeleton, cell apoptosis, endoplasmic reticulum (ER) and mitochondria. Glycine (Gly) improved the developmental potential of porcine oocytes by regulating mitochondrial and ER function. The effect of Gly in protecting oocytes against MBP-induced damage was studied. The results showed that the addition of Gly significantly decreased the rate of MBP-induced spindle abnormalities, decreased the frequency of MBP-induced mitochondria-associated ER membrane (MAM) interactions, and downregulated the protein and gene expression of the linkage molecules Mitofusin 1 (MFN1) and Mitofusin 2 (MFN2) in the MAM. Additionally, treatment with Gly restored the distribution of the 1,4,5-triphosphate receptor 1 (IP₃R1) and voltage-dependent anion channel 1 (VDAC1), further decreasing the intracellular free calcium concentration ([Ca²⁺]ᵢ) levels and mitochondrial Ca²⁺ ([Ca²⁺]ₘ) , increasing the ER Ca²⁺ ([Ca²⁺]ER) levels, and thus significantly increasing the ER levels and mitochondrial membrane potential (ΔΨ m). Gly also decreased the levels of reactive oxygen species (ROS) and increased the levels of Glutathione (GSH), oocyte apoptosis-related indicators (Caspase-3 activity and Annexin V) and oocyte apoptosis-related genes (BAX, Caspase 3 and AIFM1). Our results suggest that Gly can ameliorate microtubule cytoskeleton abnormalities and improve oocyte maturation by reducing the defective mitochondrial–ER interactions caused by MBP exposure in vitro.

Exposure of females to fine particulate matter ≤2.5 μm in diameter (PM2.5) prior to pregnancy could produce adverse impact on fertility and enhances susceptibility of the offspring to a variety of diseases. In the current study, female C57BL/6 mice (6 weeks of age) were exposed to either concentrated PM2.5 or filtered air (average PM2.5 concentration: 115.60 ± 7.77 vs. 14.07 ± 0.38 μg/m⁻³) using a whole-body exposure device for 12 weeks. Briefly, PM2.5 exposure decreased anti-Müllerian hormone level (613.40 ± 17.36 vs 759.30 ± 21.90 pg mL⁻¹, P＜0.01) and increased reactive oxygen species (ROS) level (45.39 ± 0.82 vs 24.20 ± 0.85 arbitrary unit in fluorescence assay, P＜0.01) in oocytes. The exposure increased oocyte degeneration rate (21.5% vs 5.1%, respectively (P＜0.01) and decreased the 2-cell formation rate (71.9% vs 86.0%, P < 0.01). Transcriptome profiling using RNA sequencing showed wide spectrum of abnormal expression of genes, particularly those involved in regulating the mitochondrial respiratory complex in oocytes and metabolic processes in blastocysts. The exposure decreased litter size (6 ± 0.37 vs 7 ± 0.26, P＜0.05) and weight (1.18 ± 0.02 vs 1.27 ± 0.02 g, P＜0.01). In summary, PM2.5 exposure decreased female fertility, possibly through increased ROS production in oocytes and metabolic disturbances in developing embryos. The cause-effect relationship, however, requires further investigation.

Artificial light at night (ALAN) exposes us to prolonged illumination, that adversely affects female reproduction. However, it remains to be clarified how prolonged light exposure affects oocyte meiotic maturation and quality. To this end, we exposed female mice to a constant light (CL) of 250 lux for different durations. Our findings showed that CL exposure for 7 weeks reduced the oocyte maturation rate. Meanwhile, CL exposure caused greater abnormalities in spindle assembly and chromosome alignment and a higher rate of oocyte aneuploidy than the regular light dark cycle. CL exposure also induced oxidative stress and caused mitochondrial dysfunction, which resulted in oocyte apoptosis and autophagy. Notably, our results showed that CL exposure reduced the levels of α-tubulin acetylation, DNA methylation at 5 mC, RNA methylation at m⁶A and histone methylation at H3K4me2 but increased the levels of histone methylation at H3K27me2 in oocytes. In summary, our findings demonstrate that constant bright light exposure causes oocyte meiotic defects and reduces cytoplasmic quality. These results extend the current understanding of ALAN-mediated defects in female reproduction.

Exposure to phthalates during gestation has been associated with decreased birth weight among offspring. However, the associations between preconception phthalate metabolites in follicular fluid (FF) and offspring birth weight among women undergoing in vitro fertilization (IVF) remain largely unknown. Here, we explored the associations between preconception phthalate metabolite concentrations in FF and the birth weights of singletons and twins among women undergoing IVF. We recruited 147 female participants who gave birth to 90 singletons and 57 twin infants at the Reproductive Medicine Center, Tongji Hospital, Wuhan, between November and December 2016. Each participant was asked to complete a questionnaire at the time of recruitment and provide a FF sample on the day of oocyte retrieval. The FF concentrations of eight phthalate metabolites were determined using high-performance liquid chromatography and tandem mass spectrometry. Birth outcomes were abstracted from medical records. The associations between phthalate metabolites in FF and birth weights of the singleton and twin groups were evaluated using generalized linear models (GLMs). We found that birth weight in the twin group had negative dose-response associations with maternal preconception monobenzyl phthalate (MBzP) and mono(2-ethyl-5-oxohexyl) phthalate (MEOHP) in FF (both P for trends < 0.05) and that birth weight in the singleton group had positive dose-response associations with monoethyl phthalate (MEP) and mono(2-ethyl-5 hydroxyhexyl) phthalate (MEHHP) in FF (both P for trends < 0.05). These associations persisted when we modeled as continuous variables. In addition, we observed male-specific association between decreased twin birth weight and MEOHP and MBzP and a female-specific associations between increased singleton birth weight and MEP, MEHHP and the sum of di(2-ethylhexyl) phthalate (∑DEHP) (all P for interactions < 0.05). Preconception phthalate metabolites in maternal FF may affect the birth weights of both singleton and twin newborns.

Dibutyl phthalate (DBP), one of the most widely used plasticizers, is a known environmental endocrine disruptor that impairs male and female fertility. In this study, oral administration of DBP was given to pregnant mice on 14.5 days post coitus (dpc) for 3 days; and additionally, DBP was added into the culture of 14.5 dpc fetal ovaries for 3 days. DBP exposure during gestation disturbed the progression of meiotic prophase I of mouse oocytes, specifically from the zygotene to pachytene stages. Meanwhile, the DBP-exposed pachytene oocytes showed increased homologous recombination sites and unrepaired DNA damage. Furthermore, DBP caused DNA damage by increasing oxidative stress, decreased the expression of multiple critical meiotic regulators, and consequently induced oocyte apoptosis. Moreover, the effect of DBP on meiosis I prophase involved estrogen receptors α and β. Collectively, these results demonstrated a set of meiotic defects in DBP-exposed fetal oocytes. As aberrations in homologous recombination can result in aneuploid gametes and embryos, this study provides new support for the deleterious effects of phthalates.

The environmental risk of phthalic acid esters (PAEs) is of great concern. We investigated the reproductive impairment of di-(2-ethylhexyl)-phthalate (DEHP) on Chinese rare minnow, an endemic fish inhabiting the upper streams of the Yangtze River. Chinese rare minnow larvae were exposed to environmentally relevant concentrations of DEHP (0, 4.2, 13.3, and 40.8 μg/L) for 6 months. Plasma testosterone and 17β-estradiol levels decreased in females, accompanied by downregulation of cyp19a and cyp17 gene transcription in ovary. Increases in plasma testosterone concentration were observed in males, accompanied by downregulation of cyp19a gene transcription in testes. Hepatic VTG gene transcription was upregulated in males and females. Exposure to DEHP reduced egg production and inhibited oocyte maturation in females and retarded spermiation in males. Decreased egg protein content was measured in F1 embryos. These results indicate that long-term exposure to low concentrations of DEHP (13.3 μg/L) causes endocrine disruption and impairs fish reproduction.

A large variety of anthropogenic chemicals present in the aquatic environment have been shown to be able to alter the endocrine system of exposed organisms, potentially impacting their reproductive function. The aim of this study was to assess the effects of environmental pollution on the reproductive system of wild female roach (Rutilus rutilus) from the Seine River (Normandy, France). A suite of biomarkers of endocrine disruption including gonado-somatic index, plasmatic vitellogenin, gonadal aromatase activity and histological parameters (oocyte diameter and gonad maturation) were studied. Female fish from the polluted sites showed a number of reproductive alterations, including inhibited gonad maturation, reduced oocyte growth, reduced levels of plasmatic vitellogenin and 3-fold lower gonadal aromatase activity than females collected in the reference site. Overall, these results highlight the presence of endocrine disruption in female roach from the Seine River.