The production of plastic products, which requires phthalate plasticizers, has resulted in the problems for human health, especially that of reproductive health. Phthalate exposure can induce reproductive disorders at various regulatory levels. The aim of this review was to compile the evidence concerning the association between phthalates and reproductive diseases, phthalates-induced reproductive disorders, and their possible endocrine and intracellular mechanisms. Phthalates may induce alterations in puberty, the development of testicular dysgenesis syndrome, cancer, and fertility disorders in both males and females. At the hormonal level, phthalates can modify the release of hypothalamic, pituitary, and peripheral hormones. At the intracellular level, phthalates can interfere with nuclear receptors, membrane receptors, intracellular signaling pathways, and modulate gene expression associated with reproduction. To understand and to treat the adverse effects of phthalates on human health, it is essential to expand the current knowledge concerning their mechanism of action in the organism.

https://www.mdpi.com/1660-4601/17/18/6811/pdf

Effects and Mechanisms of Phthalates' Action on Reproductive Processes and Reproductive Health: A Literature Review.

A woman's reproductive health and ability to have children directly affect numerous aspects of her life, from personal well-being and socioeconomic standing, to morbidity and lifespan. In turn, reproductive health depends on the development of correctly functioning ovaries, a process that starts early during fetal life. Early disruption to ovarian programming can have long-lasting consequences, potentially manifesting as disease much later in adulthood. A growing body of evidence suggests that exposure to chemicals early in life, including endocrine-disrupting chemicals, can cause a range of disorders later in life, such as those described in the ovarian dysgenesis syndrome hypothesis. In this Review, we discuss four specific time windows during which the ovary is particularly sensitive to disruption by exogenous insults: gonadal sex determination, meiotic division, follicle assembly and the first wave of follicle recruitment. To date, most evidence points towards the germ cell lineage being the most vulnerable to chemical exposure, particularly meiotic division and follicle assembly. Environmental chemicals and pharmaceuticals, such as bisphenols or mild analgesics (including paracetamol), can also affect the somatic cell lineages. This Review summarizes our current knowledge pertaining to environmental chemicals and pharmaceuticals, and their potential contributions to the development of ovarian dysgenesis syndrome. We also highlight knowledge gaps that need addressing to safeguard female reproductive health.

/pdf/environmental-influences-on-ovarian-dysgenesis-developmental-2t8cqjagum.pdf

Environmental influences on ovarian dysgenesis - developmental windows sensitive to chemical exposures

Background: Animal studies suggest that phthalates and bisphenol A (BPA), endocrine-disrupting chemicals found in many consumer products, may impact the timing of puberty. Objectives: We aimed to d...

/pdf/association-of-prenatal-urinary-concentrations-of-phthalates-1epqsse7j5.pdf

Association of Prenatal Urinary Concentrations of Phthalates and Bisphenol A and Pubertal Timing in Boys and Girls

Di(2-ethylhexyl) phthalate (DEHP) is a plasticizer found in polyvinyl chloride products such as vinyl flooring, plastic food containers, medical devices, and children's toys. DEHP is a ubiquitous environmental contaminant and is a known endocrine disrupting chemical. Little is known about the effects of prenatal DEHP exposure on the ovary and whether effects occur in subsequent generations. Thus, we tested the hypothesis that prenatal exposure to DEHP disrupts ovarian functions in the F1, F2, and F3 generations of female mice. To test this hypothesis, pregnant CD-1 mice were orally dosed with corn oil (vehicle control) or DEHP (20 and 200 μg/kg/day and 200, 500, and 750 mg/kg/day) daily from gestation day 10.5 until birth (7-28 dams/treatment group). F1 females were mated with untreated males to obtain the F2 generation, and F2 females were mated with untreated males to produce the F3 generation. On postnatal days 1, 8, 21, and 60, ovaries were collected and used for histological evaluation of follicle numbers and sera were used to measure progesterone, testosterone, 17β-estradiol, luteinizing hormone, and follicle stimulating hormone levels. In the F1 generation, prenatal exposure to DEHP disrupted body and organ weights, decreased folliculogenesis, and increased serum 17β-estradiol levels. In the F2 generation, exposure to DEHP decreased body and organ weights, dysregulated folliculogenesis, and disrupted serum progesterone levels. In the F3 generation, DEHP exposure accelerated folliculogenesis. These data suggest that prenatal exposure to DEHP leads to adverse multigenerational and transgenerational effects on ovarian function.

/pdf/prenatal-exposure-to-di-2-ethylhexyl-phthalate-disrupts-c7llthmeb3.pdf

Prenatal exposure to di(2-ethylhexyl) phthalate disrupts ovarian function in a transgenerational manner in female mice

Di-(2-ethylhexyl) phthalate (DEHP) is an environmental endocrine disruptor widely used in China that is harmful to the male reproductive system. Many studies have shown that DEHP causes testicular toxicity through oxidative stress, but the specific mechanism is unknown. Because the Notch pathway is a key mechanism for regulating cell growth and proliferation, we investigated whether Notch is involved in DEHP-induced testicular toxicity and whether vitamins E and C could rescue testicular impairment in Sprague-Dawley (SD) rats. Compared with the control group, we found that DEHP exposure induced testicular toxicity through oxidative stress injury, and it decreased the testosterone level (P < .01) and upregulated nuclear factor-erythroid 2 related factor (Nrf2) expression (P < .01). Therefore, because oxidative stress might be the initiating factor of DEHP-induced testicular toxicity, treatment with the antioxidant vitamins E and C activated the Notch1 signaling pathway in the testis and in Leydig cells. Treatment with vitamins E and C normalized the oxidative stress state after DEHP exposure and restored testicular development to be similar to the control group. In summary, antioxidant vitamins E and C may be used to treat DEHP-induced testicular toxicity.

Di-(2-ethylhexyl) phthalate (DEHP)-induced testicular toxicity through Nrf2-mediated Notch1 signaling pathway in Sprague-Dawley rats

DEHP exposure in utero disturbs sex determination and is potentially linked with precocious puberty in female mice.

Di (2-ethylhexyl) phthalate exposure during pregnancy disturbs temporal sex determination regulation in mice offspring

Di(2-Ethylhexyl) Phthalate Exposure In Utero Damages Sertoli Cell Differentiation Via Disturbance of Sex Determination Pathway in Fetal and Postnatal Mice

As one of the physical quantities concerned in agricultural production, soil moisture can effectively guide field irrigation and evaluate the distribution of water resources for crop growth in various regions. However, the spatial variability of soil moisture is dramatic, and its time series data are highly noisy, nonlinear, and nonstationary, and thus hard to predict accurately. In this study, taking Jiangsu Province in China as an example, the data of 70 meteorological and soil moisture automatic observation stations from 2014 to 2022 were used to establish prediction models of 0–10 cm soil relative humidity (RHs10cm) via the extreme gradient boosting (XGBoost) algorithm. Before constructing the model, according to the measured soil physical characteristics, the soil moisture observation data were divided into three categories: sandy soil, loam soil, and clay soil. Based on the impacts of various factors on the soil water budget balance, 14 predictors were chosen for constructing the model, among which atmospheric and soil factors accounted for 10 and 4, respectively. Considering the differences in soil physical characteristics and the lagged effects of environmental impacts, the best influence times of the predictors for different soil types were determined through correlation analysis to improve the rationality of the model construction. To better evaluate the importance of soil factors, two sets of models (Model_soil&atmo and Model_atmo) were designed by taking soil factors as optional predictors put into the XGBoost model. Meanwhile, the contributions of predictors to the prediction results were analyzed with Shapley additive explanation (SHAP). Six prediction effect indicators, as well as a typical drought process that happened in 2022, were analyzed to evaluate the prediction accuracy. The results show that the time with the highest correlations between environmental predictors and RHs10cm varied but was similar between soil types. Among these predictors, the contribution rates of maximum air temperature (Tamax), cumulative precipitation (Psum), and air relative humidity (RHa) in atmospheric factors, which functioned as a critical factor affecting the variation in soil moisture, are relatively high in both models. In addition, adding soil factors could improve the accuracy of soil moisture prediction. To a certain extent, the XGBoost model performed better when compared with artificial neural networks (ANNs), random forests (RFs), and support vector machines (SVMs). The values of the correlation coefficient (R), root mean square error (RMSE), mean absolute error (MAE), mean absolute relative error (MARE), Nash–Sutcliffe efficiency coefficient (NSE), and accuracy (ACC) of Model_soil&atmo were 0.69, 11.11, 4.87, 0.12, 0.50, and 88%, respectively. This study verified that the XGBoost model is applicable to the prediction of soil moisture at the provincial level, as it could reasonably predict the development processes of the typical drought event.

https://www.mdpi.com/2077-0472/13/5/927/pdf?version=1682304994

Research on Provincial-Level Soil Moisture Prediction Based on Extreme Gradient Boosting Model

Environmental endocrine-disrupting chemicals (EDCs), known to bind to estrogen/androgen receptors and mimic native estrogens, have been implicated as a main source for increasing human reproductive and developmental deficiencies and diseases. Tamoxifen (TAM) is one of the most well-known antiestrogens with defined adverse effects on the female reproductive tract, but the mechanisms related to autosomal gene regulation governing ovary maintenance in mammals remain unclear. The expression pattern and levels of key genes and proteins involved in maintaining the ovarian phenotype in mice were analyzed. The results showed that TAM induced significant upregulation of Sox9, which is the testis-determining factor gene. The results showed that TAM induced significant upregulation of Sox9, the testis-determining factor gene, and the expression level of Sox9 mRNA in the ovaries of mice exposed to 75 or 225 mg/kg bw TAM was 2- and 10-fold that in the control group, respectively (p < 0.001). Furthermore, the testicular fibroblast growth factor gene, Fgf9, was also elevated in TAM-treated ovaries. Accordingly, expression of the ovary development marker, forkhead transcription factor (FOXL2), and WNT4/FST signaling, were depressed. The levels of protein expression changed consistently with the target genes. Moreover, the detection of platelet/endothelial cell adhesion molecule 1 (PECAM-1) in TAM-treated ovaries suggested the formation of vascular endothelial cells, which is a further evidence for the differentiation of the ovaries to a testis-like phenotype. During this period, the level of 17β-estradiol, progesterone, and luteinizing hormone decreased, while that of testosterone increased by 3.3-fold (p = 0.013). The activation of a testis-specific molecular signaling cascade was a potentially important mechanism contributing to the gender disorder induced by TAM, which resulted in the differentiation of the ovaries to a testis-like phenotype in adult mice. Limited with a relatively higher exposure, the present study provided preliminary molecular insights into the sexual disorder induced by antiestrogens and compounds that interrupted estrogen signaling by other modes of action.

Effects of tamoxifen on autosomal genes regulating ovary maintenance in adult mice

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