Diethyl phthalate (DEP), bisphenol A (BPA), and external estradiol 17β-estradiol (E2) all are endocrine disrupting chemicals (EDCs). Our previous study has found that the development of ceratohyal cartilage (CH) in embryos could be disrupted when the maternal generation was exposed with 8.06 μM DEP, 2.86 μM BPA, and 1.11 μM E2. However, it is still unknown how doses of the residual EDCs in eggs cause abnormal CH development in their offspring. Microinjection is used at the 2-cell stage of embryos to mimic the maternal effect and to observe the toxicities of EDCs in embryos. Results shown that the amounts of DEP, BPA, and E2 were 1.3 × 10-6 ng, 4.7 × 10-7 ng, and 1.4 × 10-7 ng, respectively, inducing the CH angles to become bigger than the control. However, related genes to the migratory pathways of neural crest cells (NCCs) were not influenced upon BPA and E2 treatments. Both sox10 and smad3 gene expressions were up-regulated upon DEP treatment. On the other hand, the CH angles were smaller than the control upon 1.3 × 10-5, 9.4 × 10-6, and 1.4 × 10-6 ng of DEP, BPA, and E2 microinjection, respectively. Furthermore, genes related to migratory NCCs were significantly influenced upon 10-5 ng of BPA, and 10-4 ng of DEP treatments on embryos. According to the data, we suggested that 10-5-10-7 ng of EDCs in eggs could disrupt CH development as well as significantly increase the mortality on their embryos. The present study raises concern that the responses were highly sensitive in embryos through maternal effects.

Parabens, bisphenols (BPs), and triclosan (TCS) are common environmental phenols widely applied in industrial products, pharmaceuticals, and personal care products. They are endocrine disruptors and pervade the natural environment, causing significant detrimental impacts on ecosystems, including marine habitats. Therefore, in this study, 40 samples comprising coral polyps, algae, and sediments were collected from Sanya, Hainan Province, China, in which the presence and compositional profiles of parabens, BPs, and TCS were examined to identify their fate in the oceans. The results unveiled the ubiquitous occurrence of at least one paraben or bisphenol in all samples, with TCS detected in over 80% of cases. Notably, coral samples contained the most contaminants (median concentration: 9.42 ng/g dry weight-dw), followed by sediment samples (5.95 ng/g dw) and algal samples (3.58 ng/g dw). Attributed to their broadest application, methylparaben (MeP) and propylparaben (PrP) emerged as the primary paraben constituents. MeP displayed the highest median concentration in coral samples (4.42 ng/g dw), probably related to its high-water solubility and the filtration mechanism employed by the coral polyps during seawater intake. Intriguingly, bisphenol P (BPP) superseded bisphenol A (BPA) as the dominant bisphenol, especially in the algal samples, probably owing to the lipophilic character of BPP and the enhanced biodegradability of BPA within aquatic environments. The highest concentration of TCS (3.44 ng/g dw) was found in the sediment samples, associated with its long half-life in the sediments. Furthermore, the correlation between multiple parabens and TCS implies their co-use to augment antimicrobial efficacy. Future research should prioritize the examination of these phenols in diverse marine environmental media. Corresponding toxicological experiments should be conducted to visualize their transport dynamics, degradation byproducts, and toxicity to marine biota to gain insights into the risks they pose to the marine ecosystem.

The placenta operates during gestation as the primary communication organ between the mother and fetus. It is essential for gas, nutrient exchange, and fetal waste transfer. The placenta also produces a wide range of hormones and other factors that influence maternal physiology, including survival and activity of the corpus luteum of the ovary, but the means whereby the placenta shapes fetal development remain less clear, although the fetal brain is thought to be dependent upon the placenta for factors that play roles in its early differentiation and growth, giving rise to the term \"placenta-brain axis\". Placental hormones transit via the maternal and fetal vasculature, but smaller placental molecules require protection from fetal and maternal metabolism. Such biomolecules include small RNA, mRNA, peptides, lipids, and catecholamines that include serotonin and dopamine. These compounds presumably shuttle to maternal and fetal systems via protective extracellular vesicles (EVs). Placental EVs (pEVs) and their components, in particular miRNA (miRs), are known to play important roles in regulating maternal systems, such as immune, cardiovascular, and reproductive functions. A scant amount is known about how pEVs affect fetal cells and tissues. The composition of pEVs can be influenced by gestational diseases. This review will provide critical insight into the roles of pEVs as the intermediary link between maternal and fetal systems, the impact of maternal pathologies on pEV cargo contents, and how an understanding of biomolecular changes within pEVs in health and disease might be utilized to design early diagnostic and mitigation strategies to prevent gestational diseases and later offspring disorders.

Emerging contaminants are pervasive in aquatic environments globally, encompassing pharmaceuticals, personal care products, steroid hormones, phenols, biocides, disinfectants and various other compounds. Concentrations of these contaminants are detected ranging from ng/L to μg/L. Even at trace levels, these contaminants can pose significant risks to ecosystems and human health. This article systematically summarises and categorizes data on the concentrations of 54 common emerging contaminants found in the influent and effluent of wastewater treatment plants across various geographical regions: North America, Europe, Oceania, Africa, and Asia. It reviews the occurrence and distribution of these contaminants, providing spatial and causal analyses based on data from these regions. Notably, the maximum concentrations of the pollutants observed vary significantly across different regions. The data from Africa, in particular, show more frequent detection of pharmaceutical maxima in wastewater treatment plants.

The plasticizer di(2-ethylhexyl) phthalate (DEHP) is known to have endocrine-disrupting properties mediated by its many metabolites that form upon exposure in biological systems. In a previous study, we reported an inverse association between DEHP metabolites in the human ovarian follicular fluid (FF) and the responsiveness of the follicles to controlled ovarian stimulation during in vitro fertilization (IVF) treatments. Here, we explored this association further through molecular analysis of the ovarian FF samples. Ninety-six IVF patients from Swedish (N = 48) and Estonian (N = 48) infertility clinics were selected from the previous cohort (N = 333) based on the molar sum of DEHP metabolites in their FF samples to arrive at \"high\" (mean 7.7 ± SD 2.3 nM, N = 48) and \"low\" (0.8 ± 0.4 nM, N = 48) exposure groups. Extracellular miRNA levels and concentrations of 15 steroid hormones were measured across FF samples. In addition, FF somatic cells, available for the Estonian patients, were used for RNA sequencing. Differential expression (DE) and interactions between miRNA and mRNA networks revealed that the expression levels of genes in the cholesterol biosynthesis and steroidogenesis pathways were significantly decreased in the high compared to the low DEHP group. In addition, the DE miRNAs were predicted to target key enzymes within these pathways (FDR < 0.05). A decreased 17-OH-progesterone to progesterone ratio was observed in the FF of the high DEHP group (p < 0.05). Additionally, the expression levels of genes associated with inflammatory processes were elevated in the FF somatic cells, and a computational cell-type deconvolution analysis suggested an increased immune cell infiltration into the high DEHP follicles (p < 0.05). In conclusion, elevated DEHP levels in FF were associated with a significantly altered follicular milieu within human ovaries, involving a pro-inflammatory environment and reduced cholesterol metabolism, including steroid synthesis. These results contribute to our understanding of the molecular mechanisms of female reprotoxic effects of DEHP.

Dietary exposure risks of 39 multi-class Endocrine Disrupting Chemicals (EDCs) to the threatened Gangetic dolphins (Platanista gangetica) were investigated in a conservation-priority segment of the Ganga River. Elevated EDCs bioaccumulation was observed across prey fish species, with di(2-ethylhexyl) phthalate (DEHP) and di-n-butyl phthalate (DnBP) significantly contributing to the EDC burden. The concentrations of persistent organochlorines in prey revealed a shift from dioxin-like polychlorinated biphenyls (PCBs) to non-dioxin-like PCBs. The prevalence of regulated p,p\' DDT (Dichlorodiphenyltrichloroethane) and γ-HCH (Lindane) residues suggests regional non-compliance with regulatory standards. The concentration of some EDCs is dependent on the habitat, foraging behavior, trophic level and fish growth. The potential drivers of EDCs contamination in catchment includes agriculture, vehicular emissions, poor solid waste management, textile industry, and high tourist influx. Risk quotients (RQs) based on toxicity reference value were generally below 1, while the RQ derived from the reference dose highlighted a high risk to Gangetic dolphins from DEHP, DDT, DnBP, arsenic, PCBs, mercury, and cadmium, emphasizing the need for their prioritization within monitoring programs. The study also proposes a monitoring framework to provide guidance on monitoring and assessment of chemical contamination in Gangetic dolphin and habitats.

The unsustainable use of manmade chemicals poses significant threats to biodiversity and human health. Emerging evidence highlights the potential of certain chemicals to cause transgenerational impacts on metabolic health. Here, we investigate male transmitted epigenetic transgenerational effects of the anti-androgenic herbicide linuron in the pancreas of Xenopus tropicalis frogs, and their association with metabolic phenotypes. Reduced representation bisulfite sequencing (RRBS) was used to assess genome-wide DNA methylation patterns in the pancreas of adult male F2 generation ancestrally exposed to environmentally relevant linuron levels (44 ± 4.7 μg/L). We identified 1117 differentially methylated regions (DMRs) distributed across the X. tropicalis genome, revealing potential regulatory mechanisms underlying metabolic disturbances. DMRs were identified in genes crucial for pancreatic function, including calcium signalling (clstn2, cacna1d and cadps2), genes associated with type 2 diabetes (tcf7l2 and adcy5) and a biomarker for pancreatic ductal adenocarcinoma (plec). Correlation analysis revealed associations between DNA methylation levels in these genes and metabolic phenotypes, indicating epigenetic regulation of glucose metabolism. Moreover, differential methylation in genes related to histone modifications suggests alterations in the epigenetic machinery. These findings underscore the long-term consequences of environmental contamination on pancreatic function and raise concerns about the health risks associated with transgenerational effects of pesticides.

Concerns regarding man-made organic chemicals pervading our ecosystem and having adverse and detrimental effects upon organisms, including man, have now been studied for several decades. Since the 1970s, some environmental pollutants were identified as having endocrine disrupting affects. These endocrine disrupting chemicals (EDC) were initially shown to have estrogenic or anti-estrogenic properties and some were also shown to bind to a variety of hormone receptors. However, since the 1990s it has also been identified that many of these EDC additionally, have the ability of causing abnormal alterations in Ca2+ signalling pathways (also commonly involved in hormone signalling), leading to exaggerated elevations in cytosolic [Ca2+] levels, that is known to cause activation of a number of cell death pathways. The major emphasis of this review is to present a personal perspective of the evidence for some types of EDC, specifically alkylphenols and brominated flame retardants (BFRs), causing direct effects on Ca2+ transporters (mainly the SERCA Ca2+ ATPases), culminating in acute cytotoxicity and cell death. Evidence is also presented to indicate that this Ca2+ATPase inhibition, which leads to abnormally elevated cytosolic [Ca2+], as well as a decreased luminal ER [Ca2+], which triggers the ER stress response, are both involved in acute cytotoxicity.

The endocrine system and particularly thyroid hormones regulate almost all physiological processes in a timely manner in all vertebrates, from fish to reptiles to mammals, so risk assessment of endocrine disrupting chemicals (EDCs) is extremely important given their persistent presence in all environmental matrices. Resorcinol, as well as nonylphenol, octylphenol, and bisphenol A, F, S, are non-Halogenated Phenolic (non-HPCs) Chemicals known as EDCs. Resorcinol is a particular example in that most studies are based exclusively on humans while animal studies are few and often inadequate. The aim of this study was to assess the effects of exposure to different doses of resorcinol on the thyroid gland of the lizard Podarcis siculus during different periods of the thyroid gland activity cycle. Our results showed histopathologic changes in thyroid (follicular cell height increase and colloid area decrease), a thyroid weight increase in combination with serum T4 and T3 decrease, serum TSH, TRH increase in male lizards treated with 0.8,3.9,13.1, and 36.9 mg/kg/d of resorcinol. Besides, we also investigated the impacts of resorcinol treatments on hepatic 5\'ORD (type II) deiodinase and hepatic content of T3 and T4. Our findings showed that they are in agreement with in vivo in humans and in rodents data and therefore, resorcinol in reptiles may meet the WHO definition of ECDs.

Globally, pharmaceuticals and personal care products (PPCPs) are detected in surface waters receiving wastewater, yet their presence in biota, remain largely understudied. To address this, we conducted a study that measured 46 PPCPs in spot water samples and fish caught up- and downstream from wastewater treatment plants (WWTPs) in Victoria, Australia. We sampled 15 sites located along four waterways following a 3-site design: WWTP-discharge(\'hotspot\'), \'upstream\'(∼2 km) and \'downstream\'(∼2 km). Spot water and fish were also sampled at reference sites >100 km from WWTP discharge (n = 3). Additionally, spot water samples were taken from WWTP effluent outflows (n = 3). From each locality, we analysed 3-12 fish (n = 131 total). In waterways, passive samplers (POCIS; ∼28d, n = 19 PPCPs) were also deployed. Individual fish (axial muscle) and water were analysed with LC-MS-MS. We found that PPCP concentrations in environmental surface water ranged from<0.02-0.97 μg/L. In WWTP effluent, the range was <0.02-1.4 μg/L. Of the 46 PPCPs analysed, 12 were detected in spot water samples and five in fish. In water, the highest concentration detected was for antidepressant venlafaxine (3 μg/L). The most frequently detected PPCPs: venlafaxine (54.9%), metoprolol (41.2%), propranolol (29.4%), carbamazepine (29.4%), caffeine (17.6%) and sulfamethoxazole (17.6%). Out of 131 fish analysed, 35 fish had detectable levels of PPCPs in the muscle tissue. The highest muscle concentrations were: venlafaxine (150 μg/kg, redfin perch), and sertraline (100 μg/kg, eel). Bioaccumulation factors ranged from 104 to 341L/kg for venlafaxine in redfins, 21-1,260L/kg for carbamazepine in redfins and eels, and 367-3,333L/kg for sertraline in eels. Based on our human health risk calculations for venlafaxine, carbamazepine, sertraline, triclosan, and caffeine, consumption of fish does not pose a significant risk to human health. Despite this, most of the detected PPCPs in surface waters exceeded 10 ng/L trigger value, which has led to further investigations by EPA. Our study highlights the need for using multiple lines of evidence for estimating risks of PPCPs.