Occurrence of phthalate esters in the yellow and Yangtze rivers of china: Risk assessment and source apportionment.

Phthalate esters (PAEs), recognized as endocrine disruptors, are released into the environment during usage, thereby exerting adverse ecological effects. This study investigates the occurrence, sources, and risk assessment of PAEs in surface water obtained from 36 sampling points within the Yellow River and Yangtze River basins. The total concentration of PAEs in the Yellow River spans from 124.5 to 836.5 ng/L, with Dimethyl phthalate (DMP) (75.4 ± 102.7 ng/L) and Diisobutyl phthalate (DiBP) (263.4 ± 103.1 ng/L) emerging as the predominant types. Concentrations exhibit a pattern of upstream (512.9 ± 202.1 ng/L) > midstream (344.5 ± 135.3 ng/L) > downstream (177.8 ± 46.7 ng/L). In the Yangtze River, the total concentration ranges from 81.9 to 441.6 ng/L, with DMP (46.1 ± 23.4 ng/L), Diethyl phthalate (DEP) (93.3 ± 45.2 ng/L), and DiBP (174.2 ± 67.6 ng/L) as the primary components. Concentration levels follow a midstream (324.8 ± 107.3 ng/L) > upstream (200.8 ± 51.8 ng/L) > downstream (165.8 ± 71.6 ng/L) pattern. Attention should be directed towards the moderate ecological risks of DiBP in the upstream of HH, and both the upstream and midstream of CJ need consideration for the moderate ecological risks associated with Di-n-octyl phthalate (DNOP). Conversely, in other regions, the associated risk with PAEs is either low or negligible. The main source of PAEs in Yellow River is attributed to the release of construction land, while in the Yangtze River Basin, it stems from the accumulation of pollutants in lakes and forests discharged into the river. These findings are instrumental for pinpointing sources of PAEs pollution and formulating control strategies in the Yellow and Yangtze Rivers, providing valuable insights for global PAEs research in other major rivers.

[Content and Health Risks of Microplastics and Phthalate Esters in Bottled Water].

To study the content and health risks of microplastics （MPs） and phthalate esters （PAEs） in bottled water, a quantitative analysis of MPs was conducted by using Rose Bengal staining and stereomicroscopy. Seven PAEs were quantified by using gas chromatography-triple quadrupole tandem mass spectrometry （GC-MS/MS）. The daily intake of MPs was estimated and the carcinogenic and non-carcinogenic risks of PAEs were evaluated through a health risk assessment model. The results showed that the abundance of MPs in 21 bottled waters ranged from 48 n·L-1 to 216 n·L-1 （with the median abundance of 88 n·L-1）. The majority （72.1%） of MPs were fibrous in shape, and fragments accounted for only 27.9%. The average proportion of small-sized （10-50 µm） MPs was 33.9%, and that of large-sized MPs （>500 µm） was 4.3%. Most MPs were blue. The ∑(PAEs) in bottled water was 1.15-2.47 µg·L-1 （average 1.62 µg·L-1）. PAEs detected with high frequencies （100%） included dimethyl phthalate （DMP）, diethyl phthalate （DEP）, diisobutyl phthalate （DIBP）, di-n-butyl phthalate （DBP）, and di（2-ethylhexyl） phthalate （DEHP）, while the detection frequencies of butylbenzyl phthalate （BBP） and di-n-octyl phthalate （DNOP） were relatively low. The concentrations of DBP, DEHP, and DEP were all below the standard limits for drinking water in China. The ∑(PAEs) in the migration experiments was 0.61-2.04 µg·L-1 （average 1.33 µg·L-1）. The migration amounts of DBP and DEHP were also within the allowable range under the condition of 60℃ for 10 days. Seven PAEs were detected in both the bottles and caps, and the average content of DEHP in bottles was the highest, while DBP had the highest content in caps. The estimated intake of MPs （EDI） by drinking bottled water in different age groups of humans was 2.87 n·ï¼ˆkg·d）-1 for adults, 3.87 n·ï¼ˆkg·d）-1 for children, and 5.85 n·ï¼ˆkg·d）-1 for infants. The carcinogenic risks of DEHP in 21 bottled water samples and the migration test were less than the maximum acceptable risk level （1×10-6）, and the non-carcinogenic risk indices （HIs） of PAEs were all less than 1, indicating no non-carcinogenic risk to humans； however, the risk value of infants and children was higher than that of adults and should not be ignored.

Toxic effects of dibutyl phthalate on testes of adult zebrafish: evaluation of oxidative stress parameters and histopathology.

Dibutyl phthalate (DBP) is a phthalic compound and is most commonly used as a plasticizer in the polymer industry. It affects the hypothalamus-pituitary-gonadal axis and produces infertility in exposed animals. A total of 366 adult male zebrafish were used to evaluate the toxicological effects of DBP in testes following continuous exposure for 28 days. To evaluate histological changes during phase I of the study, 30 zebrafish were equally divided into five groups viz., control (RO water), vehicle control (0.01% DMSO), T0 (250 µg/L of water), T1 (500 µg/L of water), and T2 group (1000 µg/L of water). The protocol for phase II of the study was decided based on the results of phase I of the study. During phase II, for evaluation of oxidative stress parameters and gene expression profile, a total of 336 fish were equally divided into four groups viz., control, vehicle control, T1 (500 µg/L of water), and T2 (1000 µg/L of water). The activity of SOD, CAT, and TAC was significantly lower in zebrafish from the T2 group; however, a significantly increased level of MDA in the T2 group was recorded as compared to control groups. mRNA expression profile of sod, cat, and nrf2 genes was significantly downregulated in the T2 group as compared to the control group. Histopathology and proliferating cell nuclear antigen immunostaining revealed a reduction in spermatozoa with increased spermatocytes and spermatogonia in testes from T1 and T2 groups. The result indicated that DBP can induce oxidative stress and affect spermatogenesis in zebrafish testes.

The Impact of Dibutyl Phthalate on Insulin Signaling in Human Skeletal Muscle Cells.

BACKGROUND: In China, the environmental concern of Dibutyl Phthalate (DBP) exposure significantly endangers human health by inducing insulin resistance (IR). Skeletal muscle tissue plays a critical role in this process. However, the precise molecular mechanisms through which DBP interferes with the insulin signaling pathway remain to be fully elucidated. This study aims to explore the molecular mechanisms by which DBP induces IR in skeletal muscle, focusing on the phosphatidylinositol 3-kinase (PI3K)-serine/threonine kinase (AKT)-glucose transporter 4 (GLUT4) signaling pathway. METHODS: To investigate the molecular mechanisms underlying DBP-induced IR, an experimental study was established on a human skeletal muscle cell line (HSkMC). Expression levels of mRNA and proteins associated with key signaling genes within the insulin receptor (INSR)-insulin receptor substrate (IRS)-PI3K-AKT-GLUT4 pathway were assessed using quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot techniques. Additionally, this study explored the effects of DBP alone and in combination with a PI3K inhibitor (BKM120) or phosphatase and tensin homolog (PTEN) overexpression lentivirus on these signaling components. RESULTS: Results from this study demonstrated that DBP exposure significantly decreased mRNA levels of INSR, IRS1, PI3K, AKT2, and GLUT4 in HSkMC cells compared to untreated control cells. This reduction was exacerbated when DBP was combined with BKM120 or PTEN overexpression lentivirus, suggesting a synergistic effect. Furthermore, DBP treatment reduced the expression and phosphorylation of AKT2, indicating a disruption in the insulin signaling pathway. CONCLUSIONS: This study elucidates a molecular mechanism by which DBP induces IR in skeletal muscle cells, primarily through the deregulation of the PI3K-dependent insulin signaling pathway. These insights enhance comprehension of the pathophysiological changes associated with IR caused by environmental pollutants like DBP, potentially guiding future strategies for prevention and intervention.

Whole-cell biocatalysis for phthalate esters biodegradation in wastewater by a saline soil bacteria SSB-consortium.

Phthalic acid esters (PAE) are widely used as plasticizers and have been classified as ubiquitous environmental contaminants of primary concern. PAE have accumulated intensively in surface water, groundwater, and wastewaters; thus, PAE degradation is essential. In the present study, the ability of a saline soil bacteria (SSB)-consortium to degrade synthetic wastewater-phthalates with alkyl chains of different lengths, such as diethyl phthalate (DEP), di-n-butyl phthalate (DBP), benzyl butyl phthalate (BBP), and di (2-ethylhexyl) phthalate (DEHP) was characterized. A central composite design-response surface methodology was applied to optimize the degradation of each phthalate, where the independent variables were temperature (21-41 °C), pH (5.3-8.6) and PAE concentration (79.5-920.4 mg L-1), and Gas Chromatography-Mass Spectrometry was used to identify the metabolites generated during phthalate degradation. Optimal conditions were 31 °C, pH 7.0, and an initial PAE concentration of 500 mg L-1, where the SSB-consortium removed 84.9%, 98.47%, 99.09% and 98.25% of initial DEP, DBP, BBP, and DEHP, respectively, in 168h. A first-order kinetic model explained - the biodegradation progression, while the half-life of PAE degradation ranged from 12.8 to 29.8 h. Genera distribution of the SSB-consortium was determined by bacterial meta-taxonomic analysis. Serratia, Methylobacillus, Acrhomobacter, and Pseudomonas were the predominant genera; however, the type of phthalate directly affected their distribution. Scanning electron microscopy analysis showed that high concentrations (1000 mg L-1) of phthalates induced morphological alterations in the bacterial SSB-consortium. The metabolite profiling showed that DEP, DBP, BBP, and DEHP could be fully metabolized through the de-esterification and ß-oxidation pathways. Therefore, the SSB-consortium can be considered a potential candidate for bioremediation of complex phthalate-contaminated water resources.

Assessing the fate, toxicity, and ecological risk of mixtures of di(2-ethylhexyl)phthalate and di-n-butylphthalate using aquatic and terrestrial microcosms.

Di(2-ethylhexyl)phthalate (DEHP) and di-n-butylphthalate (DBP) frequently coexist in different environmental compartments. Thus, in this study, model aquatic and terrestrial microcosms were prepared to analyze the combined effect of DEHP and DBP on their fate, toxicity, and ecological risk. In the aquatic microcosms, with the addition of the same amount of DEHP and DBP, a higher total amount of DEHP was detected in water, suspended particles, and sediment than DBP due to the higher Kow and half-life of DEHP than DBP. Sediment was the major sink of both phthalates, as the highest percentages of DEHP (90.0 % âˆ¼ 95.6 %) and DBP (68.7 % âˆ¼ 78.1 %) were found in the sediment. The results of the whole sediment toxicity test showed that DBP (LC50/LC10: 6.75/1.171 µg/g dw) was more toxic than DEHP (LC50/LC10: 158.75/27.25 µg/g dw) to the tubificid oligochaete Monopylephorus limosus, with a synergistic toxic effect of the mixture of DEHP and DBP (LC50/LC10: 100.3/4.6 µg/g dw). The mobility of DEHP and DBP in soil was low during irrigation, with the release of 0.054 % âˆ¼ 2.29 % DEHP and 0.097 % âˆ¼ 1.86 % DBP. The bioconcentration factors/biota-sediment accumulation factors for DEHP (70.8-145 L/kg/0.093-0.359) in the muscle of the fish Carassius auratus were lower than those for DBP (82.2-300 L/kg/0.514-1.625). The bioaccumulation factors of DEHP and DBP for earthworms were 0.373 and 0.682, respectively. The levels of DEHP and DBP in the water and sediment of aquatic systems and in the soil of terrestrial systems might pose high ecological risks to some fish species, M. limosus and earthworms, according to the risk quotient values. These data provide valuable insights for the development of government control strategies to minimize the ecological risks of DEHP and DBP.

Antioxidants in mitigating phthalate-induced male reproductive toxicity: A comprehensive review.

Phthalates, widely used as plasticizers, have been increasingly linked to male reproductive toxicity through mechanisms including oxidative stress, endocrine disruption, inflammation, and apoptosis. This comprehensive review evaluates the protective role of various antioxidants in mitigating the detrimental effects of phthalates such as di-(2-ethylhexyl) phthalate (DEHP), di-butyl phthalate (DBP), mono-(2-ethylhexyl) phthalate (MEHP), and monobutyl phthalate (MBP) on male reproductive health. Antioxidants such as lycopene, ellagic acid, genistein, and selenium compounds exhibit significant efficacy in counteracting phthalate-induced damage by neutralizing reactive oxygen species (ROS), enhancing endogenous antioxidant defenses, reducing inflammatory responses, and preventing apoptosis. Lycopene demonstrates broad-spectrum protective effects, particularly through its high ROS-scavenging capacity and ability to preserve mitochondrial function. Ellagic acid effectively ameliorates oxidative stress and inflammation, while genistein enhances the Nrf2 pathway and restores hormonal balance, offering robust protection against reproductive toxicity. Selenium compounds improve antioxidant enzyme activities, providing essential support against oxidative damage. These findings underscore the potential of antioxidants as therapeutic agents against phthalate-induced male reproductive dysfunction. Future research should focus on optimizing antioxidant combinations, understanding dose-response relationships, and assessing long-term efficacy and safety to develop effective interventions for safeguarding male reproductive health.

Prenatal exposure to dibutyl phthalate contributes to erectile dysfunction in offspring male rats by activating the RhoA/ROCK signalling pathway.

Prenatal exposure to dibutyl phthalate (DBP) has been reported to cause erectile dysfunction (ED) in adult offspring rats. However, its underlying mechanisms are not fully understood. Previously, we found that DBP activates the RhoA/ROCK pathway in the male reproductive system. This study investigated how prenatal exposure to DBP activates the RhoA/ROCK signalling pathway, leading to ED in male rat offspring. Pregnant rats were stratified into DBP-exposed and NC groups, with the exposed group receiving 750 milligrams per kilogram per day (mg/kg/day) of DBP through gavage from days 14-18 of gestation. DBP exposure activated the RhoA/ROCK pathway in the penile corpus cavernosum (CC) of descendants, causing smooth muscle cell contraction, fibrosis, and apoptosis, all of which contribute to ED. In vitro experiments confirmed that DBP induces apoptosis and RhoA/ROCK pathway activation in CC smooth muscle cells. Treatment of DBP-exposed offspring with the ROCK inhibitor Y-27632 for 8 weeks significantly improved smooth muscle cell condition, erectile function, and reduced fibrosis. Thus, prenatal DBP exposure induces ED in offspring through RhoA/ROCK pathway activation, and the ROCK inhibitor Y-27632 shows potential as an effective treatment for DBP-induced ED.

Alterations in neurotransmitters, steroid hormones, vitellogenin, and antioxidant system induced by di-n-butyl phthalate and di-isopentyl phthalate on catfish Rhamdia quelen.

Phthalates, such as di-n-butyl phthalate (DBP) and di-isopentyl phthalate (DiPeP), are pollutants with a high potential for endocrine disruption. This study aimed to evaluate parameters of endocrine disruption in specimens of the Neotropical fish Rhamdia quelen exposed to DBP and DiPeP through their food. After 30 days of exposure, the fish were anesthetized and then euthanized, and blood, hypothalamus, liver, and gonads were collected. DBP caused statistically significant alterations in the serotoninergic system of males (5 and 25 ng/g) and females (5 ng/g) of R. quelen and it increased testosterone levels in females (25 ng/g). DiPeP significantly altered the dopaminergic system in females, reduced plasma estradiol levels (125 ng/g) and hepatic vitellogenin expression (25 ng/g), and changed the antioxidant system in gonads (125 ng/g). The results suggest that DBP and DiPeP may have different response patterns in females, with the former being androgenic and the latter being anti-estrogenic. These findings provide additional evidence regarding the molecular events involving DBP and DiPeP in the endocrine disruption potential in juvenile specimens of Rhamdia quelen.

Removal of dibutyl phthalate (DBP) by bacterial extracellular polymeric substances (EPS) via enzyme catalysis and electron transmission.

Phthalic acid esters (PAEs) showed high environmental risk due to the widely existence and toxicity. Microbial-excreted extracellular polymeric substances (EPS) showed potential of degrading organic compounds. In this study, the degradation ability and the mechanisms of EPS from two bacteria (PAEs degrader Gordonia sihwensis; electrochemically active strain Shewanella oneidensis MR-1) were investigated. Results showed that EPS of the two bacteria had different composition of C-type cytochromes, flavins, catalase, and α-glucosidase. The removal of dibutyl phthalate (DBP) by total EPS were 68% of G. sihwensis and 72% for S. oneidensis. For both bacteria, the degradation rates k of EPS were as TB-EPS > LB-EPS > S-EPS. The degradation mechanisms of EPS from the two bacteria showed difference with electrochemical active components mediated electron transmission for S. oneidensis MR-1 and enzymes catalysis for G. sihwensis. Results of this study illustrated the variation of the contribution of active components of EPS to degradation.

Contamination levels and ecological risk assessment of phthalate esters (PAEs) in the aquatic environment of Chaohu Lake.

Phthalate esters (PAEs), widely recognized as synthetic organic compounds with extensive production and utilization, are known to disrupt physiological processes in both animals and humans, even at low environmental concentrations. This study investigated the occurrence, distribution, and potential ecological risk of five representative PAEs (DMP, Dimethyl phthalate; DEP, Diethyl phthalate; DBP, Dibutyl phthalate; DiBP, Diisobutyl phthalate; DEHP, Bis(2-ethylhexyl) phthalate) in a typical lake (Chaohu Lake, China). It was found that PAEs were detected in both the aqueous (1.09-6.402 µg/L) and solid phases (0.827-6.602 µg/g) of Chaohu Lake. Notably, DiBP and DBP were the predominant PAEs in the water, and DiBP and DEHP were the most prevalent in the sediments. The concentrations of PAEs exhibited significant seasonal variations in the aqueous phases, with total PAEs in summer being nearly twice those in winter. Toxicity assessments revealed that DEHP, DBP, and DiBP posed high risks to the survival of three indicator organisms (algae, Daphnia, and fish) in the aqueous phase. In the solid phase, the exceeding rate of DiBP was as high as 92.9%. On the other hand, DBP and DEHP generally presenting moderate risk, although some sites were identified as high-risk. This study's analysis of PAEs concentrations in Chaohu Lake reveals a discernible increasing trend when compared with historical data. These findings underscore the urgent need for interventions to mitigate the ecological threats posed by PAEs in Chaohu Lake.

Indicator displacement-based colorimetric assay for dibutyl phthalate in pharmaceutical products with titanium(IV)-pyridylazo resorcinol (PAR).

Taking advantage of the competitive binding affinity towards Ti(IV) between 4-(2-pyridylazo) resorcinol (PAR) and phthalate, a simple indicator displacement (ID)-based colorimetric assay was designed for indirect determination of a well-known phthalic acid ester, dibutyl phthalate (DBP). The indicator PAR and Ti(IV) formed a purplish-red-colored Ti(IV)-PAR complex (λmax = 540 nm) at a 1:1 ratio. In the presence of pre-hydrolyzed DBP, colorless complex formation of phthalate ion (emerging from alkaline hydrolysis of DBP) with Ti(IV) resulted in a hypsochromic shift in absorbance maximum, accompanying a color change from purplish-red to yellowish-orange (λmax = 390 nm) by the release of PAR from Ti(IV)-PAR system. Based on this mechanism, the linear response range of the system for DBP was found to lie between 0.16 and 0.37 mmol L-1 with an experimental detection limit of 11.6 µmol L-1. The recommended Ti(IV)-PAR system was successfully applied to DBP-containing pharmaceutical products (as real sample) after a simple clean-up process for removing possible water-soluble interferents. The analytical results obtained from the recommended method (by applying the standard addition approach) and the reference liquid chromatography-tandem mass spectrometric (LC-MS/MS) method were statistically compared using DBP-extract of the drug samples. Consequently, a simple and selective colorimetric ID strategy was proposed for the analysis of DBP in pharmaceuticals for the first time.

Dibutyl phthalate released by solitary female locusts mediates sexual communication at low density.

Sex pheromones play a crucial role in mate location and reproductive success. Insects face challenges in finding mates in low-density environments. The population dynamics of locusts vary greatly, ranging from solitary individuals to high-density swarms, leading to multiple-trait divergence between solitary and gregarious phases. However, differences in sexual communication between solitary and gregarious locusts have not been sufficiently explored. Herein, we found that solitary locusts but not gregarious ones heavily rely on a single compound, dibutyl phthalate (DBP), for sexual communication. DBP is abundantly released by solitary female locusts and elicits strong attraction of male solitary and gregarious locusts. Solitary adult males display much higher electrophysiological responses to DBP than adult females. Additionally, LmigOr13 was identified as the DBP-specific odorant receptor expressed in neurons housed in basiconic sensilla. Male LmigOr13-/- mutants generated by CRISPR/Cas9 have low electrophysiological responses and behavioral attraction to DBP in both laboratory and field cage experiments. Notably, the attractiveness of DBP to male locusts becomes more evident at lower population densities imposed by controlling the cage size. This finding sheds light on the utilization of a sex pheromone to promote reproductive success in extremely low-density conditions and provides important insights into alternative approaches for population monitoring of locusts.

Mechanisms of exacerbation of Th2-mediated eosinophilic allergic asthma induced by plastic pollution derivatives (PPD): A molecular toxicological study involving lung cell ferroptosis and metabolomics.

Polystyrene microplastics (PS-MP) and dibutyl phthalate (DBP) are plastic pollution derivatives (PPDs) commonly found in the natural environment. To investigate the effects of PPD exposure on the risk of allergic asthma, we established a PPD exposure group in a mouse model. The dose administered for PS-MP was 0.1 mg/d and for DBP was 30 mg/kg/d, with a 5-week oral administration period. The pathological changes of airway tissue and the increase of oxidative stress and inflammatory response confirmed that PPD aggravated eosinophilic allergic asthma in mice. The mitochondrial morphological changes and metabolomics of mice confirmed that ferrotosis and oxidative stress played key roles in this process. Treatment with 100 mg/Kg deferoxamine (DFO) provided significant relief, and metabolomic analysis of lung tissue supported the molecular toxicological. Our findings suggest that the increased levels of reactive oxygen species (ROS) in the lungs lead to Th2-mediated eosinophilic inflammation, characterized by elevated IL-4, IL-5, and eosinophils, and reduced INF-γ levels. This inflammatory response is mediated by the NFκB pathway and exacerbates type I hypersensitivity through increased IL-4 production. In this study, the molecular mechanism by which PPD aggravates asthma in mice was elucidated, which helps to improve the understanding of the health effects of PPD and lays a theoretical foundation for addressing the health risks posed by PPD.

Response of wheat (Triticum aestivum L. cv.) to the coexistence of micro-/nanoplastics and phthalate esters alters its growth environment.

Micro- and nano-plastics (MPs/NPs) have emerged as a global pollutant, yet their impact on the root environment of plants remains scarcely explored. Given the widespread pollution of phthalate esters (PAEs) in the environment due to the application of plastic products, the co-occurrence of MPs/NPs and PAEs could potentially threaten the growth medium of plants. This study examined the combined effects of polystyrene (PS) MPs/NPs and PAEs, specifically dibutyl phthalate and di-(2-ethylhexyl) phthalate, on the chemical properties and microbial communities in a wheat growth medium. It was observed that the co-pollution with MPs/NPs and PAEs significantly increased the levels of oxalic acid, formic acid, and total organic carbon (TOC), enhanced microbial activity, and promoted the indigenous input and humification of dissolved organic matter, while slightly reducing the pH of the medium solution. Although changes in chemical indices were primarily attributed to the addition of PAEs, no interaction between PS MPs/NPs and PAEs was detected. High-throughput sequencing revealed no significant change in microbial diversity within the media containing both PS MPs/NPs and PAEs compared to the media with PS MPs/NPs alone. However, alterations in energy and carbohydrate metabolism were noted. Proteobacteria dominated the bacterial communities in the medium solution across all treatment groups, followed by Bacteroidetes and Verrucomicrobia. The composition and structure of these microbial communities varied with the particle size of the PS in both single and combined treatments. Moreover, variations in TOC, oxalic acid, and formic acid significantly influenced the bacterial community composition in the medium, suggesting they could modulate the abundance of dominant bacteria to counteract the stress from exogenous pollutants. This research provides new insights into the combined effects of different sizes of PS particles and another abiotic stressor in the wheat root environment, providing a critical foundation for understanding plant adaptation in complex environmental conditions.

Transcriptome mechanisms of dandelion under stress of polystyrene and dibutyl phthalate and quantitative tracing of nanoplastics.

Polystyrene nanoplastics (PS NPs) and dibutyl phthalate (DBP) pollution pose significant risks to ecosystems and contribute to bioaccumulation in plants, yet uptake mechanisms and combined toxicity are poorly understood. We used fluorescent labeling and europium-doped PS NPs to reveal the absorption and translocation of NPs by dandelions and conducted a transcriptomic analysis under PS NPs and DBP exposure. The results indicated that NPs are transported horizontally through the intercellular gaps at the root tips and primary root-lateral root junctions via the apoplastic pathway, followed by longitudinal transport through the xylem vessels under the transpiration stream. Co-exposure significantly reduced the bioconcentration factors of dandelion seedlings by 113 % but increased the NP transfer factors by 33.8 %. Transcriptomic analysis confirmed that exposure to PS NPs and DBP activated gene expression in dandelion shoots and roots. The differentially expressed genes were primarily involved in the photosynthesis, plant hormone signal transduction, and phenylpropanoid biosynthesis pathways. Weighted gene co-expression network analysis identified key genes and hub transcription factors playing crucial roles in regulating dandelion's response to combined stress. Our study provides new insights into the plant toxicity mechanism underlying the interaction between PS NPs and DBP, highlighting the adverse effects of the combined pollution on plant health.

Transcriptome-centric approach to the derivation of adverse outcome pathway networks of vascular dysfunction after long-term low-level exposure of human endothelial cells to dibutyl phthalate.

Dibutyl phthalate (DBP) is an endocrine disruptor that adversely affects reproduction; however, evidence suggests it can also impact other systems, including vascular function. The mechanisms underlying DBP-induced vascular dysfunction, particularly after long-term low-level exposure of endothelial cells to this phthalate, remain largely unknown. To address this gap, we used experimentally derived data on differentially expressed genes (DEGs) obtained after 12 weeks of exposure of human vascular endothelial cells EA.hy926 to the concentrations of DBP to which humans are routinely exposed (10-9 M, 10-8 M, and 10-7 M) and various computational tools and manual data curation to build the first adverse outcome pathway (AOP) network relevant to DBP-induced vascular toxicity. DEGs were used to infer transcription factors (molecular initiating events) and molecular functions and biological processes (key events, KEs) using the Enrichr database. The AOP-helpFinder 2.0, an artificial intelligence-based web tool, was used to link genes and KEs and assign confidence scores to co-occurred terms. We constructed the AOP networks using Cytoscape and then manually arranged KEs to depict the flow of mechanistic information across different levels of network organization. An AOP network was created for each DBP concentration, revealing several distinct high-confidence subnetworks that could be involved in DBP-induced vascular toxicity: the insulin-like growth factor subnetwork for 10-7 M DBP, the CXCL8-dependent chemokine subnetwork for 10-8 M DBP, and the fatty acid subnetwork for 10-9 M DBP. We also developed an AOP network providing a mechanistic insight into the dose-dependent effects of DBP in endothelial cells leading to vascular dysfunction. In summary, we present novel putative AOP networks describing the mechanistic flow of information involved in DBP-induced vascular dysfunction in a long-term low-level exposure scenario.

Quantitative label-free proteomic analysis of mouse ovarian antral follicles following oral exposure to a human-relevant mixture of three phthalates.

Dibutyl phthalate (DBP), di-2-ethylhexyl phthalate (DEHP), and benzyl butyl phthalate (BBP) are used in personal and medical care products. In the ovary, antral follicles are essential for steroidogenesis and ovulation. DBP, BBP, and DEHP are known to inhibit mouse antral follicle growth and ovulation in vitro, and associate with decreased antral follicle counts in women. Given that the in vivo effects of a three-phthalate mixture on antral follicles are unknown, we evaluated the effects of a human-relevant mixture of DBP, BBP, and DEHP on ovarian follicles through proteome profiling analysis. Adult CD-1 female mice were fed corn oil (vehicle), or two dose levels of a phthalate mixture based on estimated exposures in general (32 µg/kg/d; PHT 32) and occupationally exposed (500 µg/kg/d; PHT 500) populations for 10 d. Antral follicles (>250 µm) were isolated and subjected to proteome profiling via label-free tandem mass spectrometry. A total of 5,417 antral follicle proteins were detected, of which 194 were differentially abundant between vehicle and PHT 32, and 136 between vehicle and PHT 500. Bioinformatic analysis revealed significantly different responses between the two phthalate doses. Protein abundance differences in the PHT 32 exposure mapped to cytoplasm, mitochondria, and lipid metabolism; whereas those in the PHT 500 exposure mapped to cytoplasm, nucleus, and phosphorylation. When both doses altered proteins mapped to common processes, the associated predicted transcription factors were different. These findings provide novel mechanistic insight into phthalate-associated, ovary-driven reproductive outcomes in women.

Ecotoxicological evaluation and regeneration impairment of planarians by dibutyl phthalate.

Commonly utilized as a plasticizer in the food and chemical sectors, Dibutyl phthalate (DBP) poses threats to the environment and human well-being as it seeps or moves into the surroundings. Nevertheless, research on the harmfulness of DBP to aquatic organisms is limited, and its impact on stem cells and tissue regeneration remains unidentified. Planarians, recognized for their robust regenerative capabilities and sensitivity to aquatic pollutants, are emerging animal models in toxicology. This study investigated the comprehensive toxicity effects of environmentally relevant levels of DBP on planarians. It revealed potential toxicity mechanisms through the use of immunofluorescence, chromatin dispersion assay, Western blot, quantitative real-time fluorescence quantitative PCR (qRT-PCR), chromatin behavioral and histological analyses, immunofluorescence, and terminal dUTP nickel-end labeling (TUNEL). Findings illustrated that DBP caused morphological and motor abnormalities, tissue damage, regenerative inhibition, and developmental neurotoxicity. Further research revealed increased apoptosis and suppressed stem cell proliferation and differentiation, disrupting a balance of cell proliferation and death, ultimately leading to morphological defects and functional abnormalities. This was attributed to oxidative stress and DNA damage caused by excessive release of reactive oxygen species (ROS). This exploration furnishes fresh perspectives on evaluating the toxicity peril posed by DBP in aquatic organisms.

The relationship between bisphenol A and phthalates with precocious puberty in Vietnamese children.

OBJECTIVES: This study is aimed to explore the correlation between bisphenol A (BPA) and phthalates, including diethylhexylphthalate (DEHP) and dibutylphthalate (DBP), and precocious puberty (PP). METHODS: A case-control study was conducted in Ho Chi Minh City, Vietnam, from November 2021 to April 2022, involving 250 children, with 124 of them diagnosed with PP and 126 serving as controls. We assessed the levels of urinary BPA, DEHP, and DBP in all participants and examined their association with the risk of PP. RESULTS: BPA was detected in 11.3 % of PP cases but was not found in any individuals in the control group (p<0.001). Diethylhexylphthalate metabolite (MEHP) was not detected in any of the samples. Positive urinary results for dibutylphthalate metabolite (MBP) were observed in 8.1 % of PP cases and 2.4 % in the control group, with an odds ratio of 3.6 (95 % confidence interval: 0.97-13.4, p=0.03). CONCLUSIONS: The PP group exhibited a higher prevalence of positive urinary BPA and DBP levels compared to the control group.