DEHP Research Articles

From the end to the beginning: Obtaining and evaluation of flexible PVC produced via chemical recycling of post-consumer PET

Di(2-ethylhexyl) terephthalate (DEHTP) is a promising substitute for dioctyl phthalate (DOP, banned in certain countries) as a polyvinyl chloride (PVC) plasticizer. This research endeavors to present findings about the synthesis of DEHTP through the depolymerization of polyethylene terephthalate (PET) with 2-ethyl-1-hexanol, the production and assessment of PVC formulated with this plasticizer, and a comparative analysis with PVC compounded using commercial plasticizers (DOP and DEHTP). Approximately 200 post-consumer PET bottles underwent chemical recycling under various conditions, leading to complete depolymerization (99%) following a six-hour reaction at 300°C. The plasticizers were characterized by infrared spectroscopy, 1H nuclear magnetic resonance spectroscopy, and gas chromatography coupled to mass spectrometry. The flexible PVCs were tensile and hardness tested and submitted to dynamic mechanical and thermogravimetric analyses. The resulting plasticizer exhibited properties analogous to commercial DEHTP, producing flexible PVC with even better properties. For instance, the activation energy of the dehydrochlorination reaction of the flexible PVC produced with DHETP from depolymerization was 3.3% to 16.2% higher than those produced with commercial plasticizers.

Assessing Variability in Children’s Exposure to Contaminants in Food: A Longitudinal Non-Targeted Analysis Study in Miami, Florida

Food is essential for human survival; however, food can be an important route of exposure to contaminants. This study investigated the presence and distribution of anthropogenic contaminants in food consumed by families with small children in South Florida, United States, evaluating seasonal and socio-economic variabilities in chemical composition. QuEChERS protocols, followed by non-targeted analysis (NTA) using an LC-Orbitrap HRMS system, were used for the comprehensive screening of organic contaminants. The compounds were annotated and identified with the Compound Discoverer (CD) software, and contaminant distributions were analyzed using boxplots and Principal Component Analysis (PCA). The results showed significant seasonal and socio-economic differences in contaminant distributions (p < 0.05). In the wet season, a predominance of polymers and surfactants, such as dodecanedioic acid and N-dodecylacrylamide, were found in food, which might be due to increased transport of industrial pollutants during increased precipitation, while plasticizers (e.g., bis(2-ethylhexyl) phthalate) and drugs (e.g., warfarin) were more prevalent during the dry season, which could be related to less dilution effects in this period. A higher abundance of 1-nitrosopiperidine, present in cured meats, was noted in food from upper socio-economic classes, while the lower class showed higher abundance of benzocaine, a common topical anesthetic.

The associations between prenatal plastic phthalate exposure and lipid acylcarnitine levels in humans and mice.

Phthalates are ubiquitous environmental pollutants known for their endocrine-disrupting properties, particularly during critical periods such as pregnancy and early childhood. Phthalates alter lipid metabolism, but the role of prenatal exposure on the offspring lipidome is less understood. In particular, we focused on long chain acylcarnitines - intermediates of fatty acid oxidation that serve as potential biomarkers of mitochondrial function and energy metabolism. This study aimed (i) to investigate the association between prenatal phthalate exposure and the child's blood acylcarnitine concentrations and, (ii) to evaluate the impact of prenatal administration of di-(2-ethylhexyl) phthalate (DEHP) on acylcarnitine levels in mouse offspring blood, brain and liver. We conducted analyses of both a prospective birth cohort study and an experimental study in mice. From the Barwon Infant Study cohort (1074 mother-child pairs), prenatal phthalate exposure was assessed at 36 weeks' gestation and its association with acylcarnitine levels was examined in cord blood, and child's blood at 6 months, 12 months and 4 years. In mice, pregnant C57BL/6J mouse dams were exposed to 20μg/kg DEHP for 5 days mid-gestation, and offspring tissues were analyzed at 1 month of age postnatally for acylcarnitine profiles. Our findings demonstrate that prenatal phthalate levels (specifically butyl benzyl phthalate (BBzP) and diisobutyl phthalate (DiBP)) are inversely associated with total long chain acylcarnitine levels in human cord blood at birth. In contrast, BBzP was positively associated with the long chain acylcarnitines at 12 months of age. In mice, prenatal DEHP exposure for only 5 days led to decreased palmitoylcarnitine (AC16:0) levels in the brain and liver, but not in blood. Taken together, our findings highlight that prenatal phthalate exposure can alter acylcarnitine profiles, indicating disruptions in fatty acid metabolism that may have long-term effects on metabolic health.

The combination of polystyrene microplastics and di (2-ethylhexyl) phthalate promotes the conjugative transfer of antibiotic resistance genes between bacteria.

Plastic pollution has become a common phenomenon. The process of plastic degradation is accompanied by the release of microplastics and plasticizers. However, the coexistence of microplastics and plasticizers on the transfer of antibiotic resistance genes (ARGs) has not been reported until now. Here, polystyrene (PS) microplastics and plasticizer di (2-ethylhexyl) phthalate (DEHP) were used for combined treatment experiment and their effects and mechanisms on the transfer of ARGs between bacteria were explored. By increasing cell membrane permeability and the expression of correlated genes, the combined treatment group showed promoting effects on the transfer of ARGs than that of control, with the highest promoting effects observed at 1 mg/L PS and 0.1 mg/L DEHP, which was 3.0 times higher in ARGs transfer rate than that of control. It was found that PS and DEHP treatment alone also led to a higher conjugative transfer frequency, and the frequency of the combined treatment was lower than that of the corresponding single treatment group. This indicated that the effects of DEHP and microplastics on ARGs transfer might be antagonistic. Transcriptome analysis indicated that the transfer of ARGs affects bacterial ion binding, oxidative stress, and energy metabolism processes, while the expression of genes related to cell membrane permeability, DNA repair, bacterial drug resistance, and quorum sensing also increase. This study may provide new insights for explaining the combined effects of various pollutants in the environment on the spread of ARGs.

Discovery of phloridzin as a new antagonist for Di(2-ethylhexyl) phthalate-induced male reproductive toxicity based on the adverse outcome pathway network and drug-target gene set enrichment analysis.

Di(2-ethylhexyl) phthalate (DEHP) is a widespread ubiquitous phthalate environmental contaminant. The male reproductive toxicity (MRT) from exposure to DEHP and its main metabolite, mono(2-ethylhexyl) phthalate (MEHP), has been well documented. Fully elucidating its toxic mechanism and discovering effective antagonists are desirable means to reduce the health risks of DEHP. In this study, 552 genes related to MRT induced by DEHP/MEHP were screened out from the Comparative Toxicogenomics Database (CTD) and DisGeNET database. Next, we developed a global adverse outcome pathway (AOP) network based on the existed AOP-wiki. After functional enrichment analyses and mapping to the global AOP network, we found that the increased ROS level, cell cycle arrest, and increased apoptosis are key events (KEs) involved in DEHP-mediated MRT, which was validated in TM3 Leydig cell model. Among them, cellular apoptosis is the core KE in DEHP-induced MRT via network topological analysis. Eventually, we developed a novel in silico antagonist screening platform (http://43.136.69.224:3838/wlab/) based on drug-target gene set enrichment analysis (dtGSEA version 2.0). Several potential candidates that mitigate DEHP-mediated cellular apoptosis have been screened out, including quercetin, taurine, methionine, and phloridzin. Further experimental results demonstrated that phloridzin provided the most effective protection against MEHP-induced apoptosis in TM3 cells probably through the p53 and MAPK signaling pathways. Molecular docking and molecular dynamics simulations suggest that STAT3 and RUNX1 may be important targets for phloridzin to antagonize MEHP-induced MRT. Our study provides a new approach to discover the antagonists for the toxicity of environmental contaminants based on AOP network and dtGSEA methods.

Prenatal exposure to phthalates and phthalate replacements in relation to chorionic plate surface vasculature at delivery.

Pregnant people are ubiquitously exposed to endocrine-disrupting phthalates through consumer products and food. The placenta may be particularly vulnerable to the adverse effects of phthalates, with evidence from animal models suggesting impacts on placental development and vascularization. We translate this research to humans, examining gestational exposure to phthalates and phthalate replacements in relation to novel markers of chorionic plate surface vascularization. Phthalate and phthalate replacement metabolites were measured in first trimester urine from pregnant participants in the Understanding Pregnancy Signals and Infant Development (UPSIDE) cohort (n=154). At delivery, placentae underwent specialized 2D and 3D digital imaging to quantify chorionic plate surface vasculature. Using weighted quantile g-computation mixtures methods as well as multivariable linear regression models examining individual metabolites, we evaluated associations with overall chorionic plate surface area and five chorionic plate surface vascular measures, adjusting for covariates. We additionally examined interactions with placental sex. Exposure to a phthalate mixture was associated with longer total arterial arc length (β=9.64cm; 95%CI: 1.68, 17.59), shorter mean arterial arc length (β=-0.07cm; 95%CI: -0.14, -0.01), and more arterial branch points (β=5.77; 95%CI: 1.56, 9.98), but not chorionic plate surface area. In models considering individual metabolites and their molar sums, results were strongest for the metabolites of Di-isobutyl phthalate (DiBP), Di-isononyl phthalate (DiNP), and Di(2-ethylhexyl) phthalate (DEHP). Associations with metabolites of phthalate replacements tended to be in the same direction but weaker. Few sex differences were observed. Gestational phthalate exposure may be associated with alterations in placental chorionic plate surface vasculature characterized by more branching and shorter segments. These alterations may have implications for placental perfusion and suggest a placental mechanism by which phthalates may impact fetal development.

Assessing the effect of sunlight exposure and reuse of polyethylene terephthalate bottles on phthalate migration.

Nowadays, polyethylene terephthalate (PET) bottles are widely used for packaging drinks and food. However, concerns have been raised about the possible migration of harmful chemicals, particularly phthalates, from these containers into their contents. Therefore, this study investigates the effects of sunlight exposure and PET bottle reuse on phthalate migration, focusing on three common phthalates: bis(2-ethylhexyl) phthalate (DEHP), dibutyl phthalate (DBP), and benzyl butyl phthalate (BBP). The study used two experimental designs. First, new PET bottles filled with distilled water were stored in the shade and under direct sunlight for 30days. Second, PET bottles were reused to store various foods (vinegar, mint extract, salty leaves, pickled cucumber, and lemon juice) at 4°C and 40°C for 10, 30, 60, and 90days. Phthalate concentrations were analyzed using solid phase extraction followed by gas chromatography-mass spectrometry (GC/MS). The results showed that exposure of PET bottles to sunlight significantly increased phthalate migration compared to shaded storage (P<0.001). When reused, storing PET bottles at 40°C resulted in significantly higher phthalate release from the bottle walls in all storage periods than at 4°C (P<0.001)-at 40°C, longer storage times resulted in a significant increase in phthalate migration (P<0.001), while at 4°C storage time had no significant effect on phthalate levels (P<0.001). This study shows that sunlight, higher storage temperatures, and longer storage times significantly increase the migration of phthalates from PET bottles into their contents. These results highlight the importance of maintaining appropriate storage conditions and limiting the reuse of PET bottles, particularly at higher temperatures and longer storage times, to minimize potential exposure to phthalates.

Simultaneous targeted and non-targeted analysis of contaminants in fertilizers in Quebec, Canada.

In this study, an LC-MS based analytical method was developed and validated for the simultaneous targeted analysis (14 bisphenols and 14 plasticizers) and suspect screening of other plastic-related contaminants in various types of fertilizers. The ultrasound-assisted extraction method showed overall satisfactory performances, achieving a median absolute recovery of 85% for the target compounds in different types of fertilizers. The method was applied to sixteen different types of fertilizers, including fertilizing residual materials (n=8 types), one cattle manure, and seven mineral fertilizers collected in Quebec, Canada in 2022 and 2023. Relatively higher levels of the targeted bisphenols and plasticizers were detected in some fertilizing residual materials, such as municipal biosolids and deinking residues. 4-Hydroxyphenyl 4-isoprooxyphenylsulfone (D-8) and bis(2-ethylhexyl) phthalate (DEHP) were dominant contaminants in these matrixes, with concentrations up to 35.6 and 64.7μgg-1 dw, respectively. A non-targeted workflow was successfully applied to municipal biosolids and deinking residues, and >30 contaminants were identified across multiple chemical families at level 1 identification confidence, with most of them previously unreported in various types of fertilizers. For example, new color developers, N-(2-((Phenylcarbamoyl)amino)phenyl)benzenesulfonamide (NKK-1304) and 2,4-bis(phenylsulfonyl)phenol (DBSP), were reported in deinking residues. This work illustrates the complexity of the contaminant mixtures in fertilizers such as municipal biosolids and deinking residues.

Production of benzyl-based esters from used soybean cooking oil as renewable plasticizers for flexible PVC films: Exploring new applications for lipases in emerging technologies.

The objective of this study was to produce new and renewable bio-based plasticizers from used soybean cooking oil (USCO). First, USCO was completely converted into free fatty acids (FFAs) using lipase from Candida rugosa. Next, these FFAs were enzymatically esterified with benzyl alcohol in solvent-free systems. During this stage, we assessed various factors that influenced the reaction, achieving a maximum FFA conversion of 94 % within 40 min using lipase Eversa® Transform 2.0 immobilized on poly(styrene-divinylbenzene) beads. This biocatalyst maintained full activity across eight consecutive esterification cycles. In the third step, epoxy groups were introduced into the chemical structure of the synthesized benzyl esters through an in situ epoxidation process. The performance of these benzyl esters as plasticizers for flexible PVC films was then evaluated and compared to the petroleum-based plasticizer dioctyl phthalate (DOP). Incorporating epoxy groups significantly improved the compatibility of the benzyl esters with PVC, resulting in films with superior properties compared to those plasticized with DOP. This study provides valuable insights into the development of bio-based plasticizers as potential alternatives to commercial plasticizers. Additionally, the proposed process offers useful technical information for emerging applications of lipases in oleochemical processes.

In Vitro Toxicity of a DEHP and Cadmium Mixture on Sheep Cumulus-Oocyte Complexes.

Di-(2-ethylhexyl) phthalate (DEHP) and Cadmium (Cd) affect female reproduction. To date, toxicological research has focused on the effects of individual contaminants, whereas living beings are exposed to mixtures. This study analyzed the effects of a DEHP/Cd mixture on nuclear and cytoplasmic maturation of sheep cumulus-oocyte complexes (COCs) compared with single compounds. COCs recovered from slaughterhouses-derived sheep ovaries were in vitro exposed to 0.5 μM DEHP, 0.1 μM Cd, or DEHP/Cd mixture at the same concentrations during 24 h of in vitro maturation (IVM). After IVM, oocyte nuclear chromatin configuration was evaluated, and bioenergetic/oxidative parameters were assessed on expanded cumulus cells (CCs) and matured oocytes (chi-square test and one-way ANOVA; p < 0.05). Under examined conditions, oocyte nuclear maturation was never impaired. However, COC bioenergetics was affected with stronger effects for the mixture than single compounds. Indeed, the percentages of matured oocytes with healthy mitochondrial distribution patterns were reduced (p < 0.001 and p < 0.05 for mixture and single compounds, respectively). Oocyte mitochondrial membrane potential, intracellular ROS levels, and mitochondria/ROS co-localization were reduced, with the same significance level, in all contaminated conditions. CCs displayed increased ROS levels only upon mixture exposure (p < 0.001). In conclusion, in vitro exposure to the DEHP/Cd mixture affected COC quality in the sheep to a greater extent than separate compounds.

Pets and related allergens modify the association between early life DEHP exposure and respiratory outcomes in children.

Throughout the perinatal period children are exposed to complex mixtures, including indoor chemicals such as phthalates, and biological agents. However, few studies focus on interactions between early-life co-exposures to shed light on how co-exposures modify their individual effects. Therefore, our study aims to assess whether early-life exposure to pets and related biological agents, namely pet allergens and endotoxin, modifies the association between di-(2-ethylhexyl) phthalate (DEHP) and asthma and wheeze in preschoolers to gain insight into interactions. Using data from a Canadian birth cohort study (CHILD), we conducted two complementary analyses on respiratory outcomes. First, we combined pet ownership with DEHP measurements from house dust (N=726). Second, we focused on a subgroup of children with exposure measurements of both DEHP and biological agents in dust (N=261). We used multivariable logistic regression models to assess whether pets and quantified biological agent levels modify associations between DEHP and asthma at 5 years and recurrent wheeze between 2 and 5 years. Interaction terms were included in the models and stratified analyses were further conducted. Associations between DEHP and asthma and wheeze were modified by pet ownership and related biological agents. For persistent/recurrent wheeze, the association with DEHP became larger among children with dogs at home and with higher dog allergens (p-interaction <0.1) and became smaller and insignificant when exposed to cats. Similarly, for asthma, the association with DEHP tended to be larger among children with dogs (also higher dog allergens) and among children without cats (also lower cat allergens) at home, respectively. Endotoxin levels modified the association between DEHP and persistent wheeze (p-interaction < 0.1). Early-life exposure to pets and related biological agents may modify the associations between phthalates and asthma and wheeze in children. Heterogeneity in single exposure studies could be a result of differences in co-exposures among studies.

The characteristics of phthalate acid esters and bisphenol A in PM2.5 of a petrochemical city: Concentrations, compositions, and health risk assessment in Dongying.

Phthalate acid esters (PAEs) and bisphenol A (BPA) are recognized as common endocrine disruptors associated with various adverse effects on human health. However, limitations in existing systematic studies, particularly in air detection, have raised concerns about potential health risks from inhalation exposure. In this study, PM2.5 samples were collected in Dongying, a petrochemical city, from October 27 to December 6, 2021. The concentrations and compositions of PAEs and BPA in PM2.5 were analyzed, and health risks associated with inhalation exposure were assessed. The hazard index (HI) and cancer risk (CR) were calculated according to EPA standard methods for both adults and children. The mean concentrations of PAEs and BPA were determined to be 1152 and 3.7 ng/m3, respectively. BPA concentrations were found to increase during heating, whereas PAE concentrations were observed to decrease slightly. Diisobutyl phthalate (DiBP), a major PAE, was reduced by approximately 20% during heating. However, 1,4-dimethylphthalazine (DMP) and bis(2-ethylhexyl) phthalate (DEHP) were observed to increase from 4.2 to 14% and from 5.9 to 11%, respectively. It is hypothesized that variations in the concentrations and compositions of airborne PAEs and BPA were influenced by district heating. An increase in the percentage of DEHP in PM2.5 was noted on polluted days, likely influenced by saturated vapor pressure. The estimated daily intake (EDI) for children was calculated to be higher than that for adults, indicating that children were exposed to significantly greater potential risks, although overall risks were observed to be low. The results of this study provide essential baseline data, such as concentration, for the management and control of emerging pollutants like endocrine disruptors in the urban atmosphere.

Co-cultivation of Bacillus amyloliquefaciens and Trichoderma harzianum: Synergistic effects on plant growth and biocontrol of jasmine collar rot

Jasmine (Jasminum officinale) is a valuable and culturally significant flowering crop in India. Still, its cultivation is greatly impacted by collar rot disease, caused by Sclerotium rolfsii Sacc., resulting in yield losses of up to 50%. This study explores co-culture technology, utilizing Trichoderma harzianum TR(D)-4 and Bacillus amyloliquefaciens BC(M)-2, as an integrated single-product solution for the biological control of this pathogen. Field surveys conducted across major jasmine-growing districts in Tamil Nadu revealed a range of disease severity (20% - 52%) and incidence (29% - 64%). The collar rot pathogen, and biocontrol agents were isolated from surveyed locations and identified through morphological characteristics and molecular phylogenetic analysis based on ITS and 16S rDNA sequences. In vitro assays using dual-plate and paired-plate methods demonstrated that Bacillus amyloliquefaciens BC(M)-2 achieved inhibition rates of 71.34% and 78.27%, respectively, while Trichoderma harzianum TR(D)-4 exhibited inhibition rates of 86.27% and 75.43% against Sclerotium rolfsii SR(D)-5. Co-culturing these antagonistic strains synergistically improved antifungal effectiveness, achieving an 87% inhibition rate against S. rolfsii compared to their separate cultures. The synergistic interaction in co-culture promoted the production of novel compounds, including alpha-bisabolol (AB), bis(2-ethylhexyl) phthalate, and harziandione, which enhanced plant growth and inhibited S. rolfsii. Further planta studies confirmed that the co-culture significantly reduced disease incidence and enhanced plant growth in both pre-and post-inoculation strategies. This research highlights the potential of co-culturing T. harzianum TR(D)-4 and B. amyloliquefaciens BC(M)-2 as an effective and sustainable approach for managing collar rot disease in jasmine.

The benefits of removing toxic chemicals from plastics

More than 16,000 chemicals are incorporated into plastics to impart properties such as color, flexibility, and durability. These chemicals may leach from plastics, resulting in widespread human exposure during everyday use. Two plastic-associated chemicals-bisphenol A (BPA) and di(2-ethylhexyl) phthalate (DEHP)-and a class of chemicals-brominated flame retardants [polybrominated diphenyl ethers (PBDEs)]-are credibly linked to adverse health and cognitive impacts. BPA exposures are associated with ischemic heart disease (IHD) and stroke, DEHP exposure with increased all-cause mortality among persons 55 to 64 y old, and prenatal PBDE exposures in mothers with IQ losses in their children. We estimate BPA, DEHP, and PBDE exposures in 38 countries containing one-third of the world's population. We find that in 2015, 5.4 million cases of IHD and 346,000 cases of stroke were associated with BPA exposure; that DEHP exposures were linked to approximately 164,000 deaths among 55-to-64 y olds; and that 11.7 million IQ points were lost due to maternal PBDE exposure. We estimate the costs of these health impacts to be $1.5 trillion 2015 purchasing power parity dollars. If exposures to BPA and DEHP in the United States had been at 2015 levels since 2003, 515,000 fewer deaths would have been attributed to BPA and DEHP between 2003 and 2015. If PBDE levels in mothers had been at 2015 levels since 2005, over 42 million IQ points would have been saved between 2005 and 2015.

Study on the Performance of Polymer Inclusion Membrane for Gold Extraction

The efficiency of polymer inclusion membranes (PIMs) for gold extraction, particularly using Aliquat-336 as a carrier, has been extensively studied. The membrane was fabricated by combining poly(vinylidene fluoride-co-hexafluoropropylene) (PVDF-co-HFP) with dioctyl phthalate (DOP) and varying concentrations of Aliquat-336 (5, 10, 15, 20, and 25 wt.%). The optimal formulation, incorporating 20 wt.% Aliquat-336 (M5), demonstrated significant improvements in ion exchange capacity (IEC) extraction rates, achieving an impressing 1.697 meq/g and 95.96% extraction efficiency, respectively.

DEHP and Its Metabolite MEHP Alter the Insr and Glut4 Gene Expression by Blunting the Interaction of Transcription Factors in L6 Myotubes.

Endocrine-disrupting chemicals (EDCs) play an important role in the incidence of type-2 diabetes. Di-2-ethyl hexyl Phthalate (DEHP) is one of the endocrine-disrupting chemicals used as a plasticizer to impart flexibility and softness to plastic-containing materials. Mono-2-ethylhexyl Phthalate (MEHP), a DEHP's primary metabolite, is preferentially absorbed once metabolized. A previous study from our laboratory showed that DEHP and MEHP altered the key proteins such as insulin receptor (INSR) and glucose transporter-4 (GLUT4) in L6 myotubes. In a sequel to the previous study, the present study hypothesized that DEHP and its metabolite MEHP may alter the Insr and Glut4 gene expression in L6 myotubes. Therefore, to find out the molecular mechanism behind the decreased INSR and GLUT4 protein levels in the previous study, the direct effect of DEHP and its metabolite MEHP in regulating Insr and Glut4 gene transcription in L6 myotubes was studied. The L6 myotubes were exposed to 50 and 100μM DEHP and MEHP for 24h, followed by insulin stimulation for 20min. We observed decreased Insr and Glut4 mRNA levels in DEHP and MEHP-treated groups. Western blot data showed decreased protein levels of MEF2A and MyoD in treated groups. ChIP assay detected a decreased association of MEF2A and MyoD to the Glut4 gene promoter and HMGA1 to the Insr gene promoter. The study revealed that DEHP and MEHP diminished the Insr and Glut4 gene expression through weakened interaction of their transcription factors on the respective promoter.

Green tea polyphenols alleviate di (2-ethylhexyl) phthalate-induced testicular injury in mice via lncRNA-miRNA-mRNA axis.

Di(2-ethylhexyl) phthalate (DEHP) is a commonly used plasticizer known for its toxic effects on the male reproductive system. Green tea polyphenols (GTPs), recognized for their antioxidant and anti-inflammatory properties, have demonstrated protective effects on various organs, but the mechanisms by which GTPs mitigate DEHP-induced testicular damage remain unclear. Healthy male C57BL/6J mice were divided into five groups: Control, DEHP, DEHP + GTP treatment, GTP, and Oil groups. Testicular histopathological changes were assessed using hematoxylin-eosin (H&E), periodic acid-Schiff (PAS), and Masson staining. Ultrastructural alterations were examined through transmission electron microscopy. High-throughput sequencing was performed to analyze the expression of mRNA, miRNA, and lncRNA, and to construct an lncRNA-miRNA-mRNA regulatory network for identifying key regulatory axes. Mice in the DEHP group exhibited significant testicular damage, including reduced sperm count, mitochondrial deformation, and endoplasmic reticulum dilation. GTP treatment notably improved testicular structural integrity, restored sperm count, and alleviated mitochondrial and endoplasmic reticulum damage. Additionally, DEHP significantly increased activated CD8+ T cells, which were reduced with GTP treatment. High-throughput sequencing revealed that GTP treatment exerted protective effects through the regulation of six key lncRNA-miRNA-mRNA axes. GTPs significantly protect against DEHP-induced testicular damage, and the lncRNA-miRNA-mRNA regulatory axes play a potential role in this process.

DEHP impairs the oxidative stress response and disrupts trace element and mineral metabolism within the mitochondria of detoxification organs.

Di(2-ethylhexyl) phthalate (DEHP), a widely utilized plasticizer in various consumer products, is classified as an endocrine disruptor and has been implicated in numerous adverse health effects, including oxidative stress, inflammation, and metabolic disturbances. Despite the growing body of literature addressing the systemic effects of DEHP, the specific influence of DEHP-induced oxidative stress on mitochondrial function within detoxification organs, particularly the liver and kidneys, remains largely unexplored. This study evaluated the effects of DEHP exposure (0, 100, 200, and 400mg/kg/day) on mitochondrial oxidative stress, trace elements, and mineral metabolism associated with signaling pathways in the liver and kidneys of rats. Altered mitochondrial oxidative stress status was indicated by impaired glucose 6-phosphate dehydrogenase (G6PD), 6-phosphoglucerate dehydrogenase (6-PGD), glutathione reductase (GR), glutathione s-transferase (GST), and glutathione peroxidase (GPx) activities, along with significant disruptions in essential minerals and trace elements, including Na, Mg, Cu, Zn, and Fe. Key oxidative stress signaling pathways, such as NF-κB, Akt, STAT3, and CREB, glucose, and tissue homeostasis, displayed dose-dependent responses to DEHP, indicating complex regulatory mechanisms. This study represents the first comprehensive investigation into DEHP-induced mitochondrial dysfunction, highlighting its effects on oxidative stress metabolism, trace element homeostasis, and cellular signaling pathways in detoxification organs. These findings provide novel insights into the mitochondrial mechanisms underlying DEHP toxicity and underscores the need for further research into the implications of plasticizer exposure on human health.

Biodegradation of Di-2-Ethylhexyl Phthalate by Mangrove Sediment Microbiome Impacted by Chronic Plastic Waste.

Plastic pollution through the leaching of di(2-ethylhexyl) phthalate (DEHP), a widely used plasticizer, has led to the emergence of mangrove pollution. This study aimed to assess the DEHP removal efficiency of indigenous mangrove sediment microbiomes and identify key DEHP degraders using microcosm construction and metagenomic analysis. During the 35-day incubation period, the indigenous mangrove sediment microbiome, affected by chronic plastic pollution, demonstrated a 99% degradation efficiency of 200mg/kg DEHP. Spearman's correlation analysis suggested that Myxococcales, Methyloligellaceae, Mycobacterium, and Micromonospora were potentially responsible for DEHP degradation. Based on PICRUSt2, the DEHP-degrading pathway in the sediment was predicted to be an anaerobic process involving catechol metabolism through catC, pcaD, pcaI, pcaF, and fadA. Efficient bacterial isolates from the mangrove sediment, identified as Gordonia sp. and Gordonia polyisoprenivorans, were able to degrade DEHP (65-97%) within 7days and showed the ability to degrade other phthalate esters (PAEs).

DINCH Exposure Triggers Inflammatory, Oxidative, and Apoptotic Pathways in the Liver of Long-Evans Lactating Rats and Their Offspring.

1,2-cyclohexane dicarboxylic acid diisononyl ester (DINCH) is a non-phthalate plasticizer used as a replacement of di(2-ethylhexyl) phthalate (DEHP) in daily usage items. It is not known whether continuous exposure to low doses of DINCH can lead to hepatic alterations, the liver being the organ responsible for its metabolism. The aim of this study was to evaluate the activation of inflammatory and apoptotic pathways in the liver of lactating dams after DINCH exposure, and whether these effects may be observed on postnatal day 6 (PND6) offspring. Two doses of DINCH were tested by oral administration to the following three groups of Long-Evans rats: control, DINCH-lower dose (LDINCH, 30 mg/kg b.w./day), and DINCH-high dose (HDINCH, 300 mg/kg b.w./day). Inflammatory mediators (IL-1β, TNF-α, NF-κB), mitochondrial transcriptional factors (PPARγ and PGC-1α), oxidative stress markers (SOD, CAT, GSSG/GSH), and components of the mitochondrial apoptotic pathway (PUMA, BAX, BAD, Bcl-2, Bcl-xL, Cytochrome c, APAF-1, Caspase-3, AIF) were assessed by the gene and protein expression in the liver of lactating dams and offspring. Exposure to LDINCH promoted the release of pro-inflammatory cytokines such as IL-1β and TNF-α and raised oxidative stress levels (GSSG/GSH), as well as increased Caspase-3 levels and reduced anti-apoptotic proteins (Bcl-2 and Bcl-xL), both in lactating dams and PND6 offspring. Thus, constant exposure to lower doses of DINCH can disrupt inflammatory and oxidant/antioxidant homeostasis, leading to hepatic tissue damage in lactating dams and having a perinatal effect in PND6 offspring.