Project description:<p>The widespread use of agricultural plastic films has made micro- and nanoplastics (MNPs) and phthalate esters (PAEs) contaminants of emerging concern in agroecosystems. However, the interactive mechanisms underlying their combined pollution in soil-plant systems remain elusive. To fill this gap, this study investigated the interaction between submicron plastics (SMPs, 0.01% and 0.1% w/w) and di(2-ethylhexyl) phthalate (DEHP) in soil-lettuce systems. Contrary to the anticipated synergistic toxicity, DEHP significantly reduced SMP uptake into and by cracked surface cells of lettuce roots (with root concentration factors decreasing by 19%–64%), i.e., DEHP alleviated SMP-induced oxidative stress, as evidenced by reduced levels of reactive oxygen species (–26.8% and –66.7%) and antioxidant enzyme activities (–118% and –128%). Metabolomic profiling revealed that SMP exposure significantly dysregulated multiple metabolic pathways (amino acid, carbohydrate, energy, glycan, lipid, and nucleotide metabolism), while SMP+DEHP co-exposure selectively attenuated these metabolic disturbances, showing enrichment only in glycan biosynthesis/metabolism and suppressing SMP-induced perturbations in other pathways (biosynthesis of secondary metabolites, energy metabolism, and signal transduction). Microbial community analysis showed that high-level SMP exposure significantly diminished bacterial α-diversity and amplicon sequence variant (ASV) richness, whereas DEHP supplementation enhanced those of Myxococcota in the soil, potentially counterbalancing SMP-induced microbial dysbiosis. These findings collectively demonstrate that co-contamination by MNPs and plastic additives may produce antagonistic interactions rather than uniformly synergistic effects, and provide a more comprehensive evaluation of the risks of PAEs and MNPs to food security, human health, and ecological environment.</p>
Project description:In the present study, a pregnant mouse model exposed to di(2-ethylhexyl) phthalate (DEHP, one of the most common plasticizers) during primordial follicle formation was established. The single-cell transcriptome technology was applied to investigate the roles of melatonin in ovarian cells against DEHP exposure. .
Project description:Di (2-ethylhexyl) phthalate (DEHP) is a common plasticizer. Studies have revealed that DEHP exposure can cause liver damage. Green tea is one of the most popular beverages in China. Green tea polyphenols (GTPs) have been proven to have therapeutic effects on organ damage induced by heavy metal exposure. However, few study report on GTP relieving DEHP-induced liver damage.
Project description:Extracellular vesicles (EVs) are known to contain important cargo of biologically active and regulatory molecules including small non-coding RNA (sncRNA). EVs from cauda epididymis play crucial role in post-testicular maturation of sperm. We assessed levels of cauda epididymosomes sncRNAs following exposure to low dose anti-androgenic Di-n-butyl phthalate (DBP), Di(2-ethylhexyl) phthalate (DEHP), and their mixtures in mice.
Project description:RNA-seq analysis was conducted as part of an experiment investigating the effects of the phthalate, di(2-ethylhexyl) phthalate (DEHP), on the mouse fetal testis. The goal of the study was to investigate the mechanism by which phthalates interfere with Sertoli cell function, following exposure to 0, 20, 500 mg/kg/d DPeP from gestational day (GD) 17-21.
Project description:This dataset contains RNA-seq profiles of breast cancer cells treated with di(2-ethylhexyl) phthalate (DEHP) or control vehicle. The study aims to characterize transcriptomic changes induced by DEHP exposure. RNA was extracted from treated cells, sequenced, and analyzed to assess gene expression differences between DEHP-treated and control conditions. The dataset provides information on genes responsive to DEHP and may serve as a resource for studies on environmental chemical effects on breast cancer cells.
Project description:Phthalates are industrial additives widely used as plasticizers. In addition to deleterious effects on male genital development, population studies have documented correlations between phthalates exposure and impacts on reproductive tract development and on the metabolic syndrome in male adults. In this study we investigated potential mechanisms underlying the impact of di-(2-ethylhexyl)-phthalate (DEHP) on adult mouse liver in vivo. A parallel analysis of hepatic transcript and metabolic profiles from adult mice exposed to varying DEHP doses was performed. Hepatic genes modulated by DEHP are predominantly PPARα targets. However, the induction of prototypic cytochrome P450 genes strongly supports the activation of additional NR pathways, including Constitutive Androstane Receptor (CAR). Integration of transcriptomic and metabonomic profiles revealed a correlation between the impacts of DEHP on genes and metabolites related to heme synthesis and on the Rev-erbα pathway that senses endogenous heme level. Keywords: Treatment effect One-color macroarrays, 4 experimental conditions: Control mice (vehicle treated), mice treated with di-(2-ethylhexyl)-phthalate (DEHP) at 30 mg/kg/day (D30), 180 mg/kg/day (D180) or 1100 mg/kg/day (D1100) for 14 days, Biological replicates: 6 controls, 4 D30, 4 D180, 5 D1100, One replicate per array
Project description:Phthalate esters, such as DEHP (bis(2-ethylhexyl) phthalate, are a ubiquitous class of chemicals used as plasticizers in plastic products such as toys and hospital supplies. They are not covalently bound to the polymer matrix and can leach out of products. The goal of this study is to determine whether DEHP adversely affect the zebrafish (Danio rerio) microbiome-gut axis, specifically gut transcriptome. We exposed the fish to 3 ppm DEHP via food for 8 weeks to stimulate chronic exposure. To identify genomic responses of DEHP in gut, we used microarrays followed by differential gene expression analysis. The data were then mapped to changes in cell processes and signaling pathways using Pathway Studio.
Project description:Dibutyl phthalate (DBP), di-2-ethylhexyl phthalate (DEHP), and benzyl butyl phthalate (BBP) are three phthalates commonly found in consumer products, including the plastic coating of pharmaceuticals and personal care products. Folliculogenesis, a tightly regulated process occurring in the ovary, is the maturation of an immature primordial follicle to a mature antral follicle. Follicles house the oocyte and antral follicles specifically play a crucial role in ovarian steroidogenesis and ovulation. DBP, BBP, and DEHP have been associated with inhibited antral follicle growth in vitro, decreased ovulation rates in vitro, and decreased antral follicle counts in women. However, little is known about the effects of a three-phthalate mixture on antral follicles in vivo. The objective of this study was to evaluate the effects of a human relevant mixture of DBP, BBP, and DEHP on ovarian follicles through proteome profiling analysis. CD-1 female mice (60 days old) were pipet fed tocopherol stripped corn oil (vehicle control) only or a phthalate mixture (52% DBP, 36% DEHP, and 12% BBP dissolved in vehicle) which modeled human follicular fluid concentrations. The mice were treated with 32µg/kg/day (PHT Mix 32; cumulative estimate in general population) and 500µg/kg/day (PHT Mix 500; cumulative estimate in occupationally exposed individuals) for 10 consecutive days. Proteome profiling of antral follicles (>250µm) was performed via label-free tandem mass spectrometry. A total of 5,417 antral follicle proteins were identified in the three groups, of which 194 were differentially abundant between the vehicle and PHT Mix 32 group, and 136 between the vehicle and PHT Mix 500 group. Gene ontology analysis revealed that the two treatments of the phthalate mixture upregulate and downregulate distinctive processes, supporting non-monotonic effects of phthalates on the antral follicle proteome. Taken together, these results reveal that a human relevant mixture of DBP, BBP, and DEHP alters the antral follicle proteome and merits further evaluation to elucidate the molecular mechanisms by which phthalates cause negative reproductive outcomes.
Project description:Role of PPARalpha in the effects of DEHP on the hepatic expression of a selection of mouse genes related to nuclear receptor signaling. Di-(2-ethylhexyl)-phthalate (DEHP), a widely used plasticizer, is detected in consumerâs body fluids. Contamination occurs through environmental and food chain sources. In mouse liver, DEHP activates the peroxisome proliferator-activated receptor alpha (PPARalpha) and regulates the expression of its target genes. Several in vitro investigations support the simultaneous recruitment of additional nuclear receptor pathways. We investigated, in vivo, the hepatic impact of low doses of DEHP on PPARalpha activation, and the putative activation of additional signalling pathways. Wild-type and PPARalpha-deficient mice were exposed to different doses of DEHP. Gene expression profiling delineated the role of PPARalpha and revealed a PPARalpha-independent regulation of several prototypic Constitutive Androstane Receptor (CAR) target genes. This finding demonstrates that CAR also represents a transcriptional regulator sensitive to phthalates. CAR-mediated effects of DEHP provide a new rationale for most endpoints of phthalates toxicity described previously, including endocrine disruption, hepatocarcinogenesis and the metabolic syndrome. Keywords: Treatment effect One-color macroarrays, 6 experimental conditions: Wild type (WT) and PPARalpha-deficient mice (PPAR) were treated with vehicle (Ctrl) or with di-(2-ethylhexyl)-phthalate (DEHP) at 20 mg/kg/day (D20) or 200 mg/kg/day (D200) for 21 days, Biological replicates: 10 for each group, One replicate per array