Combined Enterohepatic Toxicity of Polystyrene Microplastics and Di(2-ethylhexyl) Phthalate in Mice: Gut Microbiota-Dependent Synergistic Effects.

Exposure to Phthalate Esters

Human Exposure Estimates for Phthalates

Synergistic assault of DEHP and MPs: Unmasking the ER stress-triggered autophagic injury male fertility.

Microplastics (MPs) and the plasticizer di(2-ethylhexyl) phthalate (DEHP) frequently co-occur, presenting substantial health risks to both humans and animals. While animal studies indicate adverse effects from exposure to MPs and DEHP, their potential toxicity in humans remains uncertain. This study examines the response of human hepatocellular carcinoma (HepG2) cells to concurrent exposure to synthetic spherical polystyrene (PS) particles and DEHP. We analyzed the effect of particle size on the internalization of PS-MPs using HepG2 spheres as a 3D model. The results showed that MPs at 100 nm had the highest internalization efficiency, which gradually decreased as the particle size increased to 1 and 5 μm. In addition, DEHP significantly improved the internalization of MPs, especially for 5 μm particles, which showed a 26% increase in internalization efficiency. We also evaluated changes in physiological activity. Co-exposure to MPs and DEHP resulted in significantly higher cytotoxicity than exposure to MPs alone, with a 20% reduction in cell viability. Larger particle sizes led to greater cellular damage, indicated by a 20% increase in reactive oxygen species (ROS) and a 40% rise in lactate dehydrogenase (LDH) release, suggesting membrane rupture. This study offers new insights into the potential toxicity of short-term exposure to MPs and DEHP, using HepG2 spheres to closely replicate invivo conditions.

Combined toxicity influence of polypropylene microplastics and di-2-ethylhexyl phthalate on physiological-biochemical characteristics of cucumber (Cucumis sativus L.)

Microplastics and di (2-ethylhexyl) phthalate synergistically induce apoptosis in mouse pancreas through the GRP78/CHOP/Bcl-2 pathway activated by oxidative stress

Effect of particle size and environmental conditions on the release of di(2-ethylhexyl) phthalate from microplastics

The main objective of the Endosulfan Manufacturers and Formulators Welfare Association in India is disseminating scientific facts concerning the use of endosulfan. Because endosulfan is used in several countries, the association watches for global news and information relevant to endosulfan.

Di (2-ethylhexyl) phthalate (DEHP), a widely used chemical in plastics, has various health hazards when accumulated in the environment. DEHP has been shown to cause toxicity to various organs like the liver, kidney, and reproductive organs. Phytocompounds have been used to mitigate DEHP-mediated organ toxicity. Morin hydrate (MH), a phytocompound, has also been known to protect tissue and organs against various induced toxic conditions. However, the impact of MH treatment on DEHP-induced uterine dysfunction has not yet been still investigated. Therefore, the present study has investigated the impact of MH on uterine physiology and morphology of DEHP-intoxicated mice. Twenty Swiss mice were randomly divided into four groups (n = 5): control (CN), Di (2-ethylhexyl) phthalate (DP) (500mg/kg), Di (2-ethylhexyl) phthalate (DP) + Morin hydrate (MH) (10mg/kg), and Di (2-ethylhexyl) phthalate (DP) + Morin hydrate (MH) (100mg/kg) for 14days. Our results showed that the expression of active caspase-3 was up-regulated, and Bcl2 was down-regulated in the uterus of DEHP-treated mice. Furthermore, the uterine histology also showed decreased luminal epithelium height and endometrium thickness in the DEHP-treated mice; however, myometrium layer (outer and inner) thickness was higher in DEHP-treated mice. The uterus of DEHP-treated mice also exhibited elevated oxidative stress and fibrosis, along with decreased estrogen levels and expression of estrogen receptors (ERs). MH treatment at both doses (10 and 100mg/kg) suppressed DEHP-induced uterine apoptosis (increased Bcl2 and decreased active caspase-3 expression) and fibrosis. MH also increased the circulating estrogen levels at both doses; Further ERα and ERβ expression were elevated in the MH treated in both groups). The levels of oxidative stress malondialdehyde (MDA levels) were higher in the uterus of DEHP alone and DEHP plus MH-treated mice (100mg/kg). Moreover, the antioxidant enzymes catalase, glutathione peroxidase and superoxide dismutase (Gpx and SOD) did not show a dose-dependent response to MH treatment; rather, MH showed a differential effect on these enzymes. The elevated oxidative stress in 100mg/kg MH treated uterus, despite elevated Gpx and SOD, remains unclear. Thus, these results suggest that MH ameliorates DEHP-induced uterine fibrosis, apoptosis, and histoarchitecture through ER modulation. These findings suggest that MH improves uterine structure and function in DEHP-treated mice.

Background : The study was designed to investigate renal function profile upon exposure to graded oral doses of Di (2- ethylhexyl) phthalate (DEHP) in the adult Wistar rats considering that DEHP leaches easily from plastic to foods, drinking water and the environment Methods : Twenty (20) Wistar rats were administered DEHP in the doses of 0.02mg/kg, 20mg/kg and 200mg/kg body weight in blocks A, B and C respectively through the intrapharyngeal route. Rats in block D, serving as control, were administered distill water. Both treatments and distilled water were administered at a convenient dose of 0.1ml over a 30 day duration. Serum obtained from each rat was analyzed for electrolytes (Na + , K + , Cl - ), creatinine and urea Results : Oral exposure of the rats to DEHP at the graded doses used in this study increased only the mean serum urea from 32.6 ± 2.63 mg/dl in control to 42.01 ± 3.05 mg/dl, 41.75 ± 1.93 mg/dl and 40.2 ± 2.82 mg/dl in rats treated with 0.02mg, 20mg and 200mg DEHP/body weight respectively. Other parameters of serum Na + , K + , Cl - and creatinine remain unchanged. Conclusion : Exposure to oral DEHP induced an elevation of the blood urea nitrogen irrespective of dose without affecting serum creatinine and the electrolytes Keywords : Di (2-ethylhexyl) phthalate, DEHP, Renal function, Plasticizer, Azotaemia

Combined negative effects of microplastics and plasticizer DEHP: The increased release of Nets delays wound healing in mice

Vol. 120, No. 8 News | Science SelectionsOpen AccessLong-Term Outcomes after Phthalate Exposure: Food Intake, Weight Gain, Fat Storage, and Fertility in Miceis accompanied byEffects of Di(2-ethylhexyl) Phthalate (DEHP) on Female Fertility and Adipogenesis in C3H/N Mice Wendee Holtcamp Wendee Holtcamp Search for more papers by this author Published:1 August 2012https://doi.org/10.1289/ehp.120-a320aView Article in:中文版AboutSectionsPDF ToolsDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InReddit Exposure to endocrine-disrupting chemicals (EDCs), particularly in utero, is suspected to contribute to obesity, diabetes, hypertension, and reproductive abnormalities. Di(2-ethylhexyl) phthalate (DEHP), a plasticizer found in cosmetics, fragrances, food packaging, and polyvinyl chloride, is one such EDC. Human studies have found associations between urinary metabolites of DEHP and other phthalates and increased body mass in humans, and maternal exposure to DEHP has been associated with impaired gonadal development and fertility in baby boys. However, much less is known about potential effects of DEHP on female health. In a two-part investigation, researchers documented weight and fertility changes in female mice exposed to DEHP, and then documented how exposure in utero and during lactation affected their offspring [EHP 120(8):1123–1129; Schmidt et al.].In the first study, adult female mice were given diets formulated to deliver one of three levels of DEHP (0.05, 5, or 500 mg/kg body weight) for 8 weeks. The lowest level was comparable to the tolerable daily intake for humans issued by the World Health Organization in 2003. Although outwardly healthy, dams fed all three levels of DEHP had significantly increased food intake, body weight, and visceral fat compared with controls. All treatment groups also showed increased gene expression of the hormone leptin (consistent with the animals’ increased visceral fat) and decreased expression of adiponectin (which may suggest potential effects on insulin sensitivity).As in previous studies, investigators found that at the highest level of DEHP exposure, expression of peroxisome proliferator-activated receptors alpha and gamma (PPARα and PPARγ)—which are mediators of adipogenesis and fat metabolism—was increased in the liver. However, unlike previous studies, they found a decrease in PPARα expression in visceral fat at the highest dose. The authors note that a pair-feeding design in which exposed and control animals receive the same amount of calories should be used to determine whether observed effects were a consequence of increased food intake or of metabolic effects of DEHP independent of caloric intake.In the second study, the investigators found that DEHP-exposed pups of both sexes had higher body weight at weaning than nonexposed pups. Higher body weight persisted 9 weeks after exposure ceased, and fat storage was significantly higher in female adult pups in a dose-dependent manner. These findings were surprising because DEHP is rapidly metabolized and excreted, yet the results suggest a lingering effect of in utero exposure to DEHP on body weight and fat tissue formation.At the highest DEHP exposure, a dose unlikely to be found in the environment, all dams experienced 100% spontaneous abortion. Surviving, lesser-exposed offspring were placed on a standard diet at weaning, and female offspring were mated to unexposed males. Although the total number of embryos was not reduced in pregnant females exposed to DEHP in utero, the investigators did find that 28% of the dams’ blastocysts were not viable in the low-dose group and 29% were not viable in the middle-dose group, compared with just 8% in controls. However, the difference was not statistically significant.FiguresReferencesRelatedDetailsRelated articlesEffects of Di(2-ethylhexyl) Phthalate (DEHP) on Female Fertility and Adipogenesis in C3H/N Mice15 May 2012Environmental Health Perspectives Vol. 120, No. 8 August 2012Metrics About Article Metrics Publication History Originally published1 August 2012Published in print1 August 2012 Financial disclosuresPDF download License information EHP is an open-access journal published with support from the National Institute of Environmental Health Sciences, National Institutes of Health. All content is public domain unless otherwise noted. Note to readers with disabilities EHP strives to ensure that all journal content is accessible to all readers. However, some figures and Supplemental Material published in EHP articles may not conform to 508 standards due to the complexity of the information being presented. If you need assistance accessing journal content, please contact [email protected]. Our staff will work with you to assess and meet your accessibility needs within 3 working days.

Di (2-ethyl) hexyl phthalate induces liver injury in chickens by regulating PTEN/PI3K/AKT signaling pathway via reactive oxygen species

Di (2-ethylhexyl) phthalate and polystyrene microplastics co-exposure caused oxidative stress to activate NF-κB/NLRP3 pathway aggravated pyroptosis and inflammation in mouse kidney

We studied the effect of di (2-ethylhexyl) phthalate (DEHP) on rat hair deposition of Iron (Fe), Copper (Cu), Manganese (Mn), and Zinc (Zn). Four groups, each of eight of female Wistar rats weighing 250-300 g, were randomly distributed to (1) control (corn oil-based diet), (2) DEHP 20 (20 mg DEHP per kg body weight (bw), (3) DEHP 100 (100mg DEHP kg/bw, and (4) DEHP 500 (500 mg DEHP kg/bw). The diets were fed daily for 14 days by gastric gavage before the rats were sacrificed. Hair content of Fe, Cu, Mn, and Zn was analyzed with atomic absorption spectrophotometry. There were no significant effect of DEHP on hair Fe content. However, hair Cu, Mn, and Zn were increased after DEHP 20 exposure (p<0.001). After administering DEHP 100 and DEHP 500, both Mn and Zn were decreased (p<0.001), respectively. Hair deposition of Cu, Mn, and Zn was affected by DEHP.