Role of the peroxisome proliferator-activated receptor α in responses to diisononyl phthalate

Valles, E.

doi:10.1016/s0300-483x(03)00260-9

Cited by 32 publications

(14 citation statements)

References 49 publications

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“…In fact, ppara stimulates fatty acid β-oxidation while ppary favors lipid biosynthesis and storage, leading to hepatic steatosis. Such upregulation may be explained since xeno-contaminants can interfere with nuclear transcriptional regulators, such as PPAR's, indeed DiNP and BPA are per se considered to possess PPAR activity in humans and rodents (Grün and Blumberg, 2009;Kaufmann et al, 2002;Valles et al, 2003). As previously reported (Grün and Blumberg, 2009), PPARs contain some of the largest and most promiscuous ligand binding pockets, allowing a large variety of agonist, including EDCs.…”

Section: Discussionmentioning

confidence: 83%

Endocrine disruptors in the diet of male Sparus aurata: Modulation of the endocannabinoid system at the hepatic and central level by Di-isononyl phthalate and Bisphenol A

Forner-Piquer

Mylonas

Calduch-Giner

et al. 2018

Environment International

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The increasing manufacture of plastics and their mismanagement has turned plastic into a ubiquitous waste in the marine environment. Among all the substances conforming the plastic items, the effects of a dietary Bisphenol A (BPA) and Di-isononyl phthalate (DiNP) have been evaluated in adult male gilthead sea bream, focusing on their effects in the modulation of the Endocannabinoid System (ECS). In zebrafish, the ECS has been recently chosen as a new target for the activity of some Endocrine Disrupting Chemicals (EDC), since it represents a complex lipid signaling network essential for the well-being of the organisms. The results obtained in gilthead seabream showed that BPA and DiNP altered the structure and the biochemical composition of liver, increasing the presence of lipids and triglycerides and decreasing the glycogen and phospholipids. Moreover, the addition of BPA or DiNP in the gilthead sea bream diet altered the levels of endocannabinoids (EC) and EC-like mediators in the liver. These alterations were also associated to changes at the transcriptomic level of genes involved in lipid biosynthesis and ECS metabolism. At the central level, both BPA and DiNP reduced the expression of the endocannabinoid receptor type I (cnr1) and the neuropeptide Y (npy) as well as the levels of the endocannabinoid Anandamide (AEA), suggesting a downregulation of appetite. The results herein reported highlighted the negative effects of chronic dietary exposure to DiNP or BPA on ECS functions and lipid metabolism of male gilthead sea bream liver, showing a similar disruptive activity of these contaminants at metabolic level. Moreover, the novelty of the biomarkers used evidenced possible innovative endpoints for the development of novel OEDCS test guidelines.

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Section: Discussionmentioning

confidence: 83%

Endocrine disruptors in the diet of male Sparus aurata: Modulation of the endocannabinoid system at the hepatic and central level by Di-isononyl phthalate and Bisphenol A

Forner-Piquer

Mylonas

Calduch-Giner

et al. 2018

Environment International

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“…The association of phthalates with epidemologic respiratory immunity changes is highly debated (Doelman et al 1990; Jaakkola et al 1999; Mendell 2007; Oie et al 1997). Studies in other labs have shown up-regulation of the immunosuppressive FK506 binding protein family of genes, specifically FKBP-1 and FKBP-13 , after diisononyl phthalate exposure in rodents (Valles et al 2003). …”

Section: Discussionmentioning

confidence: 99%

Concentrations of Phthalate Metabolites in Milk, Urine, Saliva, and Serum of Lactating North Carolina Women

Hines

Calafat

Silva

et al. 2009

Environ Health Perspect

213

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BackgroundPhthalates are ubiquitous in the environment, but concentrations in multiple media from breast-feeding U.S. women have not been evaluated.ObjectivesThe objective of this study was to accurately measure and compare the concentrations of oxidative monoester phthalate metabolites in milk and surrogate fluids (serum, saliva, and urine) of 33 lactating North Carolina women.MethodsWe analyzed serum, saliva, urine, and milk for the oxidative phthalate metabolites mono(3-carboxypropyl) phthalate, mono(2-ethyl-5-carboxypentyl) phthalate (MECPP), mono(2-ethyl-5-hydroxyhexyl) phthalate, and mono(2-ethyl-5-oxohexyl) phthalate using isotope-dilution high-performance liquid chromatography tandem mass spectroscopy. Because only urine lacks esterases, we analyzed it for the hydrolytic phthalate monoesters.ResultsWe detected phthalate metabolites in few milk (< 10%) and saliva samples. MECPP was detected in > 80% of serum samples, but other metabolites were less common (3–22%). Seven of the 10 urinary metabolites were detectable in ≥ 85% of samples. Monoethyl phthalate had the highest mean concentration in urine. Metabolite concentrations differed by body fluid (urine > serum > milk and saliva). Questionnaire data suggest that frequent nail polish use, immunoglobulin A, and fasting serum glucose and triglyceride levels were increased among women with higher concentrations of urinary and/or serum phthalate metabolites; motor vehicle age was inversely correlated with certain urinary phthalate concentrations.ConclusionsOur data suggest that phthalate metabolites are most frequently detected in urine of lactating women and are less often detected in serum, milk, or saliva. Urinary phthalate concentrations reflect maternal exposure and do not represent the concentrations of oxidative metabolites in other body fluids, especially milk.

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“…DINP induces peroxisome proliferation in rats ( Barber et al, 1987;Moore, 1998a;Smith et al, 2000) and mice (Kaufmann et al, 2002;Moore, 1998b;Smith et al, 2000), as determined by peroxisomal b-oxidation activity or electron microscopy. Hepatocellular proliferation and palmitoyl-CoA oxidase activity were induced in wild-type mice, but not in mice deficient in the peroxisome proliferator-activated receptor a (PPARa) (Valles et al, 2003). DINP caused a transient increase in hepatocellular proliferation in rats (Moore, 1998a) and replicative DNA synthesis in both mice and rats .…”

Section: Livermentioning

confidence: 99%

Risk assessment of oral exposure to diisononyl phthalate from children’s products

Babich

Chen

Greene

et al. 2004

Regulatory Toxicology and Pharmacology

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Role of the peroxisome proliferator-activated receptor α in responses to diisononyl phthalate

Cited by 32 publications

References 49 publications

Endocrine disruptors in the diet of male Sparus aurata: Modulation of the endocannabinoid system at the hepatic and central level by Di-isononyl phthalate and Bisphenol A

Endocrine disruptors in the diet of male Sparus aurata: Modulation of the endocannabinoid system at the hepatic and central level by Di-isononyl phthalate and Bisphenol A

Concentrations of Phthalate Metabolites in Milk, Urine, Saliva, and Serum of Lactating North Carolina Women

Risk assessment of oral exposure to diisononyl phthalate from children’s products

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