Antiestrogenic effect of paradichlorobenzene in immature mice and rats

Takahashi, Osamu; Oishi, Shogo; Yoneyama, M.; Ogata, Akio; Kamimura, Hisashi

doi:10.1007/s00204-007-0179-4

Cited by 14 publications

(4 citation statements)

References 68 publications

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“…57 It is conceivable that the enzymes induction could be transmitted by the arylhydrocarbon receptor (Ahr), although the relatively small size and polar characteristics of the halides of the mono-and dichlorobenzenes confer a limited hydrophobicity and thereby allow only for a weak binding to the Ahr. 58 3.5. Chlorinated Benzenes Modulate Oxidative Stress Proteins.…”

Section: Differential Protein Expressionmentioning

confidence: 99%

Chlorinated Benzenes Cause Concomitantly Oxidative Stress and Induction of Apoptotic Markers in Lung Epithelial Cells (A549) at Nonacute Toxic Concentrations

et al. 2010

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In industrialized countries, people spend more time indoors and are therefore increasingly exposed to volatile organic compounds that are emitted at working places and from consumer products, paintings, and furniture, with chlorobenzene (CB) and 1,2-dichlorobenzene (DCB) being representatives of the halogenated arenes. To unravel the molecular effects of low concentrations typical for indoor and occupational exposure, we exposed human lung epithelial cells to CB and DCB and analyzed the effects on the proteome level by 2-D DIGE, where 860 protein spots were detected. A set of 25 and 30 proteins were found to be significantly altered due to exposure to environmentally relevant concentrations of 10(-2) g/m(3) of CB or 10(-3) g/m(3) of DCB (2.2 and 0.17 ppm), respectively. The most enriched pathways were cell death signaling, oxidative stress response, protein quality control, and metabolism. The involvement of oxidative stress was validated by ROS measurement. Among the regulated proteins, 28, for example, voltage-dependent anion-selective channel protein 2, PDCD6IP protein, heat shock protein beta-1, proliferating cell nuclear antigen, nucleophosmin, seryl-tRNA synthetase, prohibitin, and protein arginine N-methyltransferase 1, could be correlated with the molecular pathway of cell death signaling. Caspase 3 activation by cleavage was confirmed for both CB and DCB by immunoblotting. Treatment with CB or DCB also caused differential protein phosphorylation, for example, at the proteins HNRNP C1/C2, serine-threonine receptor associated protein, and transaldolase 1. Compared to previous results, where cells were exposed to styrene, for the chlorinated aromatic substances besides oxidative stress, apoptosis was found as the predominant cellular response mechanism.

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Section: Differential Protein Expressionmentioning

confidence: 99%

Chlorinated Benzenes Cause Concomitantly Oxidative Stress and Induction of Apoptotic Markers in Lung Epithelial Cells (A549) at Nonacute Toxic Concentrations

et al. 2010

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“…Bisphenol A is an endocrine disrupting chemical used in the manufacture of polycarbonate plastics and resins found in the linings of cans and bottles, among other products (Rubin 2011). Other phenolic compounds, including benzophenone-3, 2,5- dichlorophenol, and triclosan, may also have endocrine disrupting properties (Kim and Choi 2014; Takahashi and others 2007; Wang and Tian 2015). Benzophenone-3 is an ultraviolet filter used in sunscreen and cosmetics; 2,5-dichlorophenol is a metabolite of 1,4-dichlorobenzene, a chemical used in mothballs, deodorizers, and fumigants; and triclosan is a microbicide used in antibacterial soaps and other personal care products.…”

Section: Introductionmentioning

confidence: 99%

Prenatal exposure to environmental phenols and childhood fat mass in the Mount Sinai Children's Environmental Health Study

Buckley

Herring

Wolff

et al. 2016

Environment International

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Early life exposure to endocrine disrupting chemicals may alter adipogenesis and energy balance leading to changes in obesity risk. Several studies have evaluated the association of prenatal bisphenol A exposure with childhood body size but only one study of male infants has examined other environmental phenols. Therefore, we assessed associations between prenatal exposure to environmental phenols and fat mass in a prospective birth cohort. We quantified four phenol biomarkers in third trimester maternal spot urine samples in a cohort of women enrolled in New York City between 1998 and 2002 and evaluated fat mass in their children using a Tanita scale between ages 4 and 9 years (173 children with 351 total observations). We estimated associations of standard deviation differences in natural log creatinine-standardized phenol biomarker concentrations with percent fat mass using linear mixed effects regression models. We did not observe associations of bisphenol A or triclosan with childhood percent fat mass. In unadjusted models, maternal urinary concentrations of 2,5-dichlorophenol were associated with greater percent fat mass and benzophenone-3 was associated with lower percent fat mass among children. After adjustment, phenol biomarkers were not associated with percent fat mass. However, the association between benzophenone-3 and percent fat mass was modified by child’s sex: benzophenone-3 concentrations were inversely associated with percent fat mass in girls (beta = −1.51, 95% CI = −3.06, 0.01) but not boys (beta = −0.20, 95% CI = −1.69, 1.26). Although we did not observe strong evidence that prenatal environmental phenols exposures influence the development of childhood adiposity, the potential antiadipogenic effect of benzophenone-3 in girls may warrant further investigation.

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“…Several in vitro test systems that screen for AhR ligands have been reported. First and foremost, these screenings have been implemented as operative instruments in the search for endocrine disrupters, as it has been shown that pollutants can exert anti-estrogenic effects via AhR that include a modulation of ER pathways without direct interaction with the ERs [210,211,212,213,214]. Because of this background and the high affinity of anthropogenic halogenated aromatic hydrocarbons (HAHs) for the AhR, a chemical class that includes polychlorinated biphenyls (PCBs) and polychlorinated dibenzodioxins (PCDDs), but also non-halogenated polycyclic aromatic hydrocarbons (PAHs) [194,207,208,209], toxicologists have intensively studied the AhR for a long time.…”

Section: Introductionmentioning

confidence: 99%

Potential Health-modulating Effects of Isoflavones and Metabolites via Activation of PPAR and AhR

2010

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Isoflavones have multiple actions on cell functions. The most prominent one is the activation of estrogen receptors. Other functions are often overlooked, but are equally important and explain the beneficial health effects of isoflavones. Isoflavones are potent dual PPARα/γ agonists and exert anti-inflammatory activity, which may contribute to the prevention of metabolic syndrome, atherosclerosis and various other inflammatory diseases. Some isoflavones are potent aryl hydrocarbon receptor (AhR) agonists and induce cell cycle arrest, chemoprevention and modulate xenobiotic metabolism. This review discusses effects mediated by the activation of AhR and PPARs and casts a light on the concerted action of isoflavones.

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Antiestrogenic effect of paradichlorobenzene in immature mice and rats

Cited by 14 publications

References 68 publications

Chlorinated Benzenes Cause Concomitantly Oxidative Stress and Induction of Apoptotic Markers in Lung Epithelial Cells (A549) at Nonacute Toxic Concentrations

Chlorinated Benzenes Cause Concomitantly Oxidative Stress and Induction of Apoptotic Markers in Lung Epithelial Cells (A549) at Nonacute Toxic Concentrations

Prenatal exposure to environmental phenols and childhood fat mass in the Mount Sinai Children's Environmental Health Study

Potential Health-modulating Effects of Isoflavones and Metabolites via Activation of PPAR and AhR

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