The Effects of Anthracene and Methylated Anthracenes on Gap Junctional Intercellular Communication in Rat Liver Epithelial Cells

Upham, Brad L.; Weis, Liliane M.; Rummel, Alisa M.; Masten, Susan J.; Trosko, James E.

doi:10.1006/faat.1996.0195

Cited by 42 publications

(28 citation statements)

References 26 publications

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“…Some structure-activity relationships of PAHs and GJIC have been reported by Upham et al (39), who showed that monomethyl isomers of anthracene that possessed a baylike region ( Figure 2) were more inhibitory than the parent compound or the monomethyl isomer containing no baylike region.…”

Section: Carcinogenesis As a Multistage Multimechanism Process Involvmentioning

confidence: 60%

Modulated Gap Junctional Intercellular Communication as a Biomarker of PAH Epigenetic Toxicity: Structure-Function Relationship

Upham¹,

Weis²,

Trosko³

1998

Environmental Health Perspectives

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Cancer is a multistage multimechanism process involving gene and/or chromosomal mutations (genotoxic events), altered gene expression at the transcriptional, translational, and posttranslational levels (epigenetic events), and altered cell survival (proliferation and apoptosis or necrosis), resulting in an imbalance of the organism's homeostasis. Maintenance of the organism's homeostasis depends on the intricate coordination of genetic and metabolic events between cells via extracellular and intercellular communication mechanisms. The release of a quiescent cell, whether normal or premalignant, from the suppressing effects of communicating neighbors requires the downregulation of intercellular communication via gap junctions, thereby allowing factors that control intracellular events to exceed a critical mass necessary for the cell to either proliferate or undergo apoptosis. Therefore, determining the role an environmental pollutant must play in the multistage carcinogenic process includes mechanisms of epigenetic toxicity such as the effects of a compound on gap junctional intercellular communication (GJIC). A classic example of a class of compounds in which determination of carcinogenicity focused on genotoxic events and ignored epigenetic events is polycyclic aromatic hydrocarbons (PAHs). The study of structure-activity relationships of PAHs has focused exclusively on the genotoxic and tumorinitiating properties of the compound. We report on the structure-activity relationships of two-to four-ringed PAHs on GJIC in a rat liver epithelial cell line. PAHs containing a bay or baylike region were more potent inhibitors of GJIC than the linear PAHs that do not contain these regions. These are some of the first studies to determine the epigenetic toxicity of PAHs at the epigenetic level.Environ Health Perspect 1 06(Suppl 4): 975-981 (1998). http.//ehpnetl.niehs.nih.gov/docs/ 1998/Suppl4/975-981upham/abstract.html

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Section: Carcinogenesis As a Multistage Multimechanism Process Involvmentioning

confidence: 60%

Modulated Gap Junctional Intercellular Communication as a Biomarker of PAH Epigenetic Toxicity: Structure-Function Relationship

Upham¹,

Weis²,

Trosko³

1998

Environmental Health Perspectives

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“…Another property of PAHs is their inhibitory effect on gap junctional intercellular communication. It is interesting to note that PAHs containing a bay or a baylike region (see below) are more inhibitory than PAHs lacking this structural feature (Upham et al 1996;Weiss et al 1998).…”

Section: Mechanisms Of Action Of Pahsmentioning

confidence: 99%

Cancer Risk Assessment, Indicators, and Guidelines for Polycyclic Aromatic Hydrocarbons in the Ambient Air

Boström¹,

Gerde²,

Hanberg³

et al. 2002

Environ Health Perspect

875

459

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“…BRCA1 downregulation could in turn lead to a reduced DNA repair capacity, thereby facilitating the selection (outgrowth) of cells (i.e., 'initiated cells') that carry cancer-prone mutations induced by PAHs. Trosko and colleagues [90][91][92] analyzed the effect of twelve PAHs on gap junctional intercellular communication by using the scrape loading/ dye transfer technique. The PAHs used were naphthalene, 1-methylnaphthalene, 2-methylnaphthalene, anthracene, 1-methylanthracene, 2-methylanthracene, 9-methylanthracene, 9,10-dimethylanthracene, phenanthrene, fluorene, 1-methylfluorene and fluoranthene.…”

Section: Disruption Of Brca1 Expressionmentioning

confidence: 99%

Aberrant Gene Expression and Cell Signalling/Epigenetic Effects Induced by Polycyclic Aromatic Hydrocarbons

Steinberg¹

2005

The Carcinogenic Effects of Polycyclic Aromatic Hydrocarbons

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The Effects of Anthracene and Methylated Anthracenes on Gap Junctional Intercellular Communication in Rat Liver Epithelial Cells

Cited by 42 publications

References 26 publications

Modulated Gap Junctional Intercellular Communication as a Biomarker of PAH Epigenetic Toxicity: Structure-Function Relationship

Modulated Gap Junctional Intercellular Communication as a Biomarker of PAH Epigenetic Toxicity: Structure-Function Relationship

Cancer Risk Assessment, Indicators, and Guidelines for Polycyclic Aromatic Hydrocarbons in the Ambient Air

Aberrant Gene Expression and Cell Signalling/Epigenetic Effects Induced by Polycyclic Aromatic Hydrocarbons

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