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Titolo:
MODULATED GAP JUNCTIONAL INTERCELLULAR COMMUNICATION AS A BIOMARKER OF PAH EPIGENETIC TOXICITY - STRUCTURE-FUNCTION RELATIONSHIP
Autore:
UPHAM BL; WEIS LM; TROSKO JE;
Indirizzi:
MICHIGAN STATE UNIV,DEPT PEDIAT & HUMAN DEV,FOOD SAFETY & TOXICOL CTR243 E LANSING MI 48824
Titolo Testata:
Environmental health perspectives
, volume: 106, anno: 1998, supplemento:, 4
pagine: 975 - 981
SICI:
0091-6765(1998)106:<975:MGJICA>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-INITIATING ACTIVITY; LIVER EPITHELIAL-CELLS; METHYLATED ANTHRACENES; AROMATIC-HYDROCARBONS; MUTAGENICITY; RAT; CARCINOGENESIS; FLUORANTHENE; ACTIVATION; BIOASSAY;
Keywords:
POLYCYCLIC AROMATIC HYDROCARBONS; GAP JUNCTIONAL INTERCELLULAR COMMUNICATION; EPIGENETIC TOXICITY; TUMOR PROMOTION; TUMOR INITIATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
65
Recensione:
Indirizzi per estratti:
Citazione:
B.L. Upham et al., "MODULATED GAP JUNCTIONAL INTERCELLULAR COMMUNICATION AS A BIOMARKER OF PAH EPIGENETIC TOXICITY - STRUCTURE-FUNCTION RELATIONSHIP", Environmental health perspectives, 106, 1998, pp. 975-981

Abstract

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 tumor-initiating properties of the compound. We report onthe 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.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/11/20 alle ore 15:32:41