Inhibition of GAP junctional intercellular comunication by noncoplanar polychlorinated biphenyls: inhibitory potencies and screening for potential mode(s) of action

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00027162%3A_____%2F03%3A00008481" target="_blank" >RIV/00027162:_____/03:00008481 - isvavai.cz</a>

Výsledek na webu

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DOI - Digital Object Identifier

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Jazyk výsledku

angličtina

Název v původním jazyce

Inhibition of GAP junctional intercellular comunication by noncoplanar polychlorinated biphenyls: inhibitory potencies and screening for potential mode(s) of action

Popis výsledku v původním jazyce

Inhibition of gap junctional intercellular communication (GJIC) belongs among critical epigenetic events of tumor promotion. We determined relative potencies of a series of environmentally relevant PCB congeners to inhibit GJIC in vitro in a rat liver epithelial WB-F344 cells. The nonplanar PCBs were potent inhibitors of GJIC, whereas the dioxin-like PCBs did not inhibit GJIC. In contrast to phorbol ester and epidermal growth factor, prototypal tumor promoters, noncoplanar PCB 153 elicited a long-term downregulation of GJIC (up to 48 h). Various intracellular signaling pathways potentially involved in inhibition of GJIC were screened by using specific chemical probes inhibiting serine/threonine kinases, tyrosine kinases and phspholipases. Phosphocholine/specific phospholipase or sphingomyelinase and a tyrosine kinase might be upstream regulators of PCB/induced inhibition of GJIC.

Název v anglickém jazyce

Inhibition of GAP junctional intercellular comunication by noncoplanar polychlorinated biphenyls: inhibitory potencies and screening for potential mode(s) of action

Popis výsledku anglicky

Inhibition of gap junctional intercellular communication (GJIC) belongs among critical epigenetic events of tumor promotion. We determined relative potencies of a series of environmentally relevant PCB congeners to inhibit GJIC in vitro in a rat liver epithelial WB-F344 cells. The nonplanar PCBs were potent inhibitors of GJIC, whereas the dioxin-like PCBs did not inhibit GJIC. In contrast to phorbol ester and epidermal growth factor, prototypal tumor promoters, noncoplanar PCB 153 elicited a long-term downregulation of GJIC (up to 48 h). Various intracellular signaling pathways potentially involved in inhibition of GJIC were screened by using specific chemical probes inhibiting serine/threonine kinases, tyrosine kinases and phspholipases. Phosphocholine/specific phospholipase or sphingomyelinase and a tyrosine kinase might be upstream regulators of PCB/induced inhibition of GJIC.

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

CE - Biochemie

OECD FORD obor

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Projekt

<a href="/cs/project/GA525%2F00%2FD101" target="_blank" >GA525/00/D101: In vitro metody pro detekci a studium mechanismů epigenetické toxicity cizorodých látek</a><br>

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2003

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Toxicological Sciences

ISSN

1096-6080

e-ISSN

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Svazek periodika

76

Číslo periodika v rámci svazku

1

Stát vydavatele periodika

GB - Spojené království Velké Británie a Severního Irska

Počet stran výsledku

10

Strana od-do

102-111

Kód UT WoS článku

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EID výsledku v databázi Scopus

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