The gap junctional intercellular communication is no prerequisite for the stabilization of xenobiotic metabolizing enzyme activities in primary rat liver parenchymal cells in vitro

1995 ◽  
Vol 31 (4) ◽  
pp. 266-273 ◽  
Author(s):  
Margarete Traiser ◽  
Bernd Diener ◽  
Dietmar Utesch ◽  
Franz Oesch
Keyword(s):  
Rat Liver ◽  
Intercellular Communication ◽  
Enzyme Activities ◽  
Gap Junctional Intercellular Communication ◽  
Liver Parenchymal ◽  
Metabolizing Enzyme ◽  
Parenchymal Cells ◽  
Gap Junctional

Doxorubicin induces EGF receptor-dependent downregulation of gap junctional intercellular communication in rat liver epithelial cells

2005 ◽  
Vol 386 (3) ◽  
pp. 217-223 ◽  
Author(s):  
Kotb Abdelmohsen ◽  
Claudia von Montfort ◽  
Dominik Stuhlmann ◽  
P. Arne Gerber ◽  
Ulrich K.M. Decking ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Rat Liver ◽  
Intercellular Communication ◽  
Connexin 43 ◽  
Egf Receptor ◽  
Gap Junctional Intercellular Communication ◽  
Erk Activation ◽  
Liver Epithelial Cells ◽  
Rat Liver Epithelial Cells ◽  
Gap Junctional

Abstract Exposure of rat liver epithelial cells to doxorubicin, an anthraquinone derivative widely employed in cancer chemotherapy, led to a dose-dependent decrease in gap junctional intercellular communication (GJC). Gap junctions are clusters of inter-cellular channels consisting of connexins, the major connexin in the cells used being connexin-43 (Cx43). Doxorubicin-induced loss of GJC was mediated by activation of extracellular signal-regulated kinase (ERK)-1 and ERK-2, as demonstrated using inhibitors of ERK activation. Furthermore, activation of the epidermal growth factor (EGF) receptor by doxorubicin was responsible for ERK activation and the subsequent attenuation of GJC. Inhibition of GJC, however, was not by direct phosphorylation of Cx43 by ERK-1/2, whereas menadione, a 1,4-naphthoquinone derivative that was previously demonstrated to activate the same EGF receptor-dependent pathway as doxorubicin, resulting in downregulation of GJC, caused strong phos-phorylation of Cx43 at serines 279 and 282. Thus, ERK-dependent downregulation of GJC upon exposure to quinones may occur both by direct phosphorylation of Cx43 and in a phosphorylation-independent manner.

Mutagenic and epigenetic mechanisms of zearalenone: prevention by Vitamin E

2008 ◽  
Vol 1 (3) ◽  
pp. 369-374 ◽  
Author(s):  
Z. Ouanes-Ben Othmen ◽  
S. Essefi ◽  
H. Bacha
Keyword(s):  
Vitamin E ◽  
Intercellular Communication ◽  
Chromosome Aberrations ◽  
Vero Cells ◽  
Antioxidant Vitamin ◽  
Epigenetic Mechanisms ◽  
Gap Junctional Intercellular Communication ◽  
Epigenetic Effects ◽  
Gap Junctional

It has been suggested that zearalenone, a non-steroidal estrogenic mycotoxin produced by Fusarium graminearium, causes DNA damage. However, the mutagenic properties of this toxin are controversial. The purpose of this study was to investigate both genotoxic and epigenetic effects of zearalenone in vitro. The effects of zearalenone on unscheduled DNA synthesis (UDS), induction of chromosome aberrations and inhibition of gap junctional intercellular communication were determined using Vero cells. The results show that in Vero cells, zearalenone treatment caused a concentration-dependent increase in UDS, induced chromosome aberrations and inhibited gap junctional intercellular communication. All of these effects were either prevented or reduced by co-treatment with the antioxidant vitamin E. The results support the hypothesis that in Vero cells zearalenone-induced oxidative stress is involved in and precedes all of the studied effects.

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