Abstract
Dimethylnitrosamine(DMN) is an alkylating agent and a known renal carcinogen. A short exposure of renal epithelial cells to cytotoxic concentrations of DMN influences the expression of gap junction proteins. In this study, we examined gap junctional intercellular communication and connexin 43 expression in renal epithelial cells treated with 1% DMN and also examined the effects of dibutyryl-cAMP on preventing gap junctional disturbances. Connexin 43 becomes hypophosphorylated after treatment with 1% DMN for 15 minutes, but this hypophosphorylation is inhibited by pretreatment with dibutyryl-cAMP. These results suggest that changes in gap junction protein expression are early events associated with 1% DMN treatment of renal epithelial cells, and such changes are prevented by dibutyryl-cAMP pretreatment.
MeSH terms
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Animals
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Blotting, Western
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Bucladesine / pharmacology*
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Carcinogens / antagonists & inhibitors*
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Carcinogens / toxicity
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Cell Communication / drug effects*
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Cell Communication / physiology
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Cell Membrane Permeability / drug effects
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Cell Membrane Permeability / physiology
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Connexin 43 / biosynthesis
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Connexin 43 / metabolism
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Dimethylnitrosamine / antagonists & inhibitors*
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Dimethylnitrosamine / toxicity
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Dogs
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Drug Interactions
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Epithelial Cells / cytology
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Epithelial Cells / drug effects
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Epithelial Cells / enzymology
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Epithelial Cells / metabolism
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Gap Junctions / drug effects*
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Gap Junctions / physiology
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Kidney / cytology
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Kidney / drug effects*
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Kidney / enzymology
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Kidney / metabolism
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L-Lactate Dehydrogenase / analysis
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Phosphorylation / drug effects
Substances
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Carcinogens
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Connexin 43
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Bucladesine
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L-Lactate Dehydrogenase
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Dimethylnitrosamine