Abstract
The roles of cell calcium, gap junctions and cell volume in ethanol induced gastric damage were investigated by assessing intracellular free calcium levels, the patency of gap junctions and cell volume changes in ethanol exposed gastric epithelial cell monolayers. Intracellular free calcium concentration was increased, gap junctions were closed and cell volume was decreased after exposure to 5% (vol/vol) ethanol. Since gap junctions are known to be calcium gated, it is likely that their closure is secondary to the elevated cytosolic calcium in ethanol injured cells and may have a protective function by limiting intercellular spread of impending cell injury. The mechanism of cell shrinkage and its potential contribution to ethanol injury remains to be worked out.
Published Version
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