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AJP - Gastrointestinal and Liver Physiology, Vol 265, Issue 1 133-G137, Copyright © 1993 by American Physiological Society
ARTICLES |
J. C. Barreto, G. S. Smith, D. H. Russell and T. A. Miller
Department of Surgery, University of Texas Medical School, Houston 77030.
This study was undertaken to test the hypothesis that an increase in the concentration of molecular HCl in ethanolic solutions is at least partly responsible for the severity of damage seen with acidified ethanol. To accomplish this goal, we studied the synergistic relationship of HCl and ethanol by holding ethanol constant at 50% (vol/vol) and varying the acid concentration. In another experiment, acid concentration was held constant at 150 mM HCl, and the percentage of ethanol was varied. Our hypothesis was also tested by substituting sulfate for chloride to form H2SO4, a nonpermeant molecular acid. Results of our studies clearly showed that substitution of sulfate for chloride greatly reduced gastric damage, supporting the hypothesis that diffusion of molecular HCl is contributing to the damage by acidifying cells. In all cases, acidified ethanol solutions using HCl were more damaging than the individual components alone, and the severity of the damage caused by 50% ethanol was noted to be dependent on the concentration of HCl. We therefore conclude that the severity of acidified ethanol damage is dependent on cellular acidification caused by diffusion of molecular HCl.
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