Proton permeability and lipid dynamics of gastric and duodenal apical membrane vesicles

Wilkes, Jonathan M.; Ballard, HJ; Dryden, David T. F.; Hirst, Barry H.

doi:10.1152/ajpgi.1989.256.3.g553

Cited by 16 publications

(16 citation statements)

References 17 publications

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“…In fact, an alcohol-induced increase in proton permeability Biophysical Journal was observed in gastric and duodenal mucosal epithelial membranes isolated from rabbit (Wilkes et al, 1989). It is interesting to compare their results with our present results.…”

Section: Discussionsupporting

confidence: 70%

“…It is interesting to compare their results with our present results. Wilkes et al (1989) found that, at 20°C, the proton permeability in gastric and duodenal membranes increases sharply at about 0.8-1.0 M ethanol and at about 70-90 mM benzyl alcohol. These alcohol concentrations come close to the critical alcohol concentrations for the abrupt increase in proton permeability determined at 20°C from our present DPPC study (Figs.…”

Section: Discussionmentioning

confidence: 97%

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Effects of alcohol-induced lipid interdigitation on proton permeability in L-alpha-dipalmitoylphosphatidylcholine vesicles

Zeng

Smith

Chong

1993

Biophysical Journal

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6-Carboxyfluorescein was employed to examine the effect of alcohol-induced lipid interdigitation on proton permeability in L-alpha-dipalmitoylphosphatidylcholine (DPPC) large unilamellar vesicles. Proton permeability was measured by monitoring the decrease of 6-carboxyfluorescein fluorescence after a pH gradient from 3.5 (outside the vesicle) to 8.0 (inside the vesicle) was established. At 20 degrees C and below 1.2 M ethanol, the fluorescence decrease is best described by a single exponential function. Above 1.2 M ethanol, the intensity decrease is better described by a two-exponential decay law. Using the fitted rate constants and the vesicle radii determined from light-scattering measurements, the proton permeability coefficient, P, in DPPC vesicles was calculated as a function of ethanol concentration. At 20 degrees C, P increases monotonically with increasing ethanol content up to 1.0 M, followed by an abrupt increase at 1.2 M. The vesicle size also exhibits a sudden increase at around 1.2 M ethanol, which has been shown to result from vesicle aggregation rather than vesicle fusion. The abrupt increases in P and in vesicle size occur at the concentration region close to the critical ethanol concentration for the formation of the fully interdigitated gel state of DPPC. At 14 degrees C, the abrupt change in P shifts to 1.9-2.0 M ethanol, completely in accordance with the ethanol-temperature phase diagram of interdigitated DPPC. Effects of methanol and benzyl alcohol on lipid interdigitation have also been examined. At 20 degrees C, DPPC large unilamellar vesicles exhibit a dramatic change in P at 3 M methanol and at 40 mM benzyl alcohol. These concentrations come close to the critical methanol and benzyl alcohol concentrations for the formation of fully interdigitated DPPC structures determined previously by others. It can be concluded that proton permeability increases dramatically as DPPC is transformed from the noninterdigitated gel to the fully interdigitated gel state by high concentrations of alcohol. This marked increase in proton permeability can be attributed to the combined effect of the changes in membrane thickness and surface charge density, due to the ethanol-induced lipid interdigitation. The possible effects of the increased proton permeability caused by ingested ethanol on gastric mucosal membranes are discussed.

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Section: Discussionsupporting

confidence: 70%

Section: Discussionmentioning

confidence: 97%

Effects of alcohol-induced lipid interdigitation on proton permeability in L-alpha-dipalmitoylphosphatidylcholine vesicles

Zeng

Smith

Chong

1993

Biophysical Journal

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“…In social drinking the ethanol concentration in the stomach can easily rise to 2% (28), and in moderate drinking up to 10% (13). The ethanol concentrations used in the present study are thus well within the range of real-life intragastric concentrations, giving a realistic view of the first changes caused by luminal ethanol.…”

Section: Discussionsupporting

confidence: 58%

Calcium Signaling Is Involved in EthanolInduced Volume Decrease and Gap Junction Closure in Cultured Rat Gastric Mucosal Cells

et al. 2005

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Ethanol is a well-established "barrier breaker" in gastric mucosa, but its detailed effects at the cellular level remain unclear. We have previously shown that the intracellular free calcium concentration is increased, gap junctions are closed, and cell volume is decreased after exposure to 5% (v/v) ethanol in primarily cultured rabbit gastric epithelial cells. Rat gastric mucosal (RGM) cells were grown to confluence on a coverslip or on a filter membrane. Gap junctional diffusion was measured in 5-carboxyfluorescein-loaded cells by bleaching a small area with a laser and measuring the recovery with confocal microscope. Intracellular calcium was measured spectrofluorometrically in fura-2-loaded cells. For cell volume measurements the cell monolayer was loaded with calcein and imaged along the Z-axis with a confocal microscope. The changes in fluorescence intensity were intercepted as a measure of cell volume change. TMB-8 was used to inhibit intracellular calcium release and lanthanum to block plasma membrane calcium selective ion channels, while BABTA served as an intracellular calcium chelating agent. Results showed that ethanol (7.5%, v/v) exposure increased intracellular calcium from 69 +/- 7 to 142 +/- 11 nM (N = 5; P < 0.05), decreased cell volume by -23 +/- 5% (N = 8; P < 0.05), and induced gap junction closure (fluorescence recovery from 37 +/- 9 to 15 +/- 3%; N = 6; P < 0.05). A serosal potassium channel blocker, quinine, almost completely prevented the ethanol-induced cell volume decrease (from -23 +/- 5 to -3 +/- 3%), suggesting that opening of basolateral potassium channels underlies cell shrinkage. BABTA inhibited completely (from 35 +/- 3 to 39 +/- 4 nM; N = 6; P < 0.05), and TMB-8 + lanthanum partially (from 60 +/- 6 to 92 +/- 12 nM; N = 6; P < 0.05), the ethanol-induced intracellular calcium increase. BABTA also abolished the ethanol-induced volume decrease (from -23 +/- 5 to 1 +/- 4%; N = 6; P < 0.05), while TMB-8 + lanthanum had a lesser effect on it (from -23 +/- 5 to -11 +/- 3%; N = 9; P < 0.05). They also abolished the closure of gap junctions induced by ethanol (fluorescence recovery, 38 +/- 5% for BABTA and 30 +/- 4% for TMB-8 + lanthanum). We conclude that luminal ethanol opens basolateral calcium-dependent potassium selective channels with resultant shrinkage of the cells and blocks the intercellular gap junctions. These actions are mediated by intracellular calcium signaling.

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“…Both factors have antiapoptotic and also proapoptotic functions depending on the functional state and activities of the cell, and they also contribute to gastric defense against various ulcerogenic agents (20). The ethanol concentration range used in this study is easily reached after social and moderate drinking (7,29). Fig.…”

Section: Discussionmentioning

confidence: 99%

Ethanol induced NF-κB activation protects against cell injury in cultured rat gastric mucosal epithelium

Mustonen

Hietaranta²,

Puolakkainen³

et al. 2007

American Journal of Physiology-Gastrointestinal and Liver Physi

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Proton permeability and lipid dynamics of gastric and duodenal apical membrane vesicles

Cited by 16 publications

References 17 publications

Effects of alcohol-induced lipid interdigitation on proton permeability in L-alpha-dipalmitoylphosphatidylcholine vesicles

Effects of alcohol-induced lipid interdigitation on proton permeability in L-alpha-dipalmitoylphosphatidylcholine vesicles

Calcium Signaling Is Involved in EthanolInduced Volume Decrease and Gap Junction Closure in Cultured Rat Gastric Mucosal Cells

Ethanol induced NF-κB activation protects against cell injury in cultured rat gastric mucosal epithelium

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