Effects of ethanol on active transport in the dog stomach

Tj, Sernka; Gilleland, CW; Shanbour, Linda L.

doi:10.1152/ajplegacy.1974.226.2.397

Cited by 51 publications

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“…Thus, when the mucus-bicarbonate barrier protecting the epithelial cells is im paired, ethanol can directly attack the denudated epithelium and promote also intracel lular penetration of other molecules. On the other hand ethanol was shown to inhibit transport of ions such as chloride [30,31] and sodium [30,32], the latter being an event occurring at alcohol concentrations of 6% or more [28], It has been suggested that inhibition of active Na+ transport leads to intracellular accumulation of sodium, an ions and water. The consequent swelling of epithelial cells would produce cellular dis ruption with increased permeability of the mucosa [30,32],…”

Section: Increased Mucosal Permeabilitymentioning

confidence: 99%

Effects of Ethanol on the Gastric Mucosa

Guslandi

1987

Dig Dis

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Section: Increased Mucosal Permeabilitymentioning

confidence: 99%

Effects of Ethanol on the Gastric Mucosa

Guslandi

1987

Dig Dis

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“…the mechanism of action of this agent. They include reduced gastric blood flow (3), disruption of the so-called gastric mucosal barrier (4,5), accompanied by bicarbonate leakage (6), as well as metabolic alterations deeply linked to the acid secretory activity in the damaged gastric mucosa (7)(8)(9)(10).…”

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Enhanced Intracellular Calcium Promotes Metabolic and Secretory Disturbances in Rat Gastric Mucosa during Ethanol-Induced Gastritis

Hernández-Rincón

Olguín-Martínez

Hernández‐Muñoz

2003

Exp Biol Med (Maywood)

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Changes in the Ca(2+) homeostasis have been implicated in cell injury and death. However, Ca(2+) participation in ethanol-induced chronic gastric mucosal injury has not been elucidated. We have developed a model of ethanol-induced chronic gastric injury in rats, characterized by marked alterations in plasma membranes from gastric mucosa and a compensatory cell proliferation, which follows ethanol withdrawal. Therefore, the present study explored the possible role of intracellular Ca(2+) in the oxidative metabolism and in acid secretion in this experimental model. Glucose oxidation was greatly enhanced in the injured mucosa, as evaluated by CO(2) production by isolated mucosal preparations incubated with (14)C-radiolabeled glucose in different carbons. Oxygen consumption and acid secretion (aminopyrine accumulation) were also stimulated. A predominating secretory status was morphologically identified by electron microscopy in oxyntic cells of gastric mucosa from ethanol-treated rats. A coupling between secretory and metabolic effects induced by ethanol (demonstrated by an inhibitory effect of omeprazole in both parameters) was found. These ethanol-induced effects were also inhibited by addition of Ca(2+) chelators to isolated gastric mucosa samples. Lanthanum, a Ca(2+) channel blocker, inhibited ethanol-promoted increase of oxidative metabolism. In addition, a stimulated Ca(2+) uptake by mucosal minces and increased in vivo Ca(2+) levels in cytosolic and mitochondrial fractions, were also noticed. Enhanced glucose and oxygen consumptions were associated with higher ATP and NADP+ availability, whereas cytosolic NAD/NADH ratio (assessed by mucosal levels of lactate and pyruvate) was not significantly modified by the chronic ethanol administration. In conclusion, changes in Ca(2+) homeostasis, probably mainly due to increased extracellular Ca(2+) uptake, could mediate secretory and metabolic alterations found in the gastric mucosa from rats chronically treated with ethanol.

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“…Inhibition of the active transport of chloride in the rat stomach by topical application of 20% ethanol has been demonstrated (1). Studies conducted on the isolated (2) and intact dog stomach (3) have also demonstrated inhibition of active ion transport and acid secretion. A model for active chloride transport has been described by Kasbekar and Durbin (4) which is operative through a bicarbonate-stimulated ATPase, coupling chloride movement with bicarbonate in a manner similar to ATPase-activated sodium and potassium transport.…”

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confidence: 99%

Effects of Ethanol on Bicarbonate-Stimulated ATPase, ATP, and Cyclic AMP in Canine Gastric Mucosa

Tague¹,

Shanbour²

1977

Experimental Biology and Medicine

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Although the stomach is one of the primary sites of action of ingested alcohol, there have been few studies designed to explore the mechanisms by which alcohol affects the gastric mucosa. Inhibition of the active transport of chloride in the rat stomach by topical application of 20% ethanol has been demonstrated (1). Studies conducted on the isolated (2) and intact dog stomach (3) have also demonstrated inhibition of active ion transport and acid secretion. A model for active chloride transport has been described by Kasbekar and Durbin (4) which is operative through a bicarbonate-stimulated ATPase, coupling chloride movement with bicarbonate in a manner similar to ATPase-activated sodium and potassium transport. However, unlike the sodium plus potassium ATPase, chloride is not necessary for maximal bicarbonate ATPase activity (4). The only physiological base which is known to stimulate this ATPase is bicarbonate. Simon and Sachs ( 5 ) have suggested that this enzyme may play a role in bicarbonate transport in the pancreas.To determine whether the ethanol-induced inhibition of chloride transport in the gastric mucosa is mediated by inhibition of the bicarbonate-stimulated ATPase, the effects of ethanol were evaluated on bicarbonate-stimulated ATPase activity, in vitro and in vivo ATP content, and in vivo cAMP content of dog gastric mucosa.Methods. Magnesium and magnesium plus bicarbonate-stimulated ATPase activities were determined according to Blum et al. (6) using crude homogenates of canine These investigations were supported by NIAAA Grant Number 2 R 0 1 A A 00194-04. Dr. Shanbour is the recipient of Research Scientist Development Award Number 5 K02-AA-70463-03.Author to whom reprint requests should be addressed.gastric mucosa. Gastric segments were resected from dogs fasted for 24 hr and anesthetized with 0.68 g/kg of chloralose-urethane (1:lO). The mucosa was separated from the muscular portion of the stomach using glass slides. The mucosal portion was homogenized (1 : 10) in 0.25 M ice-cold sucrose with a ground glass tissue grinder, diluted, and analyzed within 1 hr. Reaction mixtures contained the following final concentrations: 100 mM Tris-HEPES (pH 8.2), 3 mM MgC12, 3 mM ATP, homogenate equal to 2.0 mg of tissue per ml of reaction mixture, and 20 mM NaHCO, when bicarbonate stimulation was evaluated. The samples were incubated at 37" and the reaction was terminated by pipetting 0.2 ml of the reaction mixture into 0.4 ml of 5% TCA. Denatured protein was removed by centrifugation and the quantity of inorganic phosphate released during the reaction was determined by the method of Buell et al. (7).Effects of ethanol on ATP were evaluated using thin mucosal slices incubated in dog plasma gassed with 95% O2 and 5% C 0 2 at 37" with and without 20% ethanol (v/v). At varying time intervals, the tissues were removed, blotted, frozen in liquid nitrogen, pulverized, and homogenized in 5% TCA. Wet weights remained stable when three mucosal slices were incubated with 20% ethanol in dog plasma for 10, 20, and 90 min...

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Effects of ethanol on active transport in the dog stomach

Cited by 51 publications

References 0 publications

Effects of Ethanol on the Gastric Mucosa

Effects of Ethanol on the Gastric Mucosa

Enhanced Intracellular Calcium Promotes Metabolic and Secretory Disturbances in Rat Gastric Mucosa during Ethanol-Induced Gastritis

Effects of Ethanol on Bicarbonate-Stimulated ATPase, ATP, and Cyclic AMP in Canine Gastric Mucosa

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