The in vitro effect of ethanol on the histamine-sensitive adenylate cyclase system

Szücs, Mária; Karnushina, Irina

doi:10.1007/bf01991488

Cited by 8 publications

(3 citation statements)

References 7 publications

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“…This effect of ethanol can be ascribed to the enhancement of the production of cAMP in the presence of ethanol and PGE,. Little evidence exists from previous work for any actions of eth- anol on PDE (Szucs and Karnushina, 1981;Volicer et al, 1977), and our studies with forskolin-stimulated production of cAMP also give no evidence that ethanol may be acting as a PDE inhibitor. Further, the studies with forskolin provide additional evidence for the importance and specificity of G,-mediated signaling in the witnessed actions of ethanol on CAMP levels.…”

Section: Discussioncontrasting

confidence: 88%

Ethanol's Actions on cAMP‐Mediated Signaling in Cells Transfected With Type VII Adenylyl Cyclase

Yoshimura

Tabakoff

1999

Alcoholism Clin & Exp Res

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The present study indicates that, in the presence of a particular isoform of AC, moderately intoxicating concentrations of ethanol will significantly potentiate the transmitter-mediated activation of the cAMP signaling cascade. Activation of this signaling cascade may have important implications for the mechanisms by which ethanol produces intoxication and/or in the mechanisms of neuroadaptation leading to tolerance to, and physical dependence on, ethanol.

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Section: Discussioncontrasting

confidence: 88%

Ethanol's Actions on cAMP‐Mediated Signaling in Cells Transfected With Type VII Adenylyl Cyclase

Yoshimura

Tabakoff

1999

Alcoholism Clin & Exp Res

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“…Our studies, as well as others, also suggest that, at least at high concentrations, ethanol influences the receptor-adenylate cyclase cascade mechanism at several sites, at the receptor, since it influenced the binding of 125I-bTSH, at the guanyl nucleotide regulatory protein, since it altered the response to NaF and Gpp(NH)p, and at the catalytic unit of adenylate cyclase, since it altered the response to forskolin. Previous time-dependent studies have suggested that ethanol had no appreciable effect distal to the catalytic unit of AC such as on phosphodiesterase activity [31]. Ethanol at a concentration of 68 mM, that is, at a concentration lower than observed after heavy drinking (up to 98 mM), in human studies and in chronic studies in rodents significantly increased the AC response to dopamine [32].…”

Section: Discussionmentioning

confidence: 99%

Effect of ethyl alcohol on the TSH‐receptor‐cyclase system in thyroid and nonthyroid tissues

Clark

Gerend

1986

World j. surg.

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Alcohol has been documented to be an excellent stimulator of calcitonin secretion in patients with C‐cell hyperplasia and medullary thyroid carcinoma (MTC). We, therefore, investigated the effects of 3–9% ethyl alcohol (ethanol) on the binding of tracer quantities of125I‐labeled bovine thyroid‐stimulating hormone (125I‐bTSH) to its receptor in normal and neoplastic thyroid tissue as well as its effects on adenylate cyclase (AC) stimulation in an 8,000 × g particulate fraction from normal and neoplastic nonmedullary thyroid tissue from 10 patients (20 specimens). We also studied the effect of ethanol on AC activity in 16 other nonthyroidal tissues (5 parathyroid adenoma, 1 pheochromocytoma, 1 sarcoma, and normal and neoplastic breast, kidney, parotid, and colon). These studies demonstrated that ethanol increased the binding of125I‐bTSH to normal and neoplastic thyroid tissue. It also increased AC activity in all but 3 of the 20 thyroid tissues and in all but 3 of the 16 nonthyroid tissues [thyroid basal 20.9±7.1, ethanol maximum 45.9±12.3 (p<0.025); nonthyroid basal 83.0 ±21.5, ethanol maximum 137±31.1 (p<0.01) in picomoles/30 min per mg protein]. This increase was dose dependent over a range of 3–9% ethanol. There was no difference in the degree of ethanol stimulation of AC between normal (28.7±16.3) and neoplastic (21.4±7.8) thyroid or between normal (89.0±8.9) and neoplastic (75.2±23.7) nonthyroid tissues. When ethanol (5%) was given along with TSH, sodium fluoride, Gpp(NH)p, or forskolin, there was a greater increase in AC activity than when no alcohol was present. The combined effect of TSH and ethanol (140.1±49.4) at maximal concentrations was comparable or greater than the result when TSH and ethanol were added separately (121.5±41.8). Thus, ethanol stimulates TSH binding and also activates AC in nearly all normal and neoplastic human tissues. This may be important biologically as well as experimentally since some compounds used in AC assays (in particular, forskolin) are dissolved in ethanol.

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“…The acute administration of alcohol in a concentration up to 5 % stimulates in vitro adenylate cyclase (AC) activity in the stomach of the guinea pig3 dogY4 and in humans,' whereas higher ethanol concentrations up to 20% inhibit AC activity in the rat in vitro and in v~v o .~.~ In addition, in vitro ethanol also inhibits the activity of low K, 3'3'cyclic adenosine monophosphate (CAMP) phosphodiesterase (PD) of gastric mucosa in various animals and in man c0mpetitively.4-~ However, 1-5% ethanol was found to have no effect on low K, cAMP PD. 3 Since these two key enzymes of cyclic AMP metabolism control intracellular cyclic AMP concentrations, and since intracellular cyclic AMP may play a role in gastric acid secretion, acute alcohol ingestion may stimulate acid secretion at low concentrations and may inhibit acid secretion at high concentrations.…”

mentioning

confidence: 99%

Effect of Chronic Ethanol Ingestion on the Cyclic AMP System of the Upper Gastrointestinal Tract in the Rat

Seitz

Simon

Czygan

et al. 1983

Alcoholism Clin & Exp Res

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Chronic ethanol consumption significantly increases gastric adenylate cyclase (AC) activity (p less than 0.05) without influencing low Km 3',5'-cyclic adenosine monophosphate (cAMP) phosphodiesterase (PD) activity in the rat. On the other hand, in the duodenum and upper part of the jejunum, chronic ethanol feeding leads to a significant decrease of adenylate cyclase activity (p less than 0.02) and, again, does not affect low Km cAMP phosphodiesterase activity. In addition, the effect of various hormonal secretagoques on small intestinal adenylate cyclase activity was investigated. Prostaglandin I2 and D2, as well as glucagon, do not stimulate AC at all. However, small intestinal adenylate cyclase exhibits a lower sensitivity to prostaglandin E2 and vasoactive intestinal peptide (VIP), and a lower efficacy to VIP after chronic ethanol consumption when compared to controls. The decrease of both basal and stimulated AC activity following ethanol ingestion in the upper small intestine may be due to membrane alterations and tissue damage caused by ethanol. The ethanol-induced increase in gastric AC may be of relevance with respect to an increased acid secretion observed after alcohol administration.

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The in vitro effect of ethanol on the histamine-sensitive adenylate cyclase system

Cited by 8 publications

References 7 publications

Ethanol's Actions on cAMP‐Mediated Signaling in Cells Transfected With Type VII Adenylyl Cyclase

Ethanol's Actions on cAMP‐Mediated Signaling in Cells Transfected With Type VII Adenylyl Cyclase

Effect of ethyl alcohol on the TSH‐receptor‐cyclase system in thyroid and nonthyroid tissues

Effect of Chronic Ethanol Ingestion on the Cyclic AMP System of the Upper Gastrointestinal Tract in the Rat

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