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PubMed1992

Effect of acetaldehyde on ethanol absorption in the canine jejunum.

The effects of acetaldehyde on ethanol absorption from the intestinal tract were studied using canine jejunal segment. A thirty-centimeter jejunal segment with intact vascular supply was isolated, and jejunal absorption studies were performed by administering a 17% ethanol solution (0.4 g/kg) into the lumen of the jejunal segment. In the control group, blood ethanol concentrations in the portal vein increased rapidly, with a peak level of 9.8 +/- 1.9 mM 30 min after administration. In the cyanamide-pretreated group, dogs were injected intravenously with cyanamide (100 mg/kg), an inhibitor of acetaldehyde dehydrogenase, 150 min before ethanol dosing. The blood ethanol concentration in the portal vein of this group, accompanied by a high acetaldehyde concentration, increased gradually, reaching a peak of 10.7 +/- 1.84 mM 120 min after ethanol administration. Each concentration gradient corresponded to the systemic circulatory order from the portal vein for ethanol concentration, and from the hepatic vein for acetaldehyde concentration. The absorbed amount of ethanol in the control and cyanamide-pretreated groups was 94.9 +/- 4.1% and 69.3 +/- 4.8%, respectively. Pharmacokinetic analysis indicated that a presence of high acetaldehyde concentration in the blood resulted in less ethanol reaching the systemic circulation (control: 7.34 +/- 2.95 h-1, cyanamide-pretreated: 1.08 +/- 0.75 h-1). The results also suggest that the absorption of ethanol from the intestine decreases when there is a high acetaldehyde concentration in the blood.

Acetaldehyde↗
PubMedDate not supplied

Acetaldehyde induces granulocyte macrophage colony-stimulating factor production in human bronchi through activation of nuclear factor-kappa B.

Acetaldehyde, a metabolite of alcohol and primary mediator of alcohol-induced asthma, causes bronchoconstriction via histamine release from airway mast cells. Acetaldehyde also is found in cigarette smoke and may cause airway inflammation. The purpose of this study was to determine the effect of acetaldehyde on cytokine production and nuclear factor kappa B (NF-kappa B) activation in human bronchial tissues. Human bronchi were prepared from normal parts of lung tissues resected for lung cancer (n = 11). The bronchi were cultured in the presence of 5 x 10(-4) M of acetaldehyde for 24 hours and the concentrations of eotaxin, granulocyte macrophage colony-stimulating factor (GM-CSF), interleukin-5, interleukin-8, and regulated on activation, normal T cells expressed and secreted in cultured supernatants were determined by enzyme-linked immunosorbent assay. Tissues also were immunohistochemically stained for NF-kappa Bp65. Acetaldehyde significantly increased GM-CSF production from human bronchi and nuclear translocation of NF-kappa Bp65 in airway epithelium but had no effects on other cytokines. Our findings suggest that acetaldehyde potentially causes airway inflammation via increased GM-CSF production through nuclear translocation of NF-kappa B.

Acetaldehyde↗
PubMed2003

[Effects of Erk signal transduction on the cell cycle of rat hepatic stellate cells stimulated by acetaldehyde].

OBJECTIVE: To investigate the effect of PD98059 on the proliferation and cell cycle of rat hepatic stellate cells (HSCs) stimulated by acetaldehyde and explore its mechanism. METHODS: Rat HSCs stimulated by acetaldehyde were incubated with different concentrations of PD98059. Cell proliferation was assessed by MTT colorimetric assay. Cell cycle was analysed by flow cytometry. The mRNA of cyclin D1 and CDK4 were examined by RT-PCR. RESULTS: 20, 50, 100 micromol/L PD98059 could significantly inhibit the proliferation of HSCs stimulated by acetaldehyde in a does-dependent manner (0.109+/-0.020, 0.081+/-0.010 and 0.056+/-0.020 vs 0.146+/-0.030, F=31.385, P<0.05) and provoke G0/G1 phase arrest of HSCs stimulated by acetaldehyde in a does-dependent manner (61.9%+/-6.3%, 64.1%+/-3.3% and 70.9%+/-4.8% vs 55.2%+/-4.4%, F=16.402, P<0.05). 50, 100 micromol/L PD98059 could markedly inhibit cyclin D1 mRNA expression of HSC stimulated by acetaldehyde (0.56+/-0.04 and 0.46+/-0.03 vs 0.65+/-0.07, F=68.758, P<0.05) and CDK4 mRNA expression (0.39+/-0.07 and 0.33+/-0.05 vs 0.50+/-0.06, F=29.406, P<0.05). CONCLUSION: The Erk signal transduction pathway plays an important role in regulating the proliferation and cell cycle of rat hepatic stellate cells stimulated by acetaldehyde, which may be partly related to its regulative effect on the expression of cyclin D1 gene and CDK4 gene

Acetaldehyde↗
PubMedDate not supplied

[Effect of acetaldehyde on ethanol- and aldehyde-metabolising systems of the liver and brain of rats].

Lately the mechanism of craving for alcohol has been related to the local level of brain acetaldehyde occurring in ethanol consumption and depending on the activities of the brain and liver ethanol and acetaldehyde-metabolizing systems. In this connection, we studied the effect of chronic acetaldehyde intoxication on the activities of alcohol dehydrogenase (ADH), aldehyde dehydrogenase (ALDH), the microsomal ethanol oxidizing system (MEOS) and liver and brain catalase as well as ethanol and acetaldehyde levels in the blood. The results showed that the chronic acetaldehyde intoxication did not alter significantly the activities of liver ADH, MEOS and catalase as well as liver and brain ALDH. In parallel with this, the systemic acetaldehyde administration led to shortened time of ethanol narcosis and activation of catalase in the cerebellum and left hemisphere, which may indicate involvement of this enzyme into metabolic tolerance development.

Acetaldehyde↗
PubMed1992

Acetaldehyde-modified hemoglobin as a marker of alcohol consumption: comparison of two new methods.

We examined the diagnostic value of acetaldehyde-hemoglobin adducts in the detection of heavy drinking and alcoholism. Acetaldehyde adducts from red cells were measured by new chromatographic and immunologic methods. The study population included 20 men with well-documented histories of chronic alcoholism, 18 men who were heavy drinkers, 22 male healthy control subjects, and 8 control subjects with liver disease that was not related to alcohol use. In addition, 20 healthy volunteers and 5 control subjects participated in the study to determine the effect of an acute dose of ethanol. The results that were obtained by the two new methods correlated significantly (r = 0.38, p = 0.002). With both methods, the concentrations of acetaldehyde-hemoglobin adducts were found to be significantly higher in red cells of heavy drinkers (p less than 0.001) and subjects with alcoholism (p less than 0.001) when compared with control subjects. Acetaldehyde-modified hemoglobins appear to have at least the same sensitivity (chromatographic determination = 50% and immunologic determination = 50%) to detect heavy drinking as the most widely accepted conventional biochemical markers of alcohol abuse, gamma-glutamyltransferase (39%) or mean corpuscular volume (17%). In a group of 20 healthy volunteers, acetaldehyde-hemoglobin adducts increased significantly even after a single high dose of ethanol (2 gm/kg), whereas there was no change in the conventional markers of alcohol consumption at the same time. Acetaldehyde-hemoglobin adducts assays should be useful for the detection of heavy drinking in clinical settings.

Acetaldehyde↗
PubMed1991

Contribution of exogenous ethanol and endogenous substrates to acetaldehyde-adduct formation in liver injury.

Acetaldehyde was found to be transported in the blood mainly bound reversibly to 2 components of the red blood cells (RBC): a) hemoglobin, which provides binding of a high affinity, but low capacity, and b) a non-protein component (presumably cysteine), which has a lower affinity but a higher capacity. In alcoholics, the main increase in RBC-acetaldehyde binding occurred in the protein-free fraction, in association with a marked increase in RBC-cysteine. Elevated RBC-acetaldehyde persisted for at least 2 weeks after alcohol withdrawal in 83% of the blood samples from alcoholics. Even in the absence of alcohol consumption, liver injury increased acetaldehyde from sources other than ethanol. This was associated with high serum antibody titers against acetaldehyde adducts. In an animal model of non-alcoholic liver cirrhosis, a target protein for the formation of acetaldehyde adducts appears to be procollagen type I.

Acetaldehyde↗
PubMed1991

Cytotoxic T lymphocytes can be generated against acetaldehyde-modified syngeneic cells.

Acetaldehyde is a metabolic product of ethanol catabolism capable of forming protein adducts. These adducts have been found in situ and could account for the generation of anti-acetaldehyde antibodies found in various stages of alcoholic liver disease. Antibody production implicates participation of the cellular immune system. The existence of a cellular immune response poses the question of whether the body generates a cellular effector response against cells displaying these modified proteins. We have been able to show that murine splenic cells whose surface is acetaldehyde modified can generate cytotoxic T lymphocytes (CTL) in a syngeneic host when the stimulator cells carry the H-Y antigen and the responder population does not. This fact in conjunction with the finding that anti-class I antibody can block the anti-acetaldehyde CTL effector response supports the contention that the acetaldehyde-protein adducts are presented to the CTL in context with an intact class I MHC. This work supports the hypothesis that acetaldehyde-modified cells can generate a cellular immune response and may do so in pathologic states.

Acetaldehyde↗
PubMedDate not supplied

[Catecholamines in the tissues and blood of rats after administration of acetaldehyde and ethanol].

Acetaldehyde alone and in combination with acute and chronic ethanol intoxication has been studied for its effect on the concentration of epinephrine and norepinephrine in different brain areas, in the heart muscle, in adrenals and blood plasma of rats. Acetaldehyde is shown to enhance the epinephrine and norepinephrine levels in the brain areas which are non-specific for neuromediation of the mentioned catecholamines. The joint administration of acetaldehyde and ethanol increased the epinephrine concentration in adrenals probably due to the effect of acetaldehyde. On the contrary, the norepinephrine concentration in the heart decreased because of the action of ethanol. The authors' data show that acetaldehyde becomes an inductor of the mechanisms of hormone-mediator dissociation, thus altering the functions of vegetative-adrenal system. The results of the investigation support the hypothesis that acetaldehyde plays a significant role among pathogenic factors of ethanol intoxication, since it changes in a special way the catecholamine concentration in the brain and in peripheral tissues.

Acetaldehyde↗
PubMed1990

Effects of amino acids on acute alcohol intoxication in mice--concentrations of ethanol, acetaldehyde, acetate and acetone in blood and tissues.

Condensation reactions between some SH-amino acids (L-and D-cysteine 1%) and acetaldehyde (50 microM) were studied in vitro experiment. In the aqueous solution, free acetaldehyde was reduced to 41.3% by L-cysteine and to 36.4% by D-cysteine. In the reaction with human blood medium, after the medium was deproteinized with perchloric acid reagent, acetaldehyde was reduced to 47.0% by L-cysteine and to 43.8% by D-cysteine. D-Cysteine appears to have great stability of reacting acetaldehyde. In vitro experiment reactability for D-cysteine exhibited 3-8% higher than that for L-cysteine. Next, effects of some amino acids on alcohol metabolism were studied in male ICR mice. The animals were given ethanol through a gastric catheter at a dose of 2 g/kg and they were intraperitoneally injected L-cysteine (300 mg/kg), D-cysteine (300 mg/kg), L-alanine (300 mg/kg) and control (saline), respectively in the period of one hour before the injection of ethanol. Blood and tissues samples were analyzed for ethanol, acetaldehyde, acetate and acetone during alcohol intoxication in mice by head space gas chromatography. In the groups administered D-cysteine and L-cysteine, the mice showed a definitely faster oxidation and disappearance of ethanol. Especially in the D-cysteine group, ethanol levels in blood, liver and brain remained lower than that in the other groups (p less than 0.01). Acetaldehyde levels in blood, liver and brain remained low by L-cysteine. Ethanol metabolites during alcohol oxidation by chemical reactabilities of L- and D-cysteine showed different distribution in the mice, respectively. In the mice received L-alanine, acetate and acetone levels in blood, liver and brain were distinctly reduced (p less than 0.01). L-Alanine is reported to supply an abundance of pyruvic acid that performs the NAD-generating system. NAD produced is introduced to alcohol metabolism and the TCA cycle. It was thus presumed that the L- or/and D-cysteine, and L-alanine was effective in acute alcohol intoxication by heavy drinking.

Acetaldehyde↗
PubMed1987

Acetaldehyde and cardiac arrhythmias.

Administration of acetaldehyde (i.v.) into cats anesthetized with halothane elicits severe cardiac ventricular arrhythmias which begin in about 10-13 sec with bolus doses of 5-10 mg/kg, and last about 2 min. Systemic blood pressure and heart rate rise concurrently with the arrhythmias. The cardiac effects are attributed to the release of endogenous catecholamines from cardiac tissue because they are prevented by beta-adrenergic blockade and are not dependent on adrenomedullary and splenic stores of catecholamines, since acute surgical removal of these tissues does not prevent the arrhythmias and other cardiovascular changes. This indirect arrhythmogenic action of acetaldehyde has not been previously reported, probably because other investigators have used anesthetics like pentobarbital which exert an antiarrhythmic effect that masks acetaldehyde's arrhythmogenic potential. The use of halothane to sensitize the heart to catecholamines greatly enhanced the arrhythmogenic effect of acetaldehyde. The question is raised whether the concomitant industrial or medical exposure of human subjects to large amounts of exogenous or endogenous acetaldehyde and certain hydrocarbons could provide the substrate for the expression of this arrhythmogenic effect of acetaldehyde.

Acetaldehyde↗
PubMed1986

Humoral immune response to acetaldehyde adducts in alcoholic patients.

Sera of alcoholic patients were found to contain antibodies to acetaldehyde adducts as determined by immunodiffusion. Differences in antibody levels were determined by hemagglutination with acetaldehyde adduct-conjugated red blood cells. Anti-acetaldehyde adduct immunoglobulin titers in 21 healthy, non-drinking individuals ranged from 10-80, whereas 25 of 34 alcoholics had titers of 160 or above (P less than 0.001). Rabbit-polyclonal and mouse-monoclonal antibodies against acetaldehyde adducts did not agglutinate red blood cells of alcoholic patients, indicating that no detectable acetaldehyde-altered epitopes are present on erythrocyte membranes. These results suggest that acetaldehyde-induced immunogenic determinants can initiate a humoral immune response which may differentiate alcoholics from non-alcoholics.

Acetaldehyde↗
PubMed1988

Similar antagonistic effects of Ca N-acetylhomotaurinate on depression of motor activity and lethality induced by acetaldehyde or ethanol.

Among several taurine derivatives, Ca N-acetylhomotaurinate (Ca AOTA) appears to be the most active anti-acetaldehyde and anti-alcohol agent. Studies of the antagonism of the hypomotility induced by high intravenous doses of acetaldehyde or ethanol in mice and of the lethality of high intragastric doses of acetaldehyde in rats show its superiority which appears logical after systematic studies of these derivatives and their components. The reinforcing action of the nervous activity due to N-acetylation of these sulfonic aminoacids differs according to the target. Since Ca AOTA is the most active against acetaldehyde and ethanol toxicity, this central nervous action first relies on its effects on neuromodulators, neuromediators and cations primarily involved in the mechanisms of alcohol dependence through its taurine (TA) structure, its gamma-aminobutyric acid (GABA) agonist actions, its anti-opioid receptor "naloxone-like" effects and its possible activity as a subcellular Ca carrier. Ca AOTA may also intervene through its high membrane stabilizing effect. Compared with the other compounds, it appears to be the most active both in vitro on the erythrocyte membrane of the rabbit and on the human amnion membrane and ex vivo on the alcoholic rat's erythrocyte membrane. Among several taurine derivatives similarly efficient in toxicity of both acetaldehyde and ethanol, Ca AOTA is the best. Its efficiency against the most toxic metabolite of ethanol may specifically rely on Ca and TA dependence of acetaldehyde-dehydrogenase or on an aspecific mechanism such as the role of free radical scavenger due to its taurine structure. Ca AOTA appears to be a promising drug against alcoholism because of its effects on the multiple targets involved in the mechanism of alcohol dependence. A large multicentric coordinated trial has effectively confirmed the reliability of these pharmacological speculations.

Acamprosate↗
PubMed1987

Effects of acetaldehyde on the monosynaptic reflex pathway in the cat spinal cord.

The effects of acetaldehyde on monosynaptic reflexes were investigated in the cat spinal cord. Intravenous injection of lower doses of acetaldehyde (0.1-0.5 mg/kg) increased the amplitude of the ventral root monosynaptic reflex potentials elicited by the dorsal root stimulation; the amplitude was decreased at higher doses (1.0-10.0 mg/kg). Acetaldehyde hyperpolarized the motoneuron at lower and depolarized it at higher doses. In some cells, however, acetaldehyde induced an initial, brief depolarization and subsequent hyperpolarization. Depolarization increased with increasing the dose of acetaldehyde. Hyperpolarization was always associated with an increased amplitude of the monosynaptically-induced action potentials. Depolarization was accompanied by a decreased amplitude or block of the action potentials. During aldehyde-induced depolarization, antidromic action potentials were more severely depressed than orthodromic ones. The present results suggest that acetaldehyde acts predominantly on the motoneuron membrane resulting in hyperpolarization at relatively lower doses and in depolarization at higher doses.

Acetaldehyde↗
PubMed1985

Synergistic interaction between hydroquinone and acetaldehyde in the induction of sister chromatid exchange in human lymphocytes in vitro.

Hydroquinone, a metabolite of benzene, and acetaldehyde, a metabolite of ethanol, induce sister chromatid exchanges (SCEs) at relatively high concentrations. Because both compounds are reported to form glutathione conjugates, experiments were carried out to see if there was a synergistic effect when lower concentrations of both chemicals were added to human lymphocyte cultures. Hydroquinone (40 microM) increased SCEs in some individuals but not in others. However, the rate of SCE was more than doubled when cells were pretreated with diethyl maleate, which transiently depletes cellular glutathione. Acetaldehyde by itself increased SCEs at 100 microM, but it increased SCEs at 1 microM in the presence of diethyl maleate. When various concentrations of acetaldehyde were added to cultures containing 40 microM hydroquinone, synergism in the induction of SCEs was observed. The lowest effective concentration of acetaldehyde varied among individuals from 1 to 100 microM. These observations suggest that glutathione is involved in the detoxification of hydroquinone and acetaldehyde in lymphocytes and that the simultaneous presence of both chemicals may saturate this mechanism and thus increase their genotoxic potency. Genetic differences in glutathione metabolism may govern the concentration of acetaldehyde at which synergism occurs in different individuals.

Acetaldehyde↗
PubMed1979

Acute effects of acetaldehyde and ethanol on rat heart mitochondria.

The effects of acute exposure of rat heart mitochondria to ethanol (87, 65, and 45 mM) and acetaldehyde (3, 1, and 0.3 mM) were studied using both glutamate and pyruvate/malate substrates. Mitochondria assayed with pyruvate/malate substrate showed no apparent effects of acute exposure to or 30 min preincubation with ethanol at the three concentrations tested. With glutamate substrate, acute ethanol at 87 and 65 mM produced significant decreases in respiratory control ratio (RCR). With 65 and 45 mM acute ethanol, mitochondrial oxygen consumption (QO2) was significantly decreased. Acute acetaldehyde significantly decreased RCR and QO2 of mitochondria tested with both substrates. The depressive effect was more pronounced with pyruvate/malate substrate than with glutamate substrate. With pyruvate/malate substrate, the ADP/O ratio was also decreased with 3 and 1 mM acetaldehyde. Preincubation with acetaldehyde had no effect on mitochondrial function except for significantly decreased RCR after preincubation with 3 mM acetaldehyde followed by assay with glutamate substrate. The data indicate a depressant effect of acetaldehyde and ethanol on cardiac mitochondria that may contribute to abnormal cardiac biochemistry and function characteristic of alcoholic cardiomyopathy.

Acetaldehyde↗
PubMed1978

Alcohol, amino acids, and albumin synthesis. III. Effects of ethanol, acetaldehyde, and 4-methylpyrazole.

The effects of ethanol, 4-methylpyrazole (4-MP), and acetaldehyde on albumin and urea synthesis, and on polysome aggregation were studied in isolated perfused rabbit livers. Fed or fasted males served as donors and the perfusate contained ethanol, 200 mg per 100 ml, with and without 1.5 mM 4-MP; or acetaldehyde, 2 mg per 100 ml, with and without 1.5 mM 4-MP. The results indicate that in livers from fed donors ethanol depressed albumin and urea synthesis and bound polysomes were disaggregated. Perfusion with acetaldehyde caused a similar decrease in albumin and urea synthesis, but did not cause polysome disaggregation. The addition of 4-MP to the ethanol perfusates did not enhance albumin or urea synthesis but did prevent polysome disaggregation. When the donor was fasted, the addition of 4-MP to the ethanol perfusates restored urea synthesis and polysome aggregation to fasted control levels. In the livers from fasted donors, acetaldehyde did not lower albumin or urea synthesis and had no effect on polysome aggregation. The results indicate that the hepatic responses to ethanol and acetaldehyde are different if the livers are derived from fed or fasted donors, and it is not possible to ascribe the toxic effects of acetaldehyde or ethanol on albumin and urea synthesis to either agent, per se.

Acetaldehyde↗
PubMed1983

Binding of metabolically derived acetaldehyde to hepatic proteins in vitro.

Homogenates of rat liver incubated with 10 mM [14C]ethanol were analyzed for acetaldehyde production and for both stable and unstable radiolabeled acetaldehyde adducts with proteins. During incubation, formation of acetaldehyde and of 14C-labeled proteins both increased with time in a parallel manner. Acetaldehyde generation and subsequent formation of radiolabeled proteins were potentiated by supplementation of the cell-free system with NAD+ (1 mM). Cycloheximide (0.1 mM) caused no significant reduction in protein-bound radioactivity, whereas the addition of strong nucleophiles L-cysteine (5 mM) and reduced glutathione (5 mM) each decreased radiolabeling by 50 to 60%. Preheating of crude homogenates at 90 degrees C, prior to incubation with [14C]ethanol profoundly decreased subsequent production of acetaldehyde and formation of 14C-labeled proteins. The results indicate that the major source of protein-bound radioactivity derived from [14C]ethanol oxidation in this system is due to binding of enzymatically derived [14C]acetaldehyde to hepatic proteins.

Acetaldehyde↗
PubMed1982

The inhibitory action of acetaldehyde on the tonic component of the potassium-induced contracture in the guinea-pig taenia caeci.

The effect of acetaldehyde on the contractile responses induced by potassium-rich solution was studied in the guinea-pig taenia caeci. Acetaldehyde at a concentration between 1 and 50 mM reduced the tonic contraction induced by a high potassium solution containing a normal concentration of CaCl2 without affecting the phasic one. The phasic contraction was depressed only slightly at a very high concentration of acetaldehyde (100 mM). The tonic component increased with increasing external Ca concentration, and the reduction of this tonic contraction by acetaldehyde was greater at high Ca concentrations. In Ca-free, K-rich solution, carbachol induced a transient contraction. This carbachol-induced contraction in the absence of external Ca was markedly depressed at the second application of carbachol, but it reappeared after exposure to a Ca-containing solution. In this condition acetaldehyde did not affect these carbachol-responses, while it decreased a slow rise of tension during exposure of Ca. These results suggest that acetaldehyde inhibits the entry of external calcium without having an appreciable effect on the release of Ca and on the filling of the internal stores with Ca.

Acetaldehyde↗