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PubMed2000

Acetaldehyde-stimulated PKC activity in airway epithelial cells treated with smoke extract from normal and smokeless cigarettes.

Previously, we have found that acetaldehyde, a volatile component of cigarette smoke, stimulates the protein kinase C (PKC) pathway and inhibits ciliary motility. A "smokeless" cigarette (Eclipse) now exists in which most of the tobacco is not burned, reducing the pyrolyzed components in the extract. We hypothesized that acetaldehyde is a component of cigarette smoke that activates PKC in the airway epithelial cell, and therefore the Eclipse cigarette would not activate epithelial cell PKC. In this study, bovine bronchial epithelial cells (BBEC) were incubated with cigarette smoke extract (CSE) or Eclipse smoke extract (ESE). We found that PKC activity was significantly higher in cells exposed to 5% CSE than cells exposed to 5% ESE or media. When acetaldehyde levels of both extracts were measured by gas chromatography, CSE was found to have 15-20 times greater concentration (microM) of acetaldehyde than ESE. When BBEC were treated with 5% CSE, ciliary beating was further decreased from baseline levels. This decrease in ciliary beating was not observed in cells treated with ESE, suggesting that acetaldehyde contained in CSE slows cilia. These results suggest that volatile components such as acetaldehyde in cigarette smoke may inhibit ciliary motility via a PKC-dependent mechanism.

Animals↗
PubMedDate not supplied

Binding of acetaldehyde to human and Guinea pig placentae in vitro.

BACKGROUND: Significant interindividual variability exists following maternal alcohol consumption; not all children born to alcoholic women manifest the symptoms associated with foetal alcohol spectrum disorder (FASD). OBJECTIVE: To investigate the potential role of the placenta as a source of variability by determining if interindividual variability exists in the binding of acetaldehyde to human placenta. METHODS: Acetaldehyde was added to ten different human placental homogenates and subjected to equilibrium dialysis. Homogenates of placentae obtained from guinea pigs chronically exposed to ethanol throughout gestation were also dialysed in the presence of acetaldehyde to look for alterations in binding after chronic alcohol exposure. Nonlinear least-squares regression analysis was used to characterize the binding system involved. RESULTS: It was found that the amount of acetaldehyde bound to human placentae varied by as much as 3-fold among placentae. The binding profile of acetaldehyde was characterized as a two site binding system (Ka(1)=9.8 x 10(5)+/-0.7 x 10(5)l/mol, N(1)=1.1 x 10(-8)+/-0.7 x 10(-8)mol/g tissue; Ka(2)=1.6 x 10(4)+/-0.9 x 10(4)l/mol, N(2)=1.7 x 10(-7)+/-0.4 x 10(-7)mol/g tissue). Chronic alcohol exposure had no effect on the degree of acetaldehyde binding. CONCLUSION: This previously unidentified source of variability may partially explain why some foetuses are adversely affected by prenatal alcohol exposure while others are not.

Acetaldehyde↗
PubMed2000

Enhanced DNA binding and activation of transcription factors NF-kappa B and AP-1 by acetaldehyde in HEPG2 cells.

Because transcription factors NF-kappaB and activator protein-1 (AP-1) are known to regulate gene expression, we have analyzed the role of acetaldehyde in the activation of NF-kappaB and AP-1 in HepG2 cells. Binding activity and transactivation of NF-kappaB and AP-1 were determined by gel retardation assays and transfection of a luciferase reporter construct controlled by kappaB and AP-1 binding sites, respectively. Acetaldehyde enhanced the DNA binding of NF-kappaB and AP-1 by 1 and 4 h, respectively, increasing the kappaB- and AP-1-dependent luciferase expression. Supershift assays revealed the presence of NF-kappaB heterodimers p65/p50 and p50/p52, whereas nuclear c-Jun levels correlated with the DNA binding of AP-1. The enhanced binding of NF-kappaB to DNA by acetaldehyde in intact cells was accompanied by the proteolytic degradation of IkappaB-alpha. However, the addition of acetaldehyde to cytostolic extracts from untreated Hep G2 cells did not affect the DNA binding of AP-1 but activated the NF-kappaB heterodimer p65/p50 in the absence of IkappaB-alpha degradation. Preincubation of HepG2 cells with protein kinase C inhibitors abolished the enhanced DNA binding of NF-kappaB and AP-1 caused by acetaldehyde. Hence, these findings uncover a previously unrecognized role for acetaldehyde in the activation of NF-kappaB and AP-1, which may be of relevance in the alcohol-induced liver disease.

Acetaldehyde↗
PubMed2001

Sensory-nerve-mediated nasal vasodilatory response to inspired acetaldehyde and acetic acid vapors.

This study was designed to characterize the acute nasal vasodilatory responses to the sensory irritants acetaldehyde and acetic acid. For this purpose, the upper respiratory tract of the urethane-anesthetized male F344 rat was isolated by insertion of an endotracheal cannula, and irritant-laden air was drawn continuously through that site at a flow rate of 100 ml/min for 50 min. Vascular function was monitored by measuring inert vapor (acetone) uptake throughout the exposure. Both acetaldehyde and acetic acid induced an immediate concentration-dependent vasodilation as indicated by increased steady-state acetone uptake rates. This response was observed at exposure concentrations of 25 ppm or 130 ppm or higher for acetaldehyde or acetic acid, respectively. The response to either vapor was significantly diminished in rats pretreated with the sensory nerve toxin capsaicin (50 mg/kg, 7 days prior to exposure), providing evidence that sensory nerves play a role in the response. Acetaldehyde is metabolized by aldehyde dehydrogenase to acetic acid. Pretreatment with the aldehyde dehydrogenase inhibitor cyanamide (10 mg/kg, 1 h prior to exposure) reduced the vasodilatory response to 200 ppm but not to 50 ppm acetaldehyde. These results suggest that formation of acetic acid is important in the sensory nerve-mediated vasodilatory response to high, but perhaps not to low, concentrations of acetaldehyde.

Acetaldehyde↗
PubMed2005

Neurotoxic effects of alcohol and acetaldehyde during embryonic development.

Alcohol drinking during pregnancy results in abnormal fetal development, including fetal alcohol syndrome (FAS) in humans and experimental animals. FAS is characterized by two major effects, including central nervous system (CNS) dysfunction and multiple anomalies recognizable mainly as a typical face. However, the mechanisms of alcohol-induced embryotoxicity have not been clearly demonstrated. The aim of the present study was to investigate the possible mechanisms underlying ethanol-induced FAS in the developing embryo. First, ethanol-induced developmental abnormalities were investigated in vitro. Postimplantation embryos at gestation day (GD) 9.5 were cultured for 48 h and observed for morphological changes. Ethanol-mediated changes in proteins regulated apoptosis (p53 and bcl-2), antioxidant (vitamin E and catalase) activities, generation of reactive oxygen species (ROS), and oxidative DNA damage shown as 8-hydroxy-2'-deoxyguanosine (8-OHdG) were measured in embryonic midbrain cells. Alcohol or acetaldehyde significantly induced cytotoxicity in cultured rat embryonic midbrain cells. The levels of p53, bcl-2, and 8-OHdG were concomitantly changed by alcohol and acetaldehyde treatment in midbrain cells. Injured cells induced by ROS were increased by alcohol or acetaldehyde treatment in midbrain cells. Cotreatment with alcohol or acetaldehyde and catalase decreased cytotoxicity in midbrain cells. In postimplantation embryo culture, alcohol or acetaldehyde-treated embryos showed retardation of embryonic growth and development in a concentration-dependent manner. These results indicate that alcohol and its metabolite acetaldehyde induce fetal developmental abnormalities by disrupting cellular differentiation and growth. Data demonstrate that some antioxidants can partially protect against the alcohol-induced embryonic developmental toxicity.

8-Hydroxy-2'-Deoxyguanosine↗
PubMedDate not supplied

Toxicity of beta-carotene and its exacerbation by acetaldehyde in HepG2 cells.

In rats and baboons, the hepatotoxicity of chronic ethanol consumption is exacerbated by beta-carotene feeding, but the mechanism of this adverse effect is unknown. In this study, the toxicity of beta-carotene and acetaldehyde was documented by the MTT test (an assay of reduction of tetrazolium to formazan) and by lactate dehydrogenase (LDH) leakage. In HepG2 cells, beta-carotene or acetaldehyde inhibited mitochondrial reduction function as indicated by a decrease of the MTT test. beta-Carotene was inhibitory at very low concentration, in a dose-dependent manner. The combination of these two compounds resulted in an additive effect. Acetaldehyde increased LDH leakage from the HepG2 cells into the medium, whereas beta-carotene by itself did not show such an effect, but it exacerbated the toxicity of acetaldehyde when combined. In addition, this study showed that acetaldehyde and beta-carotene inhibited each other's clearance from the medium, which suggests that these two chemicals may share, at least in part, a common metabolic pathway (possibly via aldehyde dehydrogenase) in the cells, and that a competitive inhibition may exist. In conclusion, this preliminary study indicates that beta-carotene is toxic to hepatocytes, especially when combined with acetaldehyde, the metabolite of ethanol.

Acetaldehyde↗
PubMed2000

Chemical peritonitis associated with high dialysate acetaldehyde concentrations.

BACKGROUND: During the standard heat sterilization process of lactate-buffered peritoneal dialysis (PD) solutions, glucose degrades to form compounds called glucose degradation products such as acetaldehyde, formaldehyde, or glyoxal. Despite evidence that these products may be responsible for some in vitro cytotoxic effects induced by commercially available PD fluids, data on their acute or chronic effects on the human peritoneum is scarce. SUBJECTS AND METHODS: This case presentation is based on an observation of 21 aseptic peritonitis cases of unknown aetiology. All cases appeared within one month in a university hospital PD unit that had a peritonitis rate of 1 episode/26 patient months and 55 active patients on CAPD. Acetaldehyde level in the bags was assayed by gas chromatography. RESULTS: Twenty-one patients presented with signs of peritonitis including cloudy dialysate and abdominal tenderness with additional abdominal pain in 11 patients and vomiting in one. In all cases, cultures and Gram stains were negative for micro-organisms. Fever was not observed in any patient. Average dialysate white blood cell count was 1795/mm(3). All patients were free of intraperitoneal medication when symptoms appeared. Patients were using PD solutions from a newly established domestic production plant. Apparently all patients with symptoms of peritonitis used bags with the same lot number and the solution in the bags appeared to be darker in colour than that in bags with other lot numbers. Chemical analysis of the unused PD solution samples revealed acetaldehyde levels of 17-20 p.p. m. in bags containing darker solution, which is very high compared with the usual acetaldehyde level of 6 p.p.m. in heat-sterilized PD solutions. CONCLUSIONS: Based on the above findings, we hypothesize that higher levels of acetaldehyde and possibly other glucose degradation products may have been an aetiological factor in these 21 cases of chemical peritonitis. Our observation suggests that acetaldehyde, in concentrations 3-4 times higher than the usual level in commercially available PD solutions, may induce acute sterile peritonitis in CAPD patients.

Acetaldehyde↗
PubMed1988

Changes in blood acetaldehyde concentrations during acetate haemodialysis.

Hyperacetataemia during acetate haemodialysis has been associated with the development of a variety of unpleasant symptoms, although a direct toxic effect of acetate is hard to prove. Acetaldehyde, which is produced during the metabolism of ethanol to acetate, has various toxic effects including some of those reported during acetate dialysis such as nausea, headache and palpitations. Using a novel, recently developed method we studied blood acetaldehyde concentrations during acetate dialysis in 15 patients and found significant increases in five, with a mean peak value in these patients of 1.36 mumol/l (normal less than 0.4 mumol/l). These five patients also developed high blood acetate concentrations during a subsequent acetate dialysis and showed a significant correlation between blood acetaldehyde and acetate concentrations (r = 0.55, P less than 0.05). Blood acetaldehyde did not change during bicarbonate dialysis in these patients. Our results suggest that significant accumulation of acetaldehyde may occur during acetate dialysis, especially in those patients whose metabolic capacity for acetate is somehow impaired, and that acetaldehyde may contribute to some of the symptoms previously ascribed to 'acetate' intolerance.

Acetaldehyde↗
PubMed2004

Local induction of the alc gene switch in transgenic tobacco plants by acetaldehyde.

The alc promoter system, derived from the filamentous fungi Aspergillus nidulans, allows chemically regulated gene expression in plants and thereby the study of gene function as well as metabolic and developmental processes. In addition to ethanol, this system can be activated by acetaldehyde, described as the physiological inducer in A. nidulans. Here, we show that in contrast to ethanol, acetaldehyde allows tissue-specific activation of the alc promoter in transgenic tobacco plants. Soil drenching with aqueous acetaldehyde solutions at a concentration of 0.05% (v/v) resulted in the rapid and temporary induction of the alc gene expression system exclusively in roots. In addition, the split root system allows activation to be restricted to the treated part of the root. The temporary activation of the alc system by soil drenching with acetaldehyde could be prolonged over several weeks by subsequent applications at intervals of 7 d. This effect was demonstrated for the root-specific induction of a yeast-derived apoplast-located invertase under the control of the alcohol-inducible promoter system. In leaves, which exhibit a lower responsiveness to acetaldehyde than roots, the alc system was induced in the directly treated tissue only. Thus, acetaldehyde can be used as a local inducer of the alc gene expression system in tobacco plants.

Acetaldehyde↗
PubMed2003

Lactulose reduces intracolonic acetaldehyde concentration and ethanol elimination rate in rats.

BACKGROUND: Normal colonic bacteria possessing alcohol dehydrogenase activity can oxidize ethanol to acetaldehyde. Acetaldehyde recently has been shown to be a local carcinogen in humans. The aim of the study was to examine the effect of lactulose feeding on fecal and cecal pH, intracolonic acetaldehyde concentration, and total ethanol elimination rate in rats. METHODS: Sixty Wistar rats were divided into four groups. Groups 2 and 4 received lactulose daily (11 g/kg body weight for 14 days). On days 7 and 14, groups 1 and 2 received ethanol (1.5 g/kg body weight) intraperitoneally, whereas groups 3 and 4 received saline. RESULTS: Fecal and cecal pH values decreased significantly after lactulose treatment compared with the controls. Lactulose feeding reduced the total ethanol elimination rate by 13.8% (257 +/- 0.008 mg/kg/hr vs. 298 +/- 0.003 mg/kg/hr, p < 0.001) and the intracecal acetaldehyde concentration by 66.2% after ethanol (49 +/- 29 microM vs. 145 +/- 47 microM, p = 0.03) compared with the controls. CONCLUSION: Lactulose feeding to rats significantly reduces ethanol elimination rate and intraluminal acetaldehyde concentration in the colon after ethanol administration. This prebiotic thus could be used as an effective agent to block the microbial production of carcinogenic acetaldehyde in the large intestine.

Acetaldehyde↗
PubMed1989

Acetaldehyde-modified serum proteins inhibit mitogen-stimulated human lymphocyte transformation.

Sera obtained from healthy volunteers immediately before and 8 h after the rapid consumption of 1.2 g ethanol/kg body weight were dialysed against RPMI 1640 and added ab initio to microcultures of normal human lymphocytes containing 1-3 micrograms phytohaemagglutinin (PHA)/ml or 2-8 micrograms pokeweed mitogen (PWM)/ml. When compared with the pre-alcohol sera, the post-alcohol sera inhibited lymphocyte transformation after 48 h incubation with either mitogen. In other experiments, acetaldehyde-albumin complexes were generated by reacting solutions of human serum albumin with 45-720 microM acetaldehyde, and the same quantity of either unmodified albumin or acetaldehyde-modified albumin was included in freshly-prepared lymphocyte microcultures containing 3 micrograms PHA/ml or 8 micrograms PWM/ml. When compared with unmodified albumin, acetaldehyde-modified albumin inhibited lymphocyte transformation after 48 h of culture with either mitogen. The inhibition of lymphocyte transformation caused by post-alcohol sera and acetaldehyde-modified albumin was partially corrected after treatment of the proteins with 1.55 mM sodium borohydride at a pH of 9.5. The data indicate that post-alcohol sera contain a non-dialysable activity which inhibits mitogen-stimulated lymphocyte transformation in vitro and that at least part of this activity may reside in acetaldehyde-modified serum albumin.

Acetaldehyde↗
PubMedDate not supplied

The toxicity to rat cerebral cortex or topical applications of acetaldehyde, ammonia or bilirubin.

The relative toxicity of acetaldehyde, ammonia and bilirubin to cerebral cortex of rats has been tested by superfusion of the intact dura for 1 h with each toxin separately. The cortex was examined histologically after 6 days survival using a silver strain which selectively impregnates degenerating axons and their synaptic terminals. A tissue concentration of 30 mM acetaldehyde was found to cause axonal and terminal degeneration, whereas 11 mM acetaldehyde was not toxic, and did not produce any structural changes detectable by electron microscopy. In terms of tissue concentrations, acetaldehyde was at least 27 times more toxic than ethanol on a molar basis. However, the acetaldehyde concentration necessary to produce neuronal degeneration in a 1 h exposure is many times greater than ever reported in CSF in human alcoholism. Both ammonia and bilirubin are capable of causing neuronal degeneration, but we have not measured the tissue concentrations that are toxic. Comparison of molar concentrations in the superfusing fluids showed that ammonia is at least 39 times more toxic than acetaldehyde, and at least 1000 times more toxic than ethanol. Superfusion with an ethanolic solution of bilirubin (2.5mM) was strongly toxic, but this solution diluted to 50% with saline was not toxic. The possibility exists that ammonia or bilirubin may reach concentrations toxic to neurons in alcoholism, especially in the presence of liver damage.

Acetaldehyde↗
PubMed1993

Neurotoxicity and induction of fibroblast proliferation by acetaldehyde in the rabbit liver.

1. Acetaldehyde may, directly or through the formation of condensation products with biogenic amines, be involved in the pathogeny of alcoholic disease. 2. Rabbits were treated acutely (200 mg kg-1, i.p., 1 h before sacrifice) or subacutely (200 mg kg-1 per day, during 5 days; sacrificed 2 days after end of treatment) with acetaldehyde. Another group was administered 6-OHDA (2 x 50 mg kg-1 on day 0 and on day 1, killed on day 5). 3. Acetaldehyde induced a depletion of hepatic noradrenaline. Both in the acute experiments and 2 days after the subacute treatment with acetaldehyde the levels of hepatic noradrenaline were 25% of control. These effects were similar to, but less intense than those induced by 6-OHDA. 4. Both subacute acetaldehyde and 6-OHDA led to a significant increase in the density of fibroblasts in the portal tract spaces of the rabbit liver. 5. The neurotoxic effects of acetaldehyde and the subsequent increase in liver fibroblast density may play a role in the pathogenesis of alcoholic disease.

Acetaldehyde↗
PubMed1980

Problems and pitfalls in acetaldehyde determinations.

The determination of acetaldehyde in biologic samples is complicated by a variety of formation and disappearance reactions occurring in the present methods of acetaldehyde analyses. The acetaldehyde formation (ethanol oxidation) in deproteinized supernatant of tissue preparations is prevented by the use of thiourea. During deproteinization, however, it is not inhibited by thiourea, and this remains the main problem in blood acetaldehyde determinations. To circumvent this problem, the use of a correction curve is proposed which is generated by adding control blood samples to the deproteinizing agent such that the blood dilution, temperature, and the ethanol concentrations (the main factors affecting the artifactual acetaldehyde formation) in the controls are identical to those of the samples. Disappearance reactions mainly include loss of acetaldehyde due to binding and/or metabolism. The problem seems to be pronounced with human blood samples, and it is recommended that they be rapidly ( less than 5 sec) deproteinized.

Acetaldehyde↗
PubMed1983

Role of acetaldehyde and acetate in the development of ethanol-induced cardiac lipidosis, studied in isolated perfused rat hearts.

Isolated perfused rat hearts were used to study the effects of ethanol, acetaldehyde, and acetate on the cellular redox state and fatty acid metabolism in the myocardium. Ethanol had negligible effects on the cellular redox state but at high concentrations depressed the contractile activity and thereby secondarily the oxygen consumption. Acetaldehyde in concentrations below 50 microM had negligible effects on the redox state of the mitochondrial free NAD+/NADH couple, as studied by surface fluorometry of flavins and nicotinamide nucleotides. A reduction of NAD+ was observed with concentrations between 50 and 500 microM, while in the range of 0.5-1 mM the effect was biphasic, i.e., an initial reduction was followed by oxidation concomitantly with an increase in heart rate and peak systolic pressure. Acetate in millimolar concentrations caused in the coronary flow. A mitochondrial acetaldehyde dehydrogenase was revealed in the myocardium, having an apparent Km of 1.1 microM for acetaldehyde. Acetaldehyde in 50-microM concentration had no major effects on the uptake, oxidation, or lipid incorporation of oleate in the myocardium. Acetate in concentrations less than 2 mM did not affect the uptake of oleate into the myocardium, but did inhibit is oxidation and enhance its incorporation into tissue lipids in a dose-dependent manner. 2 mM acetate caused a 91% increase in oleate incorporation into tissue lipids over 30 min. The data can be interpreted as showing that acetaldehyde and acetate, the metabolites of ethanol, have metabolic effects on the myocardium, but only those of acetate are significant in concentrations encountered during ethanol oxidation in vivo. It is probable that acetate is involved in the development of ethanol-induced myocardial lipidosis, inhibiting the oxidation of fatty acids, and channelling them into the esterification pathway.

Acetaldehyde↗
PubMedDate not supplied

Mitochondrial respiration after cardiac perfusion with ethanol or acetaldehyde.

Hemodynamics, energetics, and mechanics of isolated working rat hearts were studied during perfusion with Krebs-Henseleit medium containing either ethanol (24 +/- 2 mM) or acetaldehyde (74 +/- 6 microM). After 60-min perfusion with agent, mitochondria were isolated from the hearts and assayed polarographically using glutamate, alpha-keto-glutarate, pyruvate-malate, and succinate-rotenone substrates. Hemodynamic and mechanical function of the ethanol-treated hearts declined significantly more than that of control hearts during the 60-min perfusion. The acetaldehyde-perfused hearts did not differ from the controls. A 90-sec washout period reversed the ethanol-induced depression of physiologic function. Respiratory function (respiratory control ratio and Qo2) of mitochondria isolated from the ethanol- and acetaldehyde-treated hearts was slightly, though not significantly, depressed compared with control hearts. These data indicate that ethanol and acetaldehyde, at physiologically significant concentrations, have dissimilar effects on cardiac hemodynamics and mechanics: ethanol has a direct depressive effect which is reversible; acetaldehyde has no significant effect. Mitochondrial respiration is not irreversibly affected by brief exposure to ethanol or acetaldehyde at the concentrations tested.

Acetaldehyde↗
PubMedDate not supplied

Binding properties of glycosylated albumin and acetaldehyde albumin.

Glucose and acetaldehyde react covalently with albumin to form the post-translationally modified group of proteins, the glycosylated albumins and the acetaldehyde albumins, respectively. This study contrasts the binding ability of a major acetaldehyde albumin fraction synthesized in vitro with glycosylated albumin. A microdialysis rate method, using either [14C]monoacetyldiaminodiphenyl sulfone (MADDS), a deputy ligand for bilirubin, or [14C]diazepam, was employed to evaluate binding at these two sites. Our results indicate that prolonged exposure of purified human serum albumin to acetaldehyde results in a major acetaldehyde albumin fraction that lacks the ability to bind MADDS and diazepam. This fraction migrates identically to albumin on SDS polyacrylamide gel electrophoresis, but exhibits microheterogeneity with a more acidic pI band as seen on analytical isoelectric focusing. We suggest that altered drug binding in alcoholics may be partially explained by altered binding ability of acetaldehyde albumins.

Acetaldehyde↗
PubMed1986

Oxidation of ethanol to acetaldehyde by bronchopulmonary washings: role of bacteria.

The synergistic effects of tobacco smoking and alcohol consumption on the incidence of upper respiratory cancer may be linked to their common ability to produce acetaldehyde, an irritant and potential mutagen. Since alcohol consumption in most individuals results in very low concentrations of acetaldehyde in the blood, we determined whether bronchopulmonary cellular components are capable of oxidizing ethanol to acetaldehyde. We found that significant production of acetaldehyde occurred in vitro after incubation of human bronchopulmonary washings with 25 mM ethanol. Acetaldehyde production was increased in active smokers and related to microorganisms in the bronchopulmonary tract. It was abolished by preincubation of the washings with antibiotics and was reproduced in vitro with Streptococcus pneumoniae. Normal pulmonary cells in bronchopulmonary washings did not produce acetaldehyde from ethanol.

Acetaldehyde↗