Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Acetaldehyde”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 307 records · Page 17Linked to original sources
PubMed2001

Coagulation protein function: enhancement of the anticoagulant effect of acetaldehyde by sulfated glycosaminoglycans.

In view of the increased anticoagulant effect of acetaldehyde-treated heparin, other glycosaminoglycans (GAGs) such as chondroitin sulfates A and C, dermatan sulfate (chondroitin sulfate B), heparan sulfate, and hyaluronic acid were tested for anticoagulant activity before and after exposure to acetaldehyde. Clotting times of human plasma Ci-Trol coagulation control, level I (Baxter Healthcare Corp.), were tested in the presence of 1.8, 3.0, 3.6, or 4.5 microg heparin (0.32, 0.54, 0.64, 0.81 units heparin). Additionally, 9, 27, or 90 microg of chondroitin sulfates A, B, or C was utilized in lieu of heparin. The effects of 2 microg heparin (0.36 units), chondroitin sulfates A, B, and C, (20 microg each), 2 microg heparan sulfate, and 2 microg hyaluronic acid, respectively, in the presence of 44.7 mM acetaldehyde on the clotting time of plasma were studied. It was observed that chondroitin sulfate B (dermatan sulfate) prolonged the clotting time of plasma, although to a lesser extent than heparin. Chondroitin sulfates A and C, heparan sulfate, and hyaluronic acid did not prolong clotting time. However, pretreatment of all the sulfated GAGs with acetaldehyde gave products that enhanced the anticoagulant effect of acetaldehyde, notwithstanding the lack of anticoagulant effect of the GAGs. In contrast, hyaluronic acid exhibited no effect upon clotting time nor did its acetaldehyde-treated product. Furthermore, ethanol exhibited no effect upon the clotting times of the GAG-plasma mixtures. These results suggest that sulfated GAGs may be modified by acetaldehyde, a component of plasma in chronic alcoholics, and that the resultant products may contribute to the prolonged clotting times.

Acetaldehyde↗
PubMed1999

The ethanol metabolite acetaldehyde inhibits the induction of long-term potentiation in the rat dentate gyrus in vivo.

1. Ethanol has been reported to inhibit the induction of long-term potentiation (LTP) in the hippocampus. However, the correlation between the effects of ethanol in vivo and in vitro remained unclear. In addition, previous works have little considered the possibility that the effect of ethanol is mediated by its metabolites. To solve these problems, we investigated the effects of ethanol and acetaldehyde, the first metabolite in the metabolism of ethanol, on the induction of LTP at medial perforant path-granule cell synapses in the dentate gyrus of anaesthetized rats in vivo. 2. Oral administration of 1 g kg-1 ethanol significantly inhibited the induction of LTP, confirming the effectiveness of ethanol in vivo. 3. A lower dose of ethanol (0.5 g kg-1) failed to inhibit the induction of LTP in intact rats, but significantly inhibited LTP in rats treated with disulfiram, an inhibitor of aldehyde dehydrogenase, demonstrating that LTP is inhibited by acetaldehyde accumulation following ethanol administration. 4. Intravenous injection of acetaldehyde (0.06 g kg-1) significantly inhibited the induction of LTP. 5. The inhibitory effect of acetaldehyde on LTP induction was also observed when it was injected into the cerebroventricules, suggesting that acetaldehyde has a direct effect on the brain. The intracerebroventricular dose of acetaldehyde effective in inhibiting LTP induction (0.1 - 0.15 mg brain-1) was approximately 10 fold lower than that of ethanol (1.0 - 1.5 mg brain-1). 6. It is possible that acetaldehyde is partly responsible for memory impairments induced by ethanol intoxication.

Acetaldehyde↗
PubMed2004

Acetaldehyde increases dopaminergic neuronal activity in the VTA.

Acetaldehyde is the first and principal metabolite of ethanol administered systemically. To its rise in blood, after administration of disulfiram, is ascribed the aversive reaction that should discourage alcoholics from drinking. In the present study, we sought to determine the effect of acetaldehyde on the electrophysiological properties of dopamine (DA)-containing neurons in the ventro tegmental area (VTA) of rats in vivo. Intravenous (i.v.) administration of acetaldehyde (5-40 mg/kg) readily and dose-dependently increased the firing rate, spikes/burst, and burst firing of VTA neurons. Ethanol (250-1000 mg/kg/i.v.) administration produced similar increments in electrophysiological parameters. In addition, a second group of rats was pretreated with the alcohol-dehydrogenase inhibitor 4-methyl-pyrazole (90 mg/kg) intraperitoneally (i.p.), and ethanol and acetaldehyde were administered i.v. at the same doses, 48 h later. In this group, ethanol effects were drastically reduced and the firing rate, spikes/burst, and burst firing were not significantly altered. In contrast, acetaldehyde fully retained its capacity to stimulate electrophysiological indices. The results indicate that acetaldehyde produces electrophysiological actions on VTA neurons in vivo, similar to those produced by ethanol, and significantly participate in ethanol-induced increment in DA neuronal activity. These results also suggest that acetaldehyde, by increasing DA neuronal activity in the VTA, may significantly contribute to the centrally mediated positive motivational properties of ethanol, which would oppose the well-known peripherally originating aversive properties.

Acetaldehyde↗
PubMed1972

Utilization and metabolic effects of acetaldehyde and ethanol in the perfused rat liver.

1. Removal of acetaldehyde and ethanol has been studied in perfused rat livers. 2. The maximum rate of ethanol oxidation was 2mumol/min per g of liver, which was less than the calculated capacity of the ethanol-oxidizing system. The lactate/pyruvate ratio of the medium increased with the rate of ethanol removal. At low ethanol concentrations most of the acetaldehyde formed was oxidized further, but at ethanol concentrations above 16mm about 60% of the acetaldehyde left the liver unmetabolized. 3. At lower concentrations the greater part of added acetaldehyde was oxidized, but above 5mm, 50-60% of that removed was recovered as ethanol. 4. When the reduction of acetaldehyde was blocked by pyrazole, removal was strongly diminished. There was no effect on the lactate/pyruvate ratio during oxidation of low concentrations of acetaldehyde, even in the presence of pyrazole, but at higher concentrations a gradual increase occurred. 5. The results indicate that during ethanol oxidation the ethanol/acetaldehyde pair is not in redox equilibrium with the lactate/pyruvate pair. Ethanol oxidation was abolished by addition of acetaldehyde. Under these conditions the lactate/pyruvate ratio was 1.5-1.8 times the ethanol/acetaldehyde ratio, indicating equilibration of the alcohol dehydrogenase and lactate dehydrogenase systems. 6. The results support the view that ultimately the rate of mitochondrial oxidation of NADH limits the removal of ethanol in the liver.

Acetaldehyde↗
PubMed2000

Hypochlorhydria induced by a proton pump inhibitor leads to intragastric microbial production of acetaldehyde from ethanol.

BACKGROUND: Acetaldehyde, produced locally in the digestive tract, has recently been shown to be carcinogenic in humans. AIM: To examine the effect of iatrogenic hypochlorhydria on intragastric acetaldehyde production from ethanol after a moderate dose of alcohol, and to relate the findings to the changes in gastric flora. METHODS: Eight male volunteers ingested ethanol 0.6 g/kg b.w. The pH, acetaldehyde level and microbial counts of the gastric juice were then determined. The experiment was repeated after 7 days of lansoprazole 30 mg b.d. RESULTS: The mean (+/- S.E.M.) pH of the gastric juice was 1.3 +/- 0.06 and 6.1 +/- 0.5 (P < 0.001) before and after lansoprazole, respectively. This was associated with a marked overgrowth of gastric aerobic and anaerobic bacteria (P < 0. 001), by a 2.5-fold (P=0.003) increase in gastric juice acetaldehyde level after ethanol ingestion, and with a positive correlation (r=0. 90, P < 0.001) between gastric juice acetaldehyde concentration and the count of aerobic bacteria. CONCLUSIONS: Treatment with proton pump inhibitors leads to hypochlorhydria, which associates with intragastric overgrowth of aerobic bacteria and microbially-mediated acetaldehyde production from ethanol. Since acetaldehyde is a local carcinogen in the concentrations found in this study, long-term use of gastric acid secretory inhibitors is a potential risk-factor for gastric and cardiac cancers.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2001

Effect of a cysteinyl leukotriene antagonist, pranlukast hydrate, on acetaldehyde-induced bronchoconstriction in asthmatic patients.

Acetaldehyde is a main factor of alcohol-induced asthma. We previously reported that the cysteinyl leukotriene (cys-LT) receptor antagonist, pranlukast hydrate, inhibits acetaldehyde-induced airway hyperresponsiveness in guinea pigs. The purpose of this study was to evaluate the involvement of cys-LT on bronchial responsiveness to acetaldehyde in asthmatic patients. We investigated the bronchial response to inhalation of acetaldehyde in 10 asthmatic patients, who were treated with placebo or pranlukast hydrate (225.5 mg), a cys-LT receptor antagonist, twice a day for 1 wk using a double-blind, randomized, placebo-controlled, cross-over design. Although a remarkable improvement of acetaldehyde bronchoconstriction was observed in 3 out of 10 subjects, PC(20)-AcCHO values were identical between placebo [12.0 (GSEM, 1.192) mg/ml] and pranlukast [14.7 (GSEM, 1.245) mg/ml] groups. The changes in bronchial responsiveness to acetaldehyde were similar in the six patients who had never experienced alcohol-induced asthma and the four who had. In conclusion, cys-LTs are not involved in acetaldehyde-induced bronchoconstriction.

Acetaldehyde↗
PubMed1995

Daidzin suppresses ethanol consumption by Syrian golden hamsters without blocking acetaldehyde metabolism.

Daidzin is a potent, selective, and reversible inhibitor of human mitochondrial aldehyde dehydrogenase (ALDH) that suppresses free-choice ethanol intake by Syrian golden hamsters. Other ALDH inhibitors, such as disulfiram (Antabuse) and calcium citrate carbimide (Temposil), have also been shown to suppress ethanol intake of laboratory animals and are thought to act by inhibiting the metabolism of acetaldehyde produced from ingested ethanol. To determine whether or not daidzin inhibits acetaldehyde metabolism in vivo, plasma acetaldehyde in daidzin-treated hamsters was measured after the administration of a test dose of ethanol. Daidzin treatment (150 mg/kg per day i.p. for 6 days) significantly suppresses (> 70%) hamster ethanol intake but does not affect overall acetaldehyde metabolism. In contrast, after administration of the same ethanol dose, plasma acetaldehyde concentration in disulfiram-treated hamsters reaches 0.9 mM, 70 times higher than that of the control. In vitro, daidzin suppresses hamster liver mitochondria-catalyzed acetaldehyde oxidation very potently with an IC50 value of 0.4 microM, which is substantially lower than the daidzin concentration (70 microM) found in the liver mitochondria of daidzin-treated hamsters. These results indicate that (i) the action of daidzin differs from that proposed for the classic, broad-acting ALDH inhibitors (e.g., disulfiram), and (ii) the daidzin-sensitive mitochondrial ALDH is not the one and only enzyme that is essential for acetaldehyde metabolism in golden hamsters.

Acetaldehyde↗
PubMed1999

Ethanol oxidation and acetaldehyde production in vitro by human intestinal strains of Escherichia coli under aerobic, microaerobic, and anaerobic conditions.

BACKGROUND: Many human colonic facultative anaerobic and aerobic bacteria are capable of alcohol dehydrogenase (ADH)-mediated ethanol oxidation. In this bacteriocolonic pathway for ethanol oxidation intracolonic ethanol is first oxidized by bacterial ADHs to acetaldehyde, which is further oxidized by either colonic mucosal or bacterial aldehyde dehydrogenases to acetate. The produced acetaldehyde is a highly toxic and carcinogenic agent. This study was aimed to investigate the ethanol oxidation capability and acetaldehyde formation of Escherichia coli IH 50546 and IH 50817. These intestinal E. coli strains expressed either high (IH 50546) or low (IH 50817) ADH activity. METHODS: Strains were cultured for 48 h on agar plates supplemented with ethanol under aerobic, microaerobic (6% O2), and anaerobic conditions. RESULTS: Under aerobic conditions both E. coli strains oxidized ethanol. The ethanol consumption rates (ECR) were 1.046+/-0.025 mM/h and 0.367+/-0.148 mM/h with IH 50546 and IH 50817, respectively. In the case of IH 50546 this was associated with significant acetaldehyde production (418+/-13 microM), suggesting ADH-mediated ethanol oxidation. Under microaerobic conditions only IH 50546 was able to oxidize ethanol (ECR, 0.498+/-0.074 mM/h) and to produce acetaldehyde (up to 440+/-76 microM) to significant extents. Under anaerobic conditions both strains fermented glucose to ethanol. CONCLUSIONS: This study experimentally shows the potential of certain bacteria representing normal human colonic flora to produce acetaldehyde under various atmospheric conditions that may prevail in different parts of the GI tract. This bacterial adaptation may be an essential feature of the bacteriocolonic pathway to produce toxic and carcinogenic acetaldehyde from either endogenous or exogenous ethanol.

Acetaldehyde↗
PubMed2003

Acetaldehyde, microbes, and cancer of the digestive tract.

Excessive alcohol consumption and heavy smoking are the main risk factors of upper digestive tract cancer in industrialized countries. The association between heavy drinking and cancer appears to he particularly prominent in Asian individuals who have an inherited deficient ability to detoxify the first metabolite of ethanol oxidation, acetaldehyde. Alcohol itself is not carcinogenic. However, according to cell culture and animal experiments acetaldehyde is highly toxic, mutagenic, and carcinogenic. In addition to somatic cells, microbes representing normal human gut flora are also able to produce acetaldehyde from ethanol. After the ingestion of alcoholic beverages, this results in high local acetaldehyde concentrations in the saliva, gastric juice, and the contents of the large intestine. In addition, microbes may produce acetaldehyde endogenously without alcohol administration. This review summarizes the epidemiological, genetic, and biochemical evidence supporting the role of locally produced acetaldehyde in the pathogenesis of digestive tract cancer. Special emphasis is given to those factors that regulate local acetaldehyde concentration in the contents of the gastrointestinal tract. The new evidence presented in this review may open a microbiological approach to the pathogenesis of digestive tract cancer and may have an influence on future preventive strategies.

Acetaldehyde↗
PubMed2005

Chronic consumption of ethanol leads to substantial cell damage in cultured rat astrocytes in conditions promoting acetaldehyde accumulation.

AIMS: This study aimed at comparing the cerebral cytotoxicity of ethanol and its main metabolite acetaldehyde after acute or chronic exposures of rat astrocytes in primary culture. METHODS: Cytotoxicity was evaluated on the cell reduction of viability (MTT reduction test) and on the characterization of DNA damage by single cell gel electrophoresis (or comet assay). RESULTS: Changes in astrocyte survival and in DNA integrity only occurred when the astrocytes were chronically exposed to ethanol (20 mM; 3, 6 or 9 days). On the other hand, viability and DNA integrity were deeply affected by acute exposure to acetaldehyde. Both effects were dependent on the concentration of acetaldehyde. The cytotoxic effect of acetaldehyde was also indirectly evaluated after modifications of the normal ethanol metabolism by the use of different inducers or inhibitors. In presence of ethanol, the concomitant induction of catalase (i.e. by glucose oxidase) and inhibition of aldehyde dehydrogenase (i.e. by methylene blue) led to acetaldehyde accumulation within cells. It was followed by both a reduction in viability and a substantial increase in DNA strand breaks. CONCLUSIONS: These data were thus consistent with a possible predominant role of acetaldehyde during brain ethanol metabolism. On the other hand, the effects observed after AMT could also suggest a possible direct ethanol effect and a role for free radical attacks. These data were thus consistent with a possible predominant role of acetaldehyde during brain ethanol metabolism. On the other hand, the effects observed after AMT could also suggest a possible direct ethanol effect and a role for free radical attacks.

Acetaldehyde↗
PubMed2001

The role of acetaldehyde in pregnancy outcome after prenatal alcohol exposure.

It is not known why some heavy-drinking women give birth to children with alcohol-related birth defects (ARBD) whereas others do not. The objective of this study was to determine whether the frequency of elevated maternal blood acetaldehyde levels among alcoholics is in the range of ARBD among alcoholic women. MEDLINE was searched from 1980 to 2000 using the key words acetaldehyde, pharmacokinetics, and alcoholism for controlled trials reporting blood or breath acetaldehyde levels in alcoholics and nonalcoholics. Separately, using the key words fetal alcohol syndrome, epidemiology, prevalence, incidence, and frequency, articles were identified reporting ARBD incidences among the offspring of heavy drinkers. Of 23 articles reporting acetaldehyde levels in alcoholics, four met the inclusion criteria. Forty-three studies reported on the rate of ARBD in heavy drinkers, and 14 were accepted. Thirty-four percent of heavy drinkers had a child with ARBD, and 43% of chronic alcoholics had high acetaldehyde levels. The similar frequencies of high acetaldehyde levels among alcoholics and the rates of ARBD among alcoholic women provide epidemiologic support to the hypothesis that acetaldehyde may play a major role in the cause of ARBD.

Acetaldehyde↗
PubMed1984

Blood acetaldehyde concentration gradient between hepatic and antecubital venous blood in ethanol-intoxicated alcoholics and controls.

After ethanol (0.8 g kg-1 body weight orally) significant concentrations of acetaldehyde (2-20 mumol 1(-1] were found in hepatic venous blood of moderately intoxicated non-alcoholic male Caucasians in spite of the absence of detectable levels (less than 2 mumol 1(-1] in simultaneously taken antecubital blood. In thirteen chronic alcoholics the elevation of blood acetaldehyde was more constant in the hepatic than in the peripheral vein. Fructose infusion caused a marked elevation of acetaldehyde both in the hepatic and peripheral vein of four controls, but not of four alcoholics, who eliminated ethanol about 50% faster than controls. The rate of disappearance of acetaldehyde from sampled and in vitro incubated hepatic venous blood was similar to that observed after addition of acetaldehyde in vitro to ethanol-free control blood (2 nmol ml-1 min-1 at 20 mumol 1(-1) acetaldehyde; Km about 30 mumol 1(-1]. Uptake of acetaldehyde in blood was calculated to explain maximally 30-40% of the concentration gradient between central and peripheral blood.

Acetaldehyde↗
PubMed1983

Human blood acetaldehyde levels: with improved methods, a clearer picture emerges.

New reliable methods for the determination of acetaldehyde in human blood, either from separated plasma or from acid-precipitated whole blood, demonstrate that the blood of healthy Caucasians contains at most only extremely small amounts of acetaldehyde (less than 1 microM) after moderate alcohol intoxication. On the other hand, among about 50% of the Japanese population ethanol ingestion results in elevated blood acetaldehyde levels (10-50 microM) with consequent unpleasant cardiovascular responses such as facial flushing and tachycardia, apparently because of a lack of one of the acetaldehyde-oxidizing aldehyde dehydrogenase isozymes. Elevated acetaldehyde levels may eventually occur also among intoxicated Caucasian alcoholics, primarily as a consequence of abuse-induced loss of hepatic aldehyde dehydrogenase activity, but accentuated by an accelerated ethanol oxidation rate. The elevation is probably reversible, since no acetaldehyde is seen in alcoholics after abstinence and hospital treatment. There is thus little evidence that an elevation of acetaldehyde could serve as a marker for predisposition for alcoholism.

Acetaldehyde↗
PubMedDate not supplied

A reinvestigation of the usefulness of breath analysis in the determination of blood acetaldehyde concentrations.

Human volunteers were given ethanol (0.4 g/kg) either intravenous or per os. They were also given ethanol (0.2 g/kg) intravenous 4 hr after receiving a dose of 50 mg citrated calcium carbimide, an aldehyde dehydrogenase inhibitor. During the first hour after starting the administration of ethanol, ethanol and acetaldehyde concentrations were determined in expired air, blood from the right atrium, arterial blood, and venous blood. In the absence of calcium carbimide treatment, the respective maximal blood acetaldehyde concentrations were (range): 6-30 microM (calculated from breath analysis using a blood:breath partition ratio of 190 for acetaldehyde); 0-3.5 microM (right atrium blood); and 0 microM (arterial and venous blood). After calcium carbimide treatment, the maximal blood acetaldehyde concentrations were 10-220 microM (calculated from concentrations in expired air), 38-280 microM (right atrium), 31-250 microM (arterial blood), and 7-186 microM (venous blood). With aldehyde dehydrogenase inhibition, a clear correlation existed between breath concentrations and blood concentrations. Without this inhibition, no such correlation was found. A clear arterio-venous difference was seen for acetaldehyde concentrations while they were artificially elevated by calcium carbimide. Our study suggests that factors other than the equilibration of acetaldehyde between alveolar air and pulmonary blood are of great importance in determining the concentration of acetaldehyde in expired air.

Acetaldehyde↗
PubMedDate not supplied

Formation of Schiff base adduct between acetaldehyde and rat liver microsomal phosphatidylethanolamine.

Recent studies have established the formation of acetaldehyde adducts of proteins even at low concentrations of acetaldehyde expected to occur in vivo under conditions of ethanol metabolism. Although formation of acetaldehyde adducts with phospholipids has been obtained at high pH values and at high concentrations of acetaldehyde, the occurrence of such adducts under more physiological conditions had yet to be demonstrated. Rat liver microsomes were incubated with 0.2 mM [14C]acetaldehyde at pH 7.4 and 37 degrees C. After treatment with sodium borohydride to reduce any Schiff bases formed, the phospholipids were isolated. The major radioactive component within the phospholipid fraction had chromatographic properties identical to N-ethylphosphatidylethanolamine. In addition, the nitrogenous base derived therefrom by acid hydrolysis was identical to N-ethylethanolamine. These results indicate that a Schiff base adduct between acetaldehyde and microsomal phosphatidylethanolamine had been formed during incubation of low concentrations of acetaldehyde with rat liver microsomes.

Acetaldehyde↗
PubMedDate not supplied

Exaggerated acetaldehyde response after ethanol administration during pregnancy and lactation in rats.

The exaggerated blood acetaldehyde response that has been reported after ethanol administration to pregnant rats was found to be the beginning of a much larger alteration occurring during lactation. Indeed, at the end of pregnancy, we confirmed a 4-fold increase in the acetaldehyde values above nonpregnant values after an intragastric dose of 3 g/kg ethanol. During gestational days 1 to 17, the levels did not differ. After delivery, the exaggerated acetaldehyde response to ethanol was increased, producing acetaldehyde concentrations 15-fold greater than in nonlactating controls. This response returned to nonpregnant levels with weaning and could be abolished by removing the pups at birth. The intensified response was associated with both an enhanced rate of ethanol oxidation and a decreased low Km aldehyde dehydrogenase activity in liver mitochondria. At the end of pregnancy, measurable concentrations of acetaldehyde were found in umbilical venous blood and fetal blood. However, they amounted to only one-quarter of maternal values whereas ethanol levels were similar. Thus, during late pregnancy and lactation, there is a marked increase in maternal blood acetaldehyde after ethanol intake. In the presence of a normal placenta, however, an acetaldehyde concentration gradient exists between the mother and the fetus.

Acetaldehyde↗
PubMed1986

Application of isoelectric focusing in immobilized pH gradients to the study of acetaldehyde-modified hemoglobin.

We applied the technique of isoelectric focusing (IEF) on immobilized pH gradients (LKB) to determine whether acetaldehyde-modified hemoglobins (Hb) prepared in vitro with unphysiological acetaldehyde concentrations have clinical relevance. This technique separates proteins with pl less than 0.01 and provides detail about hemoglobins not otherwise separable. We performed two kinds of studies. In one kind of study, we incubated red cells from control subjects with acetaldehyde. Products of these incubations were applied to IEF gels either directly or after reduction with sodium cyanoborohydride. Incubation of red cells with acetaldehyde in 1-150 mM concentration without cyanoborohydride reduction yielded hemoglobin bands of decreasing pl the appearance of which coincided with the disappearance of Hb A and Hb A1c. When the products of incubation were reduced with cyanoborohydride before IEF, an additional acidic Hb band appeared which we call the "anodal CNBH band." In a second kind of study, we compared IEF patterns of hemolysates from control subjects and alcoholism detoxification patients, without adding acetaldehyde. Again, samples were applied to IEF gels either directly or after reduction with cyanoborohydride. When samples were run on IEF without reduction, no differences were seen between patients and controls. When samples were reduced before IEF, an anodal CNBH band appeared having the same mobility as the band seen after in vitro incubations with acetaldehyde. These bands were often stronger in samples from patients, but not consistently so. Several experiments, including the use of glycolysis inhibitors, indicated that the anodal CNBH band is an adduct of fructose 1,6-diphosphate with hemoglobin. We suggest that in millimolar concentrations, acetaldehyde may function as an inhibitor of glycolysis at or below the aldolase step.

Acetaldehyde↗
PubMed1990

Hemoglobin-acetaldehyde adducts in human volunteers following acute ethanol ingestion.

Rabbit antibodies against albumin-acetaldehyde adduct were used in an enzyme-linked immunosorbent assay to detect acetaldehyde-hemoglobin condensates from the blood of 12 volunteers following ingestion of 1.3 to 2.9 g of ethanol per kg body weight during 8 hr. Blood samples were drawn before drinking and between 2 to 46 hr after starting the drinking session. While there were no significant increases in blood acetaldehyde levels in these samples, acetaldehyde-hemoglobin adducts were significantly increased in the samples drawn after ethanol had been eliminated from the body. Administration of ethanol (0.1 g/kg) to an Oriental flusher resulted in an increase both in blood acetaldehyde and the hemoglobin-acetaldehyde adduct levels. These results suggest that acetaldehyde-hemoglobin condensates are formed in vivo following acute ethanol ingestion. Such condensates may be of value to mark alcohol consumption.

Acetaldehyde↗