The effect of cigarette smoking on breath and whole blood-associated acetaldehyde

Six pairs (1 habitual smoker and 1 nonsmoking control) of volunteers were studied to determine the effect of smoking tobacco on breath and whole blood acetaldehyde levels. On a given study day, samples of blood and breath were obtained from both participants at -0.25, 0, 0.25, 0.50, 0.75, 1.5, 2.5, and 3.5 hour time points. The smoking volunteer was told to smoke 1-3 cigarettes between the 0 and 0.25 hour time points. Acetaldehyde levels in breath and whole blood were quantified with a fluorigenic high performance liquid chromatographic assay. Acetaldehyde in breath rose six-fold in smokers at the 0.25 hour time point and returned to levels not significantly different from baseline values found in smokers or nonsmokers by 0.50 hr. Whole blood-associated acetaldehyde measurements remained unchanged in smokers throughout the experiment and were not different from nonsmokers. In conclusion, while smoking produces appreciable levels of acetaldehyde in expired air, the partitioning of acetaldehyde associated with smoking to blood or blood proteins appears to be below the level of detection of the assay employed (picomolar). Smoking of tobacco products may not interfere with assays designed to quantify ethanol intake by measuring acetaldehyde adducts with blood proteins.     

Rapid association of acetaldehyde with hemoglobin in human volunteers after low dose ethanol

A fluorigenic high performance liquid chromatographic (HPLC) method was used to determine plasma (PA) and hemoglobin-associated (HbAA) acetaldehyde levels following a pulse of 0.3 g/kg ethanol to volunteers from whom bloods were drawn serially for 8 hours on the clinical research unit. On discharge from the research unit, the volunteers were instructed to avoid ethanol for 28 days. The results were compared to previously published results in teetotalers and alcoholic individuals reporting for treatment at an inpatient detoxification facility. Following ethanol ingestion, the peak levels of ethanol and both plasma and hemoglobin-associated acetaldehyde were detected at the 30 min time point and plasma levels were less than those associated with hemoglobin (31 +/- 16 S.D. and 159 +/- 48 S.D. nmol/g respectively, p less than 0.001). PA and HbAA returned to baseline values following ethanol ingestion within 3.5 hours. PA returned to within 1 standard deviation of levels found in teetotalers by 5 days, whereas HbAA remained elevated for the 28 days of the study. These data provide evidence that measurement of PA and HbAA may provide a useful marker for relatively acute and chronic ethanol ingestion respectively.     

Blood acetaldehyde response to ethanol ingestion during the reproductive cycle of the female rat

Acetaldehyde could mediate a number of the toxic effects of alcohol both in females and their offspring. Thus, we assessed the blood acetaldehyde response to ethanol (3 g/kg) at various stages of the female reproductive cycle. Blood levels were low throughout the various phases of the estrous cycle and during most of pregnancy. By contrast, a 4-fold rise in maternal blood acetaldehyde occurred at the end of pregnancy (day 20), continued to increase during lactation (17-fold at day 14) and returned to non-pregnant values after weaning or after pup removal at birth. Both enhanced rate of ethanol oxidation and decreased activity of the low Km aldehyde dehydrogenase in liver mitochondria contributed to the increased acetaldehyde levels. Acetaldehyde was detectable in fetal blood, but only a small fraction of the high maternal values in pregnancy reached the fetus through the umbilical vein. Chronic alcohol administration resulted in decreased fetal size and striking enlargement of the placenta with possible implications for abnormal fetal development. Thus, the high maternal acetaldehyde levels at the end of pregnancy may exert deleterious effects on many maternal organs, including those (such as placenta) which are required for normal fetal development.     

Determination of Organic Acids and Volatile Flavor Substances in Kefir during Fermentation

The production of organic acids and volatile flavor components was measured during kefir starter culture fermentation. Samples were collected at 0, 5, 10, 15, and 22 h of fermentation (final pH=4.6). Samples were analyzed for orotic, citric, pyruvic, uric, lactic, acetic, butyric, propionic and hippuric acids by HPLC. Acetaldehyde, ethanol, acetoin and diacetyl production were monitored using GC equipped with headspace autosampler. Levels of orotic, citric, and pyruvic acids slightly decreased during fermentation. Hippuric acid was totally consumed by 15 h of incubation. Acetic, propionic, and butyric acids and diacetyl were not detected. Production of ethanol began only after 5 h of incubation whereas acetaldehyde and acetoin increased during fermentation.     

Studies of urine-associated acetaldehyde as a marker for alcohol intake in mice.

A study was undertaken in 16 male C57BL mice to evaluate the effect of ethanol intake via the drinking water (10% v/v) on urinary-associated acetaldehyde. Eight received ethanol and 8 served as controls. Urinary-associated acetaldehyde (UAA) was measured using a fluorigenic high performance chromatographic assay. Ethanol consumption did not impair growth over the two weeks of the experiment. Following administration of ethanol, UAA increased and remained significantly elevated over levels seen in controls until ethanol administration ceased (11.3 +/- 3.6 SEM microM for ethanol-consuming mice vs. 0.69 +/- 0.33 microM for controls). Ethanol in the urine was found to interfere with the assay for acetaldehyde. However, following cessation of ethanol, acetaldehyde in urine was found to be significantly elevated in urine at 24 hours, after ethanol levels were no longer detectable. In conclusion, measurement of urinary-associated acetaldehyde discriminates ethanol-consuming from nonconsuming mice during ethanol ingestion as well as 24 hours following cessation of ethanol when ethanol levels are no longer detectable in urine. Thus measurement of urinary acetaldehyde may be a useful marker for monitoring ethanol intake.     

STUDIES ON THE CHRONOPHARMACOLOGY OF ETHANOL

Male subjects (n = 10) were given ethanol (0.75 g/kg) at fourequally spaced times in the 24 hr cycle (9 am, 3 pm, 9 pm, 3am) in random order. Blood ethanol concentrations were monitoredby breath analysis and measurements were made of the blood orplasma levels of ethanol, acetaldehyde, acetate, pyruvate, lactateand cortisol. Blood pressure, heart rate and body temperaturewere measured before and at 60 and 120 min after ethanol administrationand the effects of ethanol on a number of behavioural parametersand mood were studied. After ethanol ingestion, there was asignificant decrease in body temperature, systolic blood pressure,plasma cortisol and pyruvate levels, whilst acetate levels andthe lactate:pyruvate ratio were significantly increased. Standingsteadiness, critical flicker fusion threshold and divided attentiontracking control were significantly impaired under ethanol andself-report data indicated a significant decrease in alertness,co-ordination, concentration and attentiveness. Although a significantlyhigher peak blood ethanol concentration was attained at the9 am session, other time-of-day differences did not reach significanceand the pharmacokinetics of ethanol were essentially unchanged.Since the only significant diurnal variations in the responseto ethanol identified in this study (apart from the subjectiveresults) were for plasma cortisol concentrations and body temperature(both of which are well known to exhibit diurnal rhythmicity),it appears that major circadian variability in the metabolicand/or behavioural effects of ethanol is unlikely to occur.     

Lack of aldehyde dehydrogenase ameliorates oxidative stress induced by single-dose ethanol administration in mouse liver.

Polymorphism of aldehyde dehydrogenase 2 (ALDH2), denoted ALDH2*2, is far more common in East Asian countries. Acetaldehyde, an intermediate metabolite of ethanol, is metabolized very slowly in people who have ALDH2*2, as the mutated ALDH2 lacks acetaldehyde metabolizing activity. On the other hand, it is well established that metabolism of ethanol causes oxidative stress in liver tissue. To examine the consequences of this polymorphism on ethanol-induced oxidative stress in liver tissue, we conducted a study using Aldh2 knockout mice. Aldh2+/+ and Aldh2-/- mice were orally administered ethanol at a dose of 5g/kg body weight. Levels of malondialdehyde, an indicator of oxidative stress, and glutathione, a key antioxidant, in liver tissue were analyzed 0-24h after administration. Levels of malondialdehyde were significantly lower in Aldh2-/- mice than in Aldh2+/+ mice at 12h after injection, while levels of glutathione were higher in Aldh2-/- mice than in Aldh2+/+ mice at 6 and 12h after injection. Our results suggest that a lack of ALDH ameliorates ethanol-induced oxidative stress in liver tissue.     

Acetaldehyde and alcohol levels in pregnant rats and their fetuses

Alcohol and acetaldehyde blood levels were measured in chronic alcoholic pregnant rats and their fetuses at 15, 19 and 21 days of gestation. Similar ethanol concentrations were found in fetal and maternal blood in all gestation periods studied, however levels in amniotic fluid were higher than in mother's blood, especially in the early stages of gestation. Acetaldehyde concentrations were always lower in fetal than in maternal blood although increasing throughout gestation. The levels in fetal blood and amniotic fluid compared to maternal blood, were ca. 40, 50 and 70% at 15, 19 and 21 days of gestation, respectively; those for the placenta and fetal tissues were lower, i.e., 25, 40 and 50%. Similar alcohol and acetaldehyde ratios (fetus/mother's concentration) were obtained when pregnant non-alcoholic rats were administered cyanamide and ethanol (2 g/kg) at 11, 15, 19 and 21 days of gestation. These results demonstrate that ethanol freely crosses the placental barrier, but there is a concentration gradient of acetaldehyde between mother and fetus which varies with gestation age.     

Influence of chronic alcohol ingestion on acetaldehyde-induced depression of rat cardiac contractile function

Long-standing ethanol consumption acts as a chronic cardiac stress and often leads to alcoholic cardiomyopathy. We have recently shown that the acute ethanol-induced depression in myocardial contraction was substantiated by chronic ethanol ingestion. Acetaldehyde (ACA), the main ethanol metabolite, has been considered to play a role in ethanol-induced cardiac dysfunction. To evaluate the ACA-induced cardiac contractile response following chronic ethanol ingestion, mechanical properties were examined using left ventricular papillary muscles and myocytes from rats fed with control or ethanol-enriched diet. Muscles and myocytes were electrically stimulated at 0.5 Hz and contractile properties analysed included peak tension development (PTD) and peak shortening (PS). Intracellular Ca(2+) transients were measured as fura-2 fluorescence intensity changes (DeltaFFI). Papillary muscles from ethanol-consuming animals exhibited reduced baseline PTD and attenuated responsiveness to increase of extracellular Ca(2+). Acute ACA (0.3-10 mM) addition elicited a dose-dependent depression of PTD. However, the inhibition magnitude was significantly reduced in ethanol-treated rats. Myocytes from both control and ethanol-treated rats exhibited comparable ACA-induced depression in both PS and DeltaFFI. Collectively, these data suggest that the ACA-induced depression of myocardial contraction is reduced at the multicellular level, but unchanged at the single cell level, following chronic ethanol ingestion.     

Acetaldehyde inhibits the anti-elastase activity of α1-antitrypsin

There are genetic and exogenous factors responsible for α₁-antitrypsin (α₁-AT) deficiency which may lead to cirrhosis of the liver and emphysema. The present study was initiated on a biochemical level in order to determine whether acetaldehyde, the major product of ethanol metabolism, is capable of influencing the physiological effect of α₁-AT upon elastase, an enzyme which is capable of inducing emphysema. The effects of acetaldehyde and ethanol upon elastase and α₁-AT were tested. Acetaldehyde at 0.3-M and 1.2-M concentrations inhibited the anti-elastase activity of α₁-AT. Acetaldehyde at 0.03-M and 0.07-M concentrations did not affect elastase activity and had a slight effect at 0.12-M levels. Equivalent amounts of ethanol were without influence upon elastase activity or α₁-AT function. These data provide biochemical support for the possibility that heterozygous males with lower than normal α₁-AT levels may be at much higher risk to develop liver disease, emphysema, and α₁-AT deficiency as a consequence of chronic exposure to ethanol and concommitent circulating acetaldehyde levels.     

MEASURING AND REPORTING THE CONCENTRATION OF ACETALDEHYDE IN HUMAN BREATH

Most of the acetaldehyde generated during the metabolism ofethanol becomes tightly bound to endogenous molecules such ashaemoglobin, amino acids and certain phospholipids. Free acetaldehydepasses the blood-brain bamer and traces of this toxic metaboliteare excreted through the lungs and can be detected in the expiredair. The blood/air partition coefficient of acetaldehyde at34 %C, the average temperature of endexpired air, is about 190:1.Because of various problems associated with measuring acetaldehydein blood samples, several research groups have instead investigatedthe analysis of acetaldehyde in breath which offers an indirectand alternative approach for clinical and research purposes.However, care is needed when interpreting the results of breathacetaldehyde measurements, because of the possibility of localformation from microflora inhabiting the upper airways and mouth.The concentration of acetaldehyde exhaled in breath after drinkingalcohol demonstrates large inter-individual differences dependingon various genetic (racial) and environmental factors. Moreover,acetaldehyde is an endogenous metabolite and even without drinkingany alcohol the concentrations expelled in breath span from0.2 to 0.6 nmol/l, with higher levels observed in smokers andabstinent alcoholics. Breath acetaldehyde concentration reachedbetween 5 and 50 nmol/l in European subjects who drank a moderatedose of ethanol (0.4–0.8 g/kg), with the highest valuesseen in smokers. The concentration of breath acetaldehyde inJapanese subjects after drinking alcohol reached between 200and 500 nmol/l at the peak. These much higher levels followbecause a large proportion of Orientals (40–50%) inheritan inactive form of the low K_m mitochondrial isoenzyme of aldehydedehydrogenase (ALDH₂). The highest concentrations of breathacetaldehyde were seen in healthy Caucasians who drank a smalldose of alcohol (0.25 g/kg) after taking the alcohol-sensitizingdrug calcium carbimide, which blocks the action of ALDH isozymes.During the most intense acetaldehyde-flush reaction, breathacetaldehyde reached between 200 and 1300 nmol/l, but even theseabnormally high concentrations did not interfere with the analysisof ethanol in breath by means of non-specific infrared analyserscurrently used in many countries for testing drinking drivers.     

Effect of acetaldehyde on urinary salsolinol in healthy man after ethanol intake

The effect of acetaldehyde on urinary salsolinol (6, 7-dihydroxy-l-methyl-1,2,3,4-tetrahydroisoquinoline) after ethanol intake was investigated. Healthy Japanese male volunteers were divided into two groups, i.e., a normal aldehyde dehydrogenase (ALDH) group of 13 subjects with a low Km isozyme of ALDH and a deficient group of 12 subjects. The subjects were given 0.4 or 0.8 g/kg of ethanol. Blood ethanol and acetaldehyde levels, urinary excretions of salsolinol, norepinephrine, epinephrine and dopamine were determined. A significant elevation of salsolinol in urine was found after intake of 0.8 g/kg of ethanol in the two groups, but the increase in the deficient group was greater than that in the normal group, while 0.4 g/kg of ethanol did not affect the excretion of salsolinol in either group. Blood acetaldehyde was highly correlated with urinary salsolinol (r = 0.88, p less than 0.001) and the correlation coefficient was greater than that between blood ethanol and salsolinol.     

Evidence of acetaldehyde-protein adduct formation in rat brain after lifelong consumption of ethanol

Acetaldehyde, the first metabolite of ethanol, has been shown to be capable of binding covalently to liver proteins in vivo, which may be responsible for a variety of toxic effects of ethanol. Acetaldehyde-protein adducts have previously been detected in the liver of patients and experimental animals with alcoholic liver disease. Although a role for acetaldehyde as a possible mediator of ethanol-induced neurotoxicity has also been previously suggested, the formation of protein-acetaldehyde adducts in brain has not been examined. This study was designed to examine the occurrence of acetaldehyde-protein adducts in rat brain after lifelong ethanol exposure. A total of 27 male rats from the alcohol-preferring (AA) and alcohol-avoiding (ANA) lines were used. Four ANA rats and five AA rats were fed 10-12% (v/v) ethanol for 21 months. Both young (n = 10) and old (n = 8) rats receiving water were used as controls. Samples from frontal cortex, cerebellum and liver were processed for immunohistochemical detection of acetaldehyde adducts. In four (two ANA, two AA rats) of the nine ethanol-exposed rats, weak or moderate positive reactions for acetaldehyde adducts could be detected both in the frontal cortex and cerebellum, whereas no such immunostaining was found in the remaining five ethanol-treated rats or in the control rats. The positive reaction was localized to the white matter and some large neurons in layers 4 and 5 of the frontal cortex, and to the molecular layer of the cerebellum. Interestingly, the strongest positive reactions were found among the ANA rats, which are known to display high acetaldehyde levels during ethanol oxidation. We suggest that acetaldehyde may be involved in ethanol-induced neurotoxicity in vivo through formation of adducts with brain proteins and macromolecules.     

Application of static headspace gas chromatography for determination of acetaldehyde in beer

Acetaldehyde is a natural by-product of the fermentation process, and its determination and quantitative analysis help to evaluate whether complete and proper fermentation has taken place. A new method was developed for sensitive determination and quantitative analysis of acetaldehyde in beer in our laboratory. Separation and determination of acetaldehyde were carried out by static headspace gas chromatography (HS–GC) with various experimental conditions. Calibration curves were obtained by plotting peak area versus concentration, and correlation coefficient of 6 standard level additions was ≥0.999. Measuring precision for acetaldehyde was ≤0.16% R.S.D. (relative standard deviation) under the condition of HS (25 psi)/GC (16 psi) when compared to HS (21 psi)/GC (16 psi). Configuration of two level temperatures made all the detecting values existing between upper control limit (UCL) and lower control LCL (limit) in comparison with one level configuration. In addition, the detecting threshold ranged from 0.5 to 12.1 μg mL^?1 using proposed parameters. Data displayed that accuracy and precision of detection were reliable for routine monitoring in beer. The method built in our laboratory could be used successfully to analyze the concentration of acetaldehyde in beer in the future.     

Comparative measurements of total body water in healthy volunteers by online breath deuterium measurement and other near-subject methods

BACKGROUND: We developed a new near-subject approach, using flowing afterglow-mass spectrometry (FA-MS) and deuterium dilution, which enables the immediate measurement of total body water (TBW) from single exhalations. OBJECTIVES: The objectives were to show the efficacy of the new FA-MS method in measuring TBW in healthy subjects and to compare these measurements with values derived from multifrequency bioelectrical impedance analysis, skinfold-thickness (SFT) measurements, and both recent and historical published regression equations. DESIGN: After baseline measurement of breath deuterium abundance, 24 healthy subjects ingested 0.3 g D(2)O/kg body wt. A second breath sample was taken after 3 h to measure the increase in deuterium, from which TBW was calculated. Bioelectrical impedance analysis was carried out with a multifrequency analyzer, and SFT was measured by a single trained observer. Methods were compared with the use of Pearson's correlation coefficient and Bland-Altman analyses. RESULTS: TBW measures obtained by all methods were highly correlated (r = 0.95-0.98, P < 0.001), especially those between FA-MS, SFT measurement, and recent regression equations. The mean values obtained were within 2% of those published for age-matched control subjects and varied by 1-6% when all methods were compared. Systematic bias was greatest when FA-MS was compared with bioelectrical impedance analysis, which tended to underestimate TBW in smaller, female subjects. No bias related to subject size was observed in a comparison of FA-MS with SFT measurement or with more recent regression equations. CONCLUSIONS: FA-MS is a simple and effective new approach to TBW measurement in healthy subjects. The difficulty of using population-derived equations to estimate TBW in individual subjects is emphasized.     

Comparison of serum fatty acid ethyl esters and urinary 5-hydroxytryptophol as biochemical markers of recent ethanol consumption

AIMS: To examine the effects of an acute dose of ethanol on serum fatty acid ethyl esters (FAEEs) concentration and urinary 5-hydroxytryptophol (5-HTOL)/5-hydroxyindole-3-acetic acid (5-HIAA) ratio. METHODS: Sixteen (14 male, 2 female) heavy alcohol drinkers were tested in a single, 2-day long session. Six participants received 1.5 g/l of ethanol/l of body water (approximately 0.75 g/kg of body weight, low dose group: LD) and 10 participants received 2.0 g/l of ethanol ( approximately 1.0 g/kg of body weight, high dose group: HD) in four divided doses every 20 min. Blood, urine, and breath samples were collected repeatedly over 36 h following the ingestion of ethanol and were analyzed for the presence of FAEE, 5-HTOL/5-HIAA, and ethanol, respectively. Serum gamma-glutamyltransferase (GGT), a marker of chronic ethanol use, was also included. RESULTS: The breath ethanol level peaked approximately 1 h after the last dose, at 95 and 120 mg/dl for the LD and HD groups, respectively. The mean ratio of urinary 5-HTOL/5-HIAA was significantly elevated 5 and 9 h after ethanol administration, but returned to baseline 13 h after ethanol administration. This ratio was twice as high for the HD group compared with the LD group. Serum levels of FAEEs were significantly elevated at 5 h, but not 13 h after ethanol administration. There were no time-dependent changes in serum GGT levels. CONCLUSIONS: Measuring the levels of FAEE and 5-HTOL/5-HIAA ratio provides a convenient method to detect recent, particularly binge-type, ethanol use, but these measures may have limited applicability in detecting ethanol use in traditional clinical trial settings.     

REDUCTIONS IN BREATH ETHANOL READINGS IN NORMAL MALE VOLUNTEERS FOLLOWING MOUTH RINSING WITH WATER AT DIFFERING TEMPERATURES

Blood ethanol concentrations were measured sequentially. overa period of hours. using a Lion AE-D2 alcolmeter, in 12 healthymale subjects given oral ethanol 0.5 g/kg body wt. Readingswere taken before and after rinsing the mouth with water atvarying temperatures. Mouth rinsing resulted in a reductionin the alcolmeter readings at all water temperatures tested.The magnitude of the reduction was greater after rinsing withwater at lower temperatures. This effect occurs because rinsingcools the mouth and dilutes retained saliva. This finding shouldbe taken into account whenever breath analysis is used to estimateblood ethanol concentrations in experimental situations.     

Effect of ethanol challenge on serum glycoproteins in alcoholic and non-alcoholic liver disease

The effects of acute ethanol challenge on serum glycoprotein concentrations in man were studied. Serum levels of haptoglobin, alpha-2-macroglobulin and pre-albumin were measured fasting and 6 hr after oral ethanol 0.75 g/kg body weight in 8 healthy controls, 13 patients with alcoholic liver disease and 13 with non-alcoholic-related liver damage, both patient groups being further subdivided into those with and without cirrhosis. Basal levels of haptoglobin were significantly higher in non-cirrhotic alcoholics than controls and pre-albumin levels were lower in non-alcohol-related cirrhotic liver disease. In response to ethanol challenge, no consistent change was observed in any group, nor was there any significant difference between groups. There was, however, a significant correlation (r = 0.53, P less than 0.005) between the percentage changes in haptoglobin and alpha-2-macroglobulin. In 16 subjects (2 controls, 8 alcoholics and 6 non-alcoholics) blood levels of ethanol and acetaldehyde were measured serially: there was no relationship between the peak or mean concentration and the glycoprotein response. This study does not substantiate other reports which claimed to be able to predict the severity and reversibility of alcoholic liver disease on the basis of the serum glycoprotein response to ethanol: ethanol challenge with measurement of serum glycoproteins cannot substitute for proper histological assessment.     

Hypothalamic and serum catecholamines in ethanol and acetaldehyde treated guinea-pigs. Relation to moderate short-term cold exposure

Adult guinea-pigs were treated with ethanol (2.5 g/kg, IP) or acetaldehyde (100 mg/kg, IP) and exposed to moderate cold (+4 degrees C) for 50 minutes. Controls were given 0.9% NaCl solution. The hypothalamic catecholamines norepinephrine (NE) and dopamine (DA) and also norepinephrine and epinephrine (E) in the serum were analyzed by high-performance liquid chromatography with an electrochemical detector. Blood glucose, free fatty acids and glycogen in the liver and skeletal muscle were also measured. Acetaldehyde caused a similar drop in colon temperature as did ethanol, but neither could prevent cold-induced vasoconstriction in the ear lobe. Ethanol significantly reduced the concentration of NE in the hypothalamus compared to the controls. Acetaldehyde had a tendency to lower hypothalamic NE. There was no significant difference between drug-treated groups in NE concentration. Neither ethanol nor acetaldehyde had any effect on hypothalamic DA. In the ethanol group serum E and glucose were significantly elevated compared to the acetaldehyde group. Serum glucose was also higher compared to the controls, and the difference in serum E concentration near the level of significance. No significant differences were found between the groups in serum NE, FFA or skeletal muscle and liver glycogen concentration. The results point to a possible central effect of ethanol during a short-term moderate cold exposure. The effects of acetaldehyde on neuronal tissue remain speculative, but a possible effect on noradrenergic neurons cannot be ruled out. Although the hypothermic effect of acetaldehyde corresponded that of ethanol, further experiments are required to elucidate the role of acetaldehyde in ethanol-induced hypothermia.     

Acetaldehyde production and metabolism by human indigenous and probiotic Lactobacillus and Bifidobacterium strains

Many human gastrointestinal facultative anaerobic and aerobic bacteria possess alcohol dehydrogenase (ADH) activity and are therefore capable of oxidizing ethanol to acetaldehyde. We examined whether human gastrointestinal lactobacilli (three strains), bifidobacteria (five strains) and probiotic Lactobacillus GG ATCC 53103 are also able to metabolize ethanol and acetaldehyde in vitro. Acetaldehyde production by bacterial suspensions was determined by gas chromatography after a 1-h incubation with 22 mM ethanol. To determine the acetaldehyde consumption, the suspensions were incubated with 50 microM or 500 microM acetaldehyde as well as with 500 microM acetaldehyde and 22 mM ethanol, i.e. under conditions resembling those in the human colon after alcohol intake. The influence of growth media and bacterial concentration on the ability of lactobacilli to metabolize acetaldehyde and to produce acetate from acetaldehyde were determined. ADH and aldehyde dehydrogenase (ALDH) activities were determined spectrophotometrically. Neither measurable ADH nor ALDH activities were found in aerobically grown Lactobacillus GG ATCC 53103 and Lactobacillus acidophilus ATCC 4356 strains. All the lactobacilli and bifidobacteria strains revealed a very limited capacity to oxidize ethanol to acetaldehyde in vitro. Lactobacillus GG ATCC 53103 had the highest acetaldehyde-metabolizing capacity, which increased significantly with increasing bacterial concentrations. This was associated with a marked production of acetate from acetaldehyde. The type of the growth media had no effect on acetaldehyde consumption. Addition of ethanol to the incubation media diminished the acetaldehyde-metabolizing capacity of all strains. However, in the presence of ethanol, Lactobacillus GG ATCC 53103 still demonstrated the highest capacity for acetaldehyde metabolism of all strains. These data suggest a beneficial impact of Lactobacillus GG ATCC 53103 on high gastrointestinal acetaldehyde levels following alcohol intake. The possible clinical implications of this finding remain to be established in in vitro studies.