bluuebunny/crossref_metadata_2025_split huggingface dataset:
Acetaldehyde Production and Other ADH‐Related Characteristics of Aerobic Bacteria Isolated From Hypochlorhydric Human Stomach
Authors: Väkeväinen Satu , Tillonen Jyrki , Blom Mikko , Jousimies‐Somer Hannele , Salaspuro Mikko 
Published: April 2006

Background: Acetaldehyde is a known local carcinogen in the digestive tract in humans. Bacterial overgrowth in the hypochlorhydric stomach enhances production of acetaldehyde from ethanol in vivo after alcohol ingestion. Therefore, microbially produced acetaldehyde may be a potential risk factor for alcohol‐related gastric and cardiac cancers. This study was aimed to investigate which bacterial species and/or groups are responsible for acetaldehyde formation in the hypochlorhydric human stomach and to characterize their alcohol dehydrogenase (ADH) enzymes.Methods: After 7 days of treatment with 30 mg of lansoprazole twice a day, a gastroscopy was performed on eight volunteers to obtain hypochlorhydric gastric juice. Samples were cultured and bacteria were isolated and identified; thereafter, their acetaldehyde production capacity was measured gas chromatographically by incubating intact bacterial suspensions with ethanol at 37°C. Cytosolic ADH activities, Km values, and protein concentration were determined spectrophotometrically.Results: Acetaldehyde production of the isolated bacterial strains (n= 51) varied from less than 1 to 13,690 nmol of acetaldehyde/109 colony‐forming units/hr. ADH activity of the strains that produced more than 100 nmol of acetaldehyde/109 colony‐forming units/hr (n= 23) varied from 3.9 to 1253 nmol of nicotinamide adenine dinucleotide per minute per milligram of protein, and Km values for ethanol ranged from 0.65 to 116 mM and from 0.5 to 3.1 M (high Km). There was a statistically significant correlation (r= 0.64, p < 0.001) between ADH activity and acetaldehyde production from ethanol in the tested strains. The most potent acetaldehyde producers were Neisseria and Rothia species and Streptococcus salivarius, whereas nearly all Stomatococcus, Staphylococcus, and other Streptococcus species had a very low capacity to produce acetaldehyde.Conclusions: This study demonstrated that certain bacterial species or groups that originate from the oral cavity are responsible for the bulk of acetaldehyde production in the hypochlorhydric stomach. These findings provide new information with the respect to the local production of carcinogenic acetaldehyde in the upper digestive tract of achlorhydric human subjects.
Prolonged Ethanol Treatment Enhances Lipopolysaccharide/Phorbol Myristate Acetate‐Induced Tumor Necrosis Factor‐α Production in Human Monocytic Cells
Authors: Zhang Zili , Bagby Gregory J. , Stoltz David , Oliver Peter , Schwarzenberger Paul O. , Kolls Jay K. 
Published: April 2006

Background: Ethanol (EtOH) is known to alter host immune responses and cytokine production. Acute EtOH exposure can suppress tumor necrosis factor (TNF)‐α production, which attenuates pulmonary defense against infection. Previous studies in our laboratory show that acute EtOH inhibited TNF‐α production by a posttranscriptional process, namely suppression of TNF‐α‐converting, enzyme‐mediated, ectodomain shedding. However, chronic EtOH has been shown to augment TNF‐α production, and this has been associated with EtOH‐induced liver injury. To further characterize this paradoxical effect of EtOH on TNF‐α production, we developed an in vitro model by using Mono Mac 6 cells, a human monocytic cell line.Methods: Mono Mac 6 cells were treated with EtOH (0–75 mM) for 1 to 7 days. TNF‐α production was induced by lipopolysaccharide and phorbol myristate acetate and quantitated by enzyme‐linked immunosorbent assay. Generation of reactive oxygen species (ROS) was assayed by using a specific fluorogenic reagent.Results: Acute EtOH initially inhibited lipopolysaccharide/phorbol myristate acetate‐induced TNF‐α production in Mono Mac 6 cells. However, during chronic EtOH exposure, this inhibition was reversed gradually over time. By day 6 after EtOH treatment, Mono Mac 6 cells demonstrated significant up‐regulation of TNF‐α production. Moreover, chronic EtOH induced the generation of ROS in these Mono Mac 6 cells. Scavenging ROS by Mn(III)tetrakis(1‐methyl‐4pyridyl)porphyrin pentachloride and N‐acetyl‐L‐cysteine attenuated chronic EtOH‐enhanced TNF‐α production.Conclusion: These results suggest that ROS induction is involved in EtOH‐enhanced TNF‐α production by monocytes. This study also provides insight into the mechanisms of alteration of TNF‐α production in different EtOH exposure settings.
Inhibition of Hematopoietic Progenitor Cell Proliferation by Ethanol in Human Immunodeficiency Virus Type 1 Tat‐Expressing Transgenic Mice
Authors: Prakash Om , Rodriguez Vicente E. , Tang Zhen‐Ya , Zhou Peng , Coleman Roy , Dhillon Gundeep , Shellito Judd E. , Nelson Steve 
Published: April 2006

Background: A number of hematological abnormalities are associated with both human immunodeficiency virus type 1 (HIV‐1) infection and alcohol abuse. There is little information on how alcohol abuse might further influence the survival and growth of hematopoietic progenitors in HIV‐infected individuals in the presence of immune system abnormalities and anti‐HIV drugs. Because there is evidence that viral transactivator Tat itself can induce hematopoietic suppression, in this study we examined the role of ethanol as a cofactor in transgenic mice that expressed HIV‐1 Tat protein.Methods: Tat transgenic mice and nontransgenic littermates were given ethanol (20% v/v) and the anti‐HIV drug 3′‐azido‐3′‐deoxythymidine (AZT; 1 mg/ml) in drinking water. Immunosuppression in mice was induced by weekly intraperitoneal injections of anti‐CD4 antibody. Hematopoiesis was examined by erythroid colony forming unit (CFU‐E) and granulocyte/macrophage colony‐forming unit (CFU‐GM) assays of the bone marrow progenitor cells.Results: Administration of ethanol for 7 weeks resulted in a 50% decrease in the proliferative capacity of CFU‐E‐ and CFU‐GM‐derived progenitors from transgenic mice compared with that of ethanol‐treated nontransgenic controls. Similar decreases also were observed in transgenic mice treated with AZT or a combination of AZT and ethanol. Furthermore, ethanol and AZT were significantly more toxic to the granulopoietic progenitors (40–50% inhibition) than to the erythropoietic progenitors (10–20% inhibition) in Tat transgenic mice. Although a 10 day exposure of Tat transgenic and nontransgenic mice to a combination of ethanol and AZT had no suppressive effect on the erythropoietic and granulopoietic progenitor cells, there was a marked decrease (40–60%) in CFU‐GM in mice made immunodeficient by CD4+ T‐lymphocyte depletion. The ethanol‐treated Tat transgenic mice but not the nontransgenic littermates also showed a significant decrease (25%) in CFU‐GM.Conclusion: Our in vivo study strongly suggests that ethanol ingestion in HIV‐1‐infected individuals, particularly those on antiretroviral drugs, might increase bone marrow toxicity and contribute to HIV‐1‐associated hematopoietic impairment.
A Rodent Model of Alcoholic Heart Muscle Disease and Its Evaluation by Echocardiography
Authors: Kim Shann D. , Beck Jennifer , Bieniarz Teresa , Schumacher Autumn , Piano Mariann R. 
Published: April 2006

Background: Transthoracic echocardiography was used in a rodent animal model to determine whether long‐term alcohol consumption (8 and 12 months) was associated with the development of a dilated cardiomyopathy. We also investigated whether alcohol‐induced changes in cardiac structure corresponded to activation of the renin‐angiotensin system and the natriuretic peptide (NP) system.Methods: Male rats received either the Lieber‐DeCarli liquid alcohol diet (EtOH) (9%v/v) (n= 8) or control diet (CON) (n= 8). Echocardiography (echo) was used to determine left‐ventricular (LV) dimensions, and isolated heart studies (Langendorff and atrium) were used to assess ex vivo contractility. Plasma and tissue angiotensin‐I converting enzyme (ACE) activity was measured. Gene expression, plasma, and tissue levels of the NPs were determined by northern blot analysis and radioimmunoassay, respectively.Results: After 8 months of alcohol consumption, there was a trend for the end diastolic dimension, end systolic dimension, and LV mass to be greater in the 8 month EtOH group compared with the CON group. However, after 12 months of alcohol consumption, significant increases were found between the groups in several echo parameters. Tissue ACE activity (nmoles/min/mg protein) was greater in the 12 month EtOH group compared with the 12 month CON and 8 month EtOH group (p < 0.05). We found no differences between groups in gene expression (messenger RNA), plasma, and tissue levels of the NPs.Conclusions: Echocardiography revealed that 8 to 12 months of alcohol consumption was associated with the development of a dilated cardiomyopathy. However, this was not preceded by an increase in tissue ACE activity, and these changes occurred in the absence of increased plasma and LV tissue levels of the NPs.
Ethanol Consumption and the Susceptibility of Mice to Listeria monocytogenes Infection
Authors: Salerno Joseph A. , Waltenbaugh Carl , Cianciotto Nicholas P. 
Published: April 2006

Background: It is well known that excessive alcohol consumption correlates with increased infectious disease. However, the molecular microbiological and immunological bases for ethanol‐induced alterations in host defense are largely unknown.Methods: To study the effect of alcohol consumption on the pathogenesis of intracellular bacteria, we examined the relative susceptibility of alcohol‐fed mice to a virulent strain of Listeria monocytogenes.Results: Based on lethal dose 50% determinations, survival curve analysis, and bacterial burden, alcohol consumption did not increase the susceptibility of C57BL/6, BALB/c, or A/J mice to systemic infection by strain EGD. Mice fed an ethanol‐containing liquid diet showed slightly reduced susceptibility to Listeria. Alcohol consumption modestly decreased bacterial numbers in the spleen but not the liver. We also found that mice fed a typical solid diet were more sensitive to EGD infection than were animals fed a control liquid‐containing diet.Conclusions: This study indicates that alcohol consumption may not always increase infectious disease progression.
Effect of 4‐Methylpyrazole on Endogenous Plasma Ethanol and Methanol Levels in Humans
Authors: Sarkola Taisto , Eriksson C.J. Peter 
Published: April 2006

Background: Endogenous methanol and ethanol levels are found in human blood. It is assumed that these compounds are derived mainly from microflora in the gastrointestinal tract and that the small amounts formed are consequently eliminated, mainly in the liver, by the alcohol dehydrogenase (ADH) pathway. The objective of the present study was to investigate the effect of 4‐methylpyrazole (4‐MP), a specific ADH inhibitor, on endogenous plasma methanol and ethanol levels in healthy women and men.Methods: A double‐blind placebo‐controlled interventional study was carried out.Results: A significant elevation in plasma endogenous ethanol and methanol levels was observed after intake of 4‐MP (10–15 mg/kg p.o.). For methanol levels, a linear increase from 20 ± 14 μmol/l before intake to 39 ± 22 μmol/l at 420 min from intake of 4‐MP (levels 20 ± 14 μmol/l and 14 ± 9 μmol/l during the corresponding placebo time points) was found. For ethanol, concentrations increased from levels below detection limit (i.e., < 5 μmol/l, determined by headspace gas chromatography) before intake to 30 ± 20 μmol/l at 195 min from intake of 4‐MP. A small increase in ethanol levels, to 13 ± 8 μmol/l, but not in methanol levels, was observed after the intake of lingonberry juice containing no ethanol or methanol. No sex differences in the ethanol and methanol levels before or after the intake of 4‐MP were found.Conclusions: The present study provides conclusive evidence for a constant endogenous production as well as clearance of ethanol and methanol in humans. In addition, the study shows that the ethanol and methanol produced are, at least in part, eliminated by the ADH pathway.
Local Cerebral Glucose Utilization Rates in Alcohol‐Naïve High–Alcohol‐Drinking (HAD) and Low–Alcohol‐Drinking (LAD) Rats
Authors: Learn Jennifer E. , Smith Daniel G. , McBride William J. , Lumeng Lawrence , Li Ting‐Kai 
Published: April 2006

Background: The present study compared baseline local cerebral glucose utilization (LCGU) values within reward‐relevant brain regions in alcohol‐naïve, adult male high–alcohol‐drinking (HAD) and low–alcohol‐drinking (LAD) rats from replicate lines 1 and 2.Methods: 2‐[14C]Deoxyglucose ([14C]2‐DG) was injected (125 μCi/kg) intravenously during the rats’ dark cycle. Timed arterial blood samples were collected over 45 min and assayed for glucose as well as [14C]2‐DG content. Rats were then decapitated; their brains quickly removed and frozen in isopentane at −50°C. Coronal sections from each brain were apposed to film and exposed for 2 days. Image densities were analyzed using quantitative autoradiography.Results: Data were collected from several key limbic (nucleus accumbens, ventral tegmental area, olfactory tubercle, amygdala, hippocampus, ventral pallidum, and septum), basal ganglia, cortical (medial prefrontal, frontal, parietal, temporal, occipital, entorhinal, pyriform, and cingulate), and subcortical (thalamus, habenula, and superior colliculus) structures. Because there were no significant differences between the replicates within each drinking line, data from the two replicates were combined to determine drinking line differences. When both replicate lines were combined, there were trends toward higher (approximately 15%) LCGU rates in HAD (n= 15) versus LAD (n= 16) rats within the parietal and occipital cortices, but neither of these line differences reached statistical significance (p < 0.01).Conclusions: The findings suggested that, within the HAD and LAD replicate rat lines, the selection for alcohol preference did not lead to differences in functional brain activity, as measured with the 2‐DG method.
Patterns of Cognitive‐Motor Development in Children With Fetal Alcohol Syndrome From a Community in South Africa
Authors: Adnams Colleen M. , Kodituwakku Piyadasa W. , Hay Andrea , Molteno Chris D. , Viljoen Denis , May Philip A. 
Published: April 2006

Background: Even though fetal alcohol syndrome (FAS) has been reported in nonwestern nations, there is a paucity of information on neurodevelopment in the affected children from those nations. This article reports on a study of cognitive‐motor development in a group of children with FAS from a community in the Western Cape Province in South Africa.Methods: Thirty‐four children with FAS and 34 controls from grade 1 (school entry level) classes participated. The two groups comprised Afrikaans‐speaking children of mixed ancestry (South African Colored) and were matched for age, sex, and family income. The Griffiths Mental Development Scales were used to assess cognitive motor development of the participants.Results: A multivariate analysis of covariance was performed to test the group effect on the combined Griffiths subscales adjusting for maternal education. The results showed a significant group effect. Follow‐up analyses revealed that a combination of four subscales (Speech and Hearing, Performance, Practical Reasoning, and Eye and Hand Coordination) primarily contributed to the overall effect. Although there was a marginal effect on the Personal‐Social subscale, no significant effect on the Locomotor (gross motor) subscale was found.Conclusions: The results showed that the FAS group was markedly deficient only in higher‐order cognitive‐motor competencies.
Moderate Alcohol Consumption and Postprandial Plasma Lipids in Men With Different Risks for Coronary Heart Disease
Authors: Hendriks Henk F.J. , van Haaren Marian R.T. , Leenen Rianne , Schaafsma Gertjan 
Published: April 2006

Background: Moderate alcohol consumption is associated with a reduced coronary heart disease (CHD) risk. Epidemiologic studies have provided conflicting data which suggests that CHD protection may be modulated or may not be modulated by a person's CHD risk profile.Methods: We examined the effects of moderate alcohol consumption (35 g/day) on postprandial lipoprotein metabolism in two groups of healthy middle‐aged men who had different plasma total cholesterol, triglyceride concentrations, and body mass index (BMI), which are three major risk factors for CHD; 11 men had lower plasma lipids and BMI (L‐men) and 11 men had higher plasma lipids and BMI (H‐men). The effects of alcohol on postprandial lipoprotein metabolism were studied in a crossover design after an acute moderate alcohol intake both after a period of abstinence (alcohol‐free beer) and after a period of moderate alcohol consumption (alcohol containing beer).Results: Moderate alcohol consumption changed plasma total cholesterol, total triglycerides, and HDL composition in the postprandial period. Alcohol‐induced changes were essentially the same over time in both L‐men and H‐men. However, changes occurred at a different overall plasma concentration for total cholesterol and total triglycerides. Also, the postprandial response to an acute moderate alcohol dose after a period of abstinence seemed not to essentially differ from the response to an acute moderate alcohol dose after a 4‐week period of moderate alcohol consumption.Conclusions: These results suggest that men who differ in risk for CHD, based on plasma lipids and BMI, but without previous or underlying disease, have a similar postprandial lipid response to a moderate dose of alcohol.
Effect of Chronic Ethanol Consumption on Protective T‐Helper 1 and T‐Helper 2 Immune Responses Against the Parasites Leishmania major and Strongyloides stercoralis in Mice
Authors: Krolewiecki Alejandro J. , Leon Shalom , Scott Phillip A. , Nolan Thomas J. , Schad Gerhard A. , Abraham David 
Published: April 2006

Background: Chronic alcohol consumption has been associated with significant increases in the prevalence of infectious diseases, and it has been suggested that these increases are caused by a direct effect of ethanol on the immune response. The objective of this study was to determine whether chronic ethanol consumption would affect the development of protective immunity to Leishmania major, which is controlled by the T‐helper 1 (Th1) subset of CD4 cells, and Strongyloides stercoralis, which is controlled by the Th2 subset.Methods: Mice were fed ethanol‐containing liquid diet (25% ethanol‐derived calories), liquid isocaloric diet without ethanol, or solid chow and then exposed to either of the two parasites. The ability of the mice chronically consuming alcohol to eliminate the infections was determined, as were the levels of parasite‐specific humoral and cellular immune responses.Results: Mice chronically consuming alcohol were capable of eliminating both of these infections in a manner identical to the control mice. In addition, splenocytes from mice chronically consuming alcohol infected with L. major produced nitric oxide at the same levels as in control mice. Antibody responses were altered in a manner suggesting an increase in Th2 immunity and a decrease in Th1 immunity in the mice chronically consuming alcohol. In mice chronically consuming alcohol that were infected with S. stercoralis, eosinophils migrated to the parasite's microenvironment, and antibodies were produced at levels equivalent to those seen in control mice.Conclusions: Mice maintained on an ethanol‐containing liquid diet had some alteration in their ability to produce Th1 and Th2 immune responses yet were capable of generating unimpaired protective Th1 and Th2 responses.
Regulation of Milk Intake After Exposure to Alcohol in Mothers' Milk
Authors: Mennella Julie A. 
Published: April 2006

Objective: Contrary to the folklore which claims that drinking alcohol during lactation benefits both mother and infant, previous research in our laboratory revealed that breastfed infants consumed significantly less milk during the immediate hours after their mothers’ consumption of an alcoholic beverage. Because breastfed infants are clearly capable of regulating milk intake, the present study tested the hypothesis that infants would compensate for the diminished milk intake if their mothers then refrained from drinking alcohol.Methods: A within‐subjects design that controlled for time of day was implemented because of the great individual and daily variation in both milk composition and intake. To this end, 12 exclusively breastfed infants and their mothers were tested on 2 days separated by 1 week. Each woman drank a 0.3 g/kg dose of alcohol in orange juice on one testing day and orange juice alone on the other; the order was counterbalanced. The infants’ behaviors were monitored for the next 16 hr, the first 4 hr of monitoring on each test day occurred at the Monell Center. The infants fed on demand and immediately before and after each feeding, infants were weighed without a change in clothing.Results: Consistent with previous findings, infants consumed significantly less milk during the 4 hr immediately after exposure to alcohol in mothers’ milk compared with the control condition. Compensatory increases in intake were then observed during the 8 to 16 hr after exposure when mothers refrained from drinking alcohol.Conclusions: These findings demonstrate that short‐term exposure to small amounts of alcohol in mothers’ milk produces distinctive changes in the infants’ patterns of feeding.
Ethanol Dependence Has Limited Effects on GABA or Glutamate Transporters in Rat Brain
Authors: Devaud Leslie L. 
Published: April 2006

Background: Neuroadaptations of GABAergic and glutamatergic systems appear to play an important role in both the acute as well as chronic effects of ethanol. Chronic ethanol intake leads to the development of ethanol tolerance and dependence that is associated with a decrease in GABAergic and an increase in glutamatergic function. The present report assessed the involvement of GABA and glutamate transporters in the chronic ethanol‐induced adaptations of these two neuronal systems.Methods: Male and female rats were made ethanol dependent by 2‐week administration of ethanol in a liquid diet. Levels of GABA (GAT‐1, GAT‐3) and glutamate (GLT‐1, EAAC‐1) transporters were assayed by immunoblotting. Transporter function was assessed by [3H]GABA and [3H]glutamate uptake assays.Results: Ethanol dependence did not alter levels of GABA or glutamate transporters in cerebral cortex compared with pair‐fed control values. There were increases in some, but not all, transporter levels in hippocampus and hypothalamus with the development of ethanol dependence. A decreased rate of uptake was observed for GABA in cerebral cortex. There was no change in maximal GABA uptake or in glutamate uptake (Vmax).Conclusions: These results suggest that alterations in GABA and glutamate transporters have only a limited role in neuroadaptations to chronic ethanol intake in rats. However, the observed alterations were region‐specific, supporting the complex responses to chronic ethanol exposure and suggesting that neuroadaptations of GABAergic and glutamatergic systems vary across the brain.