TL;DR: This work investigates the specific activities and cofactor specificities of all relevant oxidoreductases in cell extracts of H2/CO2-grown C. autoethanogenum cells and proposes metabolic schemes that allow the chemiosmotic synthesis of 0.14 to 1.5 mol ATP per mol ethanol synthesized from CO2 and H2.
Abstract: Most acetogens can reduce CO2 with H2 to acetic acid via the Wood-Ljungdahl pathway, in which the ATP required for formate activation is regenerated in the acetate kinase reaction. However, a few acetogens, such as Clostridium autoethanogenum, Clostridium ljungdahlii, and Clostridium ragsdalei, also form large amounts of ethanol from CO2 and H2. How these anaerobes with a growth pH optimum near 5 conserve energy has remained elusive. We investigated this question by determining the specific activities and cofactor specificities of all relevant oxidoreductases in cell extracts of H2/CO2-grown C. autoethanogenum. The activity studies were backed up by transcriptional and mutational analyses. Most notably, despite the presence of six hydrogenase systems of various types encoded in the genome, the cells appear to contain only one active hydrogenase. The active [FeFe]-hydrogenase is electron bifurcating, with ferredoxin and NADP as the two electron acceptors. Consistently, most of the other active oxidoreductases rely on either reduced ferredoxin and/or NADPH as the electron donor. An exception is ethanol dehydrogenase, which was found to be NAD specific. Methylenetetrahydrofolate reductase activity could only be demonstrated with artificial electron donors. Key to the understanding of this energy metabolism is the presence of membrane-associated reduced ferredoxin:NAD+ oxidoreductase (Rnf), of electron-bifurcating and ferredoxin-dependent transhydrogenase (Nfn), and of acetaldehyde:ferredoxin oxidoreductase, which is present with very high specific activities in H2/CO2-grown cells. Based on these findings and on thermodynamic considerations, we propose metabolic schemes that allow, depending on the H2 partial pressure, the chemiosmotic synthesis of 0.14 to 1.5 mol ATP per mol ethanol synthesized from CO2 and H2.
IMPORTANCE Ethanol formation from syngas (H2, CO, and CO2) and from H2 and CO2 that is catalyzed by bacteria is presently a much-discussed process for sustainable production of biofuels. Although the process is already in use, its biochemistry is only incompletely understood. The most pertinent question is how the bacteria conserve energy for growth during ethanol formation from H2 and CO2, considering that acetyl coenzyme A (acetyl-CoA), is an intermediate. Can reduction of the activated acetic acid to ethanol with H2 be coupled with the phosphorylation of ADP? Evidence is presented that this is indeed possible, via both substrate-level phosphorylation and electron transport phosphorylation. In the case of substrate-level phosphorylation, acetyl-CoA reduction to ethanol proceeds via free acetic acid involving acetaldehyde:ferredoxin oxidoreductase (carboxylate reductase).
TL;DR: Iridium-mediated dehydrogenation of ethanol to acetaldehyde has led to the development of an ethanol-to-butanol process operated at a lower temperature.
Abstract: A highly selective (>99%) tandem catalytic system for the conversion of ethanol (up to 37%) to n-butanol, through the Guerbet process, has been developed using a bifunctional iridium catalyst coupled with bulky nickel or copper hydroxides. These sterically crowded nickel and copper hydroxides catalyze the key aldol coupling reaction of acetaldehyde to exclusively yield the C4 coupling product, crotonaldehyde. Iridium-mediated dehydrogenation of ethanol to acetaldehyde has led to the development of an ethanol-to-butanol process operated at a lower temperature.
TL;DR: In this article, metal ions-modified cryptomelane-type manganese oxide octahedral molecular sieves M′-OMS-2 (M′-=Co,Ce,Cu) were synthesized and characterized by XRD, BET, EDS, ICP, TEM, XPS, FTIR, H 2 -TPR in a post plasma-catalysis system.
TL;DR: The Guerbet coupling of ethanol into butanol was investigated using multiproduct steady-state isotopic transient kinetic analysis (SSITKA) in a comparative study between stoichiometric hydroxyapatite (HAP) and magnesia (MgO) catalysts at 613 and 653 K, respectively.
Abstract: The Guerbet coupling of ethanol into butanol was investigated using multiproduct steady-state isotopic transient kinetic analysis (SSITKA) in a comparative study between stoichiometric hydroxyapatite (HAP) and magnesia (MgO) catalysts at 613 and 653 K, respectively. The steady-state catalytic reactions were conducted in a gas-phase, fixed-bed, differential reactor at 1.3 atm total system pressure. Multiproduct SSITKA results showed that the mean surface residence time of reactive intermediates leading to acetaldehyde was significantly shorter than that of intermediates leading to butanol on both HAP and MgO. This finding may suggest that the dehydrogenation of ethanol to acetaldehyde is fast on these surfaces compared with C–C bond formation. If adsorbed acetaldehyde is a key reaction intermediate in the Guerbet coupling of ethanol into butanol, then SSITKA revealed that the majority of adsorbed acetaldehyde produced on the surface of MgO desorbs into the gas-phase, whereas the majority of adsorbed acetal...
TL;DR: In this article, a series of the Au-Cu/SiO2 catalysts including low-loaded samples with an overall metal content less than 0.5% was synthesized by a redox method.
TL;DR: In this paper, the conversion of ethanol to propene was examined on Ni ion-loaded silica MCM-41(Ni-M41), Sc-modified In2O3 (Sc/In 2O3), and a solid solution of Y2O 3-CeO2.
TL;DR: In this paper, the authors showed that Cu nanoparticles supported on a mesoporous carbon act as an active catalyst for the dehydrogenation of ethanol to acetaldehyde with excellent selectivity and in an atom-economic fashion.
Abstract: The front cover artwork for Issue 18/2015 is provided by the Advanced Energy Materials Group of Dalian University of Technology, PR China The image shows that Cu nanoparticles supported on a mesoporous carbon act as an active catalyst for the dehydrogenation of ethanol to acetaldehyde with excellent selectivity and in an atom-economic fashion See the Full Paper itself at http://dxdoiorg/101002/cctc201500501
TL;DR: In this article, the effect of ZnO on ethanol conversion to 1,3-butadiene (BD) was investigated and the highest BD yield was achieved at ratio of MgO:SiO2 = 1:1.
Abstract: Effect of ZnO on ethanol conversion to 1,3-butadiene (BD) on ZnO/MgO–SiO2 catalysts consists in the enhancement of selectivity and yield of BD due to higher rate of ethanol dehydrogenation to acetaldehyde. It has been shown that two types of Lewis acid sites formed in the contact zones of MgO–SiO2 and ZnO–SiO2 in the catalysts play an important role in BD synthesis from ethanol. The highest BD yield is achieved at ratio of MgO:SiO2 = 1:1.
TL;DR: In this article, the interaction between malvidin 3-glucoside, the main anthocyanin in red wine made from Vitis vinifera grapes, and (+)-catechin and the effect on this interaction of ferric ions and acetaldehyde was examined.
Abstract: The interaction between malvidin 3-glucoside, the main anthocyanin in red wine made from Vitis vinifera grapes, and (+)-catechin and the effect on this interaction of ferric ions and acetaldehyde was examined. In the models not containing acetaldehyde losses of malvidin 3-glucoside were observed, but there were only negligible losses of catechin; no new compounds were observed. In the presence of acetaldehyde the formation of new compounds was determined by high performance liquid chromatography; this formation coincided with rapid losses in the concentrations of malvidin 3-glucoside and catechin. A molecular ion at m/z 809 was determined by FAB MS, corresponding to a dimer consisting of malvidin 3-glucoside linked to catechin by an acetaldehyde bridge, according to a mechanism previously suggested by TIMBER-LAKE and BRIDLE (1976). Concurrent with the losses in anthocyanins, qualitative and quantitative changes in visible colour were also observed, consisting of changes in the wavelength of maximum absorbance (λ max ) and in maximum absorbance intensity (A max ). Models containing malvidin 3-glucoside plus catechin or catechin plus ferric ions showed a marked decrease in their λ max from 525 nm to 440 nm; there was little net effect of the ferric ions on these changes. The model containing acetaldehyde showed a large increase in A max while the λ max showed a bathochromic shift from 524 nm to 557 nm; colour decreased after achieving a maximum and the λ max decreased slightly. Changes in colour monitored by measuring hue angle, chroma and L* value are also reported.
TL;DR: These ALDHs are not only biomarkers for CRC and pancreatic cancer but also play important mechanistic role in cancer initiation, progression, and eventual prognosis.
Abstract: Colorectal cancer (CRC) and pancreatic cancer are two very significant contributors to cancer-related deaths. Chronic alcohol consumption is an important risk factor for these cancers. Ethanol is oxidized primarily by alcohol dehydrogenases to acetaldehyde, an agent capable of initiating tumors by forming adducts with proteins and DNA. Acetaldehyde is metabolized by ALDH2, ALDH1B1, and ALDH1A1 to acetate. Retinoic acid (RA) is required for cellular differentiation and is known to arrest tumor development. RA is synthesized from retinaldehyde by the retinaldehyde dehydrogenases, specifically ALDH1A1, ALDH1A2, ALDH1A3, and ALDH8A1. By eliminating acetaldehyde and generating RA, ALDHs can play a crucial regulatory role in the initiation and progression of cancers. ALDH1 catalytic activity has been used as a biomarker to identify and isolate normal and cancer stem cells; its presence in a tumor is associated with poor prognosis in colon and pancreatic cancer. In summary, these ALDHs are not only biomarkers for CRC and pancreatic cancer but also play important mechanistic role in cancer initiation, progression, and eventual prognosis.
TL;DR: It is demonstrated for the first time that ALDH2 deficiency results in markedly increased exposure of the gastric mucosa to acetaldehyde after intragastric administration of alcohol, providing concrete evidence for a causal relationship between acetaldehyde and gastric carcinogenesis.
Abstract: Acetaldehyde (ACH) associated with alcoholic beverages is Group 1 carcinogen to humans (IARC/WHO). Aldehyde dehydrogenase (ALDH2), a major ACH eliminating enzyme, is genetically deficient in 30–50% of Eastern Asians. In alcohol drinkers, ALDH2-deficiency is a well-known risk factor for upper aerodigestive tract cancers, i.e., head and neck cancer and esophageal cancer. However, there is only a limited evidence for stomach cancer. In this study we demonstrated for the first time that ALDH2 deficiency results in markedly increased exposure of the gastric mucosa to acetaldehyde after intragastric administration of alcohol. Our finding provides concrete evidence for a causal relationship between acetaldehyde and gastric carcinogenesis. A plausible explanation is the gastric first pass metabolism of ethanol. The gastric mucosa expresses alcohol dehydrogenase (ADH) enzymes catalyzing the oxidation of ethanol to acetaldehyde, especially at the high ethanol concentrations prevailing in the stomach after the consumption of alcoholic beverages. The gastric mucosa also possesses the acetaldehyde-eliminating ALDH2 enzyme. Due to decreased mucosal ALDH2 activity, the elimination of ethanol-derived acetaldehyde is decreased, which results in its accumulation in the gastric juice. We also demonstrate that ALDH2 deficiency, proton pump inhibitor (PPI) treatment, and L-cysteine cause independent changes in gastric juice and salivary acetaldehyde levels, indicating that intragastric acetaldehyde is locally regulated by gastric mucosal ADH and ALDH2 enzymes, and by oral microbes colonizing an achlorhydric stomach. Markedly elevated acetaldehyde levels were also found at low intragastric ethanol concentrations corresponding to the ethanol levels of many foodstuffs, beverages, and dairy products produced by fermentation. A capsule that slowly releases L-cysteine effectively eliminated acetaldehyde from the gastric juice of PPI-treated ALDH2-active and ALDH2-deficient subjects. These results provide entirely novel perspectives for the prevention of gastric cancer, especially in established risk groups.
TL;DR: In this article, a faster production of acetaldehyde could be considered to shorten the aging process of Sherry wines, which is a relevant carbonyl compound in wines and one of the main responsible for the particular personality of sherry wines.
Abstract: Sherry wines are consumed worldwide and are principally produced in the Jerez and Montilla-Moriles regions of southern Spain. Acetaldehyde is a relevant carbonyl compound in wines and one of the main responsible for the particular personality of Sherry wines with a ripe apple odor descriptor. Aldehyde dehydrogenase plays an important role in yeast acetaldehyde metabolism. Acetaldehyde contents in Sherry wines subjected to biological aging strongly depend on yeast populations, and the formation of velum depends on specific amino acids, oxygen availability, and the composition of the wine. Both biological and oxidative aging processes increase the acetaldehyde content in Sherry, although some of the acetaldehyde is oxidized to acetic acid and subsequently transformed into acetyl-CoA. In sensory terms, 1,1-diethoxyethane and other acetals, acetoin, and sotolon are the main compounds formed from acetaldehyde in Sherry wines. The chemical browning pathway of wine by the condensation between phenols and acetaldehyde is especially important in Sherry wines. Acetaldehyde can inhibit the velum formation at higher concentration than its threshold tolerance; also, it could be responsible for the high mitochondrial DNA polymorphism observed in flor yeasts. Usually, acetaldehyde is used to control the biological aging of Fino Sherry. A faster production of acetaldehyde could be considered to shorten the aging process of Sherry. In recent years, the acetaldehyde formed during ethanol metabolism in alcoholic beverages has been associated with carcinogenic processes; however, no systematic data are available about this statement.
TL;DR: In this paper, the major factors, including catalyst, temperature, weight hourly space velocity (WHSV), and molar ratio of ammonia to glycerol, which may affect the pyridine production were investigated systematically.
TL;DR: In this paper, the results of qualitative and quantitative data regarding VOC adsorption on P25 TiO2 have been determined under both dry and humid conditions, and the Langmuir model parameters (adsorption constant (K), reversible and irreversible maximum adsorbed amounts (qm,rev and qm,irr) are determined for each VOC.
TL;DR: An approach in which a pharmacologic agent recruited another ALDH to metabolize acetaldehyde to temporarily increase metabolism of acetaldehyde in vivo is described, focused on ALDH3A1, which is enriched in the upper aerodigestive track, and identified Alda-89 as a small molecule that enables ALDH 3A1 to metabolizing acetaldehyde.
Abstract: Correcting a genetic mutation that leads to a loss of function has been a challenge. One such mutation is in aldehyde dehydrogenase 2 (ALDH2), denoted ALDH2*2. This mutation is present in ∼ 0.6 billion East Asians and results in accumulation of toxic acetaldehyde after consumption of ethanol. To temporarily increase metabolism of acetaldehyde in vivo, we describe an approach in which a pharmacologic agent recruited another ALDH to metabolize acetaldehyde. We focused on ALDH3A1, which is enriched in the upper aerodigestive track, and identified Alda-89 as a small molecule that enables ALDH3A1 to metabolize acetaldehyde. When given together with the ALDH2-specific activator, Alda-1, Alda-89 reduced acetaldehyde-induced behavioral impairment by causing a rapid reduction in blood ethanol and acetaldehyde levels after acute ethanol intoxication in both wild-type and ALDH2-deficient, ALDH2*1/*2, heterozygotic knock-in mice. The use of a pharmacologic agent to recruit an enzyme to metabolize a substrate that it usually does not metabolize may represent a novel means to temporarily increase elimination of toxic agents in vivo.
TL;DR: In this article, Cabernet Sauvignon wines with low and high levels of SO2 and glutathione (GSH) were treated with microoxygenation (MOx) in a 23 L pilot experiment.
Abstract: Cabernet Sauvignon wines with low and high levels of SO2 and glutathione (GSH) were treated with microoxygenation (MOx) in a 23 L pilot experiment. Treatment generally increased O2, aldehydes, and derived products while decreasing anthocyanins, vanillin reactive flavonoids, and SO2. During the treatment, when free SO2 was depleted in the low GSH wine, dissolved oxygen levels collapsed, with a concomitant increase of acetaldehyde, pyranoanthocyanins, polymeric pigments, and acetaldehyde acetals. This outcome indicates a possible acceleration of the Fenton oxidation of ethanol and other oxidation reactions by way of direct free radical reactions with oxygen. In wines containing high levels of GSH, anthocyanins were protected, revealing a protective effect for GSH for the first time. However, the protection was only partial, and while GSH may be effective in preventing the loss of volatile thiols, its use does not prevent color stabilization in red wines. Because both SO2 and GSH are able to modulate the reactions initiated by MOx, but have somewhat dissimilar reactions, it may be possible to manage oxidation outcomes by choosing one or the other during wine processing and aging. Because SO2 and O2 levels are related to large differences in MOx reaction rates, those levels are candidate indicators of the rate of MOx oxidation. Alternatively, the levels of acetaldehyde acetals may be useful indicators of the cumulative extent of oxidation under MOx conditions.
TL;DR: In this paper, a detailed kinetic analysis of chemical effects of hydrogen addition on laminar premixed stoichiometric methane-air flames was conducted at atmospheric pressure, and the results illustrate that the chemical effects led the methane profile to move towards the upstream side and suppress the formation of acetylene and ketene.
TL;DR: A series of ZrO2-SiO2 catalysts synthesized by sol-gel method were investigated for the 1,3-butadiene formation from bioethanol and acetaldehyde as discussed by the authors.
Abstract: A series of ZrO2–SiO2 catalysts synthesized by sol–gel method were investigated for the 1,3-butadiene formation from bioethanol and acetaldehyde. The influence of ZrO2 content and reaction conditions on catalytic performance were studied. The catalysts were characterized by N2 adsorption–desorption analysis, temperature-programmed desorption of NH3 (NH3-TPD), IR spectroscopy of adsorbed pyridine (Py-IR), Fourier Transform Infrared Resonance (FTIR), X-ray diffraction (XRD) and Transmission Electron Microscope (TEM). These characterization results indicated that suitable intensity of acid sites, especially Lewis acid, are very crucial to obtain an active catalyst. The catalysts showed significantly higher selectivity for C4 chemicals, and 2 wt% ZrO2 content reached the highest selectivity to BD (69.7%), at space velocity (WHSV) of 1.8 h−1.
TL;DR: Very volatile organic compounds, such as methanol, acetaldehyde, ethanol, acetone, acetonitrile, and dichloromethane were extracted from water samples using a needle-type extraction device based on purge and trap analysis by introducing carbon molecular sieves as the extraction medium.
TL;DR: This new rapid, simple method is demonstrated for the measurement of carbonyl compounds in a range of wines of different ages and grape varieties and offers good specificity, high recovery and low limits of detection.
TL;DR: Electronic structure calculations of the pertinent stationary points on the potential energy surface show that carboxylic acids can act effectively as catalysts in the hydration of acetaldehyde, and postreactive diol-acid complexes are significantly stable, suggesting the possibility of long-lived hygroscopic species that could act as a seed molecule for condensation of secondary organic aerosols.
Abstract: Electronic structure calculations of the pertinent stationary points on the potential energy surface show that carboxylic acids can act effectively as catalysts in the hydration of acetaldehyde. Barriers to this catalyzed process correlate strongly with the pKa of the acid, providing the potential to provide the predictive capacity of the effectiveness of carboxylic acid catalysts. Transition states for the acid-catalyzed systems take the form of pseudo-six-membered rings through the linear nature of their hydrogen bonds, which accounts for their relative stability compared to the more strained direct and water-catalyzed systems. When considered as a stepwise reaction of a dimerization followed by reaction/complexation, it is likely that collisional stabilization of the prereactive complex is more likely than reaction in the free gas phase, although the catalyzed hydration does retain the potential to proceed on water surfaces or in droplets. Lastly, it is observed that postreactive diol-acid complexes are significantly stable (∼12-17 kcal/mol) relative to isolated products, suggesting the possibility of long-lived hygroscopic species that could act as a seed molecule for condensation of secondary organic aerosols.
TL;DR: In this paper, the influence of the metal on the catalytic performance of M/MgCuCr2O4 (M = ǫ, Ag, Pd, Pt, Au) catalysts was investigated to better understand the metal support synergy for the aerobic oxidation of ethanol.
TL;DR: In this article, the structure and surface properties of the MgO/SiO2 catalyst were studied by both experimental characterization and the simulation method, and the results indicated that ethanol mainly adsorbed on mgO surface.
Abstract: The structure and surface properties of the MgO/SiO2 catalyst were studied by both experimental characterization and the simulation method. The adsorption properties of ethanol on different MgO/SiO2 surfaces were researched by the density functional theory method and the result is that ethanol mainly adsorbed on MgO surface. The role of SiO2 in increasing the MgO crystal defects in the MgO/SiO2 has been obtained and the electronic properties of ethanol molecule before and after adsorption on the catalyst surfaces were compared. The initial step of ethanol dehydrogenation and the dehydration to 1,3-butadiene process, which is the dehydrogenation of ethanol to acetaldehyde reaction, on the flat sites, stepped sites and kinked sites was examined through the molecular simulation method. We investigated the preferable surface for the reaction of ethanol dissociation to an ethoxy group and the more active surface for the reaction of dehydrogenation of ethanol to acetaldehyde. The research results suggested that the stepped MgO surface is more active for the reaction of dehydrogenation of ethanol to acetaldehyde.
TL;DR: This chapter will critically evaluate the concept of carcinogenic levels of acetaldehyde, which has been raised in the literature, and discuss how data from acetaldehyde genotoxicity are and can be utilized in physiologically based models to evaluate exposure risk.
Abstract: Among various potential mechanisms that could explain alcohol carcinogenicity, the metabolism of ethanol to acetaldehyde represents an obvious possible mechanism, at least in some tissues. The fundamental principle of genotoxic carcinogenesis is the formation of mutagenic DNA adducts in proliferating cells. If not repaired, these adducts can result in mutations during DNA replication, which are passed on to cells during mitosis. Consistent with a genotoxic mechanism, acetaldehyde does react with DNA to form a variety of different types of DNA adducts. In this chapter we will focus more specifically on N 2-ethylidene-deoxyguanosine (N2-ethylidene-dG), the major DNA adduct formed from the reaction of acetaldehyde with DNA and specifically highlight recent data on the measurement of this DNA adduct in the human body after alcohol exposure. Because results are of particular biological relevance for alcohol-related cancer of the upper aerodigestive tract (UADT), we will also discuss the histology and cytology of the UADT, with the goal of placing the adduct data in the relevant cellular context for mechanistic interpretation. Furthermore, we will discuss the sources and concentrations of acetaldehyde and ethanol in different cell types during alcohol consumption in humans. Finally, in the last part of the chapter, we will critically evaluate the concept of carcinogenic levels of acetaldehyde, which has been raised in the literature, and discuss how data from acetaldehyde genotoxicity are and can be utilized in physiologically based models to evaluate exposure risk.
TL;DR: It is reported that ethanol drinking increased ALDH2 production in the oesophagus of wild-type mice, and levels of acetaldehyde-derived DNA damage represented by N2-ethylidene-2′-deoxyguanosine were higher in the Oesophagi of Aldh2-knockout mice than in wild- type mice upon ethanol consumption.
Abstract: Acetaldehyde is an ethanol-derived definite carcinogen that causes oesophageal squamous cell carcinoma (ESCC). Aldehyde dehydrogenase 2 (ALDH2) is a key enzyme that eliminates acetaldehyde, and impairment of ALDH2 increases the risk of ESCC. ALDH2 is produced in various tissues including the liver, heart, and kidney, but the generation and functional roles of ALDH2 in the oesophagus remain elusive. Here, we report that ethanol drinking increased ALDH2 production in the oesophagus of wild-type mice. Notably, levels of acetaldehyde-derived DNA damage represented by N(2)-ethylidene-2'-deoxyguanosine were higher in the oesophagus of Aldh2-knockout mice than in wild-type mice upon ethanol consumption. In vitro experiments revealed that acetaldehyde induced ALDH2 production in both mouse and human oesophageal keratinocytes. Furthermore, the N(2)-ethylidene-2'-deoxyguanosine levels increased in both Aldh2-knockout mouse keratinocytes and ALDH2-knockdown human keratinocytes treated with acetaldehyde. Conversely, forced production of ALDH2 sharply diminished the N(2)-ethylidene-2'-deoxyguanosine levels. Our findings provide new insight into the preventive role of oesophageal ALDH2 against acetaldehyde-derived DNA damage.
TL;DR: Evidence strongly suggests that brain-generated EtOH metabolites play a major role in the early ("first-hit") development of alcohol reinforcement and in the generation of relapse-like drinking.
Abstract: This review analyzes literature that describes the behavioral effects of 2 metabolites of ethanol (EtOH): acetaldehyde and salsolinol (a condensation product of acetaldehyde and dopamine) generated in the brain. These metabolites are self-administered into specific brain areas by animals, showing strong reinforcing effects. A wealth of evidence shows that EtOH, a drug consumed to attain millimolar concentrations, generates brain metabolites that are reinforcing at micromolar and nanomolar concentrations. Salsolinol administration leads to marked increases in voluntary EtOH intake, an effect inhibited by mu-opioid receptor blockers. In animals that have ingested EtOH chronically, the maintenance of alcohol intake is no longer influenced by EtOH metabolites, as intake is taken over by other brain systems. However, after EtOH withdrawal brain acetaldehyde has a major role in promoting binge-like drinking in the condition known as the "alcohol deprivation effect"; a condition seen in animals that have ingested alcohol chronically, are deprived of EtOH for extended periods, and are allowed EtOH re-access. The review also analyzes the behavioral effects of acetate, a metabolite that enters the brain and is responsible for motor incoordination at low doses of EtOH. Also discussed are the paradoxical effects of systemic acetaldehyde. Overall, evidence strongly suggests that brain-generated EtOH metabolites play a major role in the early ("first-hit") development of alcohol reinforcement and in the generation of relapse-like drinking.
TL;DR: Evidence suggests that ALDH2 Glu504Lys SNP is a potential candidate genetic risk factor for a variety of chronic diseases such as cardiovascular disease, cancer, and late-onset Alzheimer's disease.
Abstract: Aldehyde dehydrogenase (ALDH) 2 is a mitochondrial enzyme that is known for its important role in oxidation and detoxification of ethanol metabolite acetaldehyde. ALDH2 also metabolizes other reactive aldehydes such as 4-hydroxy-2-nonenal and acrolein. The Glu504Lys single nucleotide polymorphism (SNP) of ALDH2 gene, which is found in approximately 40% of the East Asian populations, causes defect in the enzyme activity of ALDH2, leading to alterations in acetaldehyde metabolism and alcohol-induced "flushing" syndrome. Evidence suggests that ALDH2 Glu504Lys SNP is a potential candidate genetic risk factor for a variety of chronic diseases such as cardiovascular disease, cancer, and late-onset Alzheimer's disease. In addition, the association between ALDH2 Glu504Lys SNP and the development of these chronic diseases appears to be affected by the interaction between the SNP and lifestyle factors such as alcohol consumption as well as by the presence of other genetic variations.
TL;DR: This work generates and characterized a global Aldh1b1 knockout mouse line and shows for the first time the functional in vivo role of ALDH1B1 in acetaldehyde metabolism and in maintaining glucose homeostasis.
TL;DR: A proteomic and exometabolomic study was conducted on Saccharomyces cerevisiae flor yeast strain growing under biofilm formation condition (BFC) with ethanol and glycerol as carbon sources and results were compared with those obtained under no biofilm Formation condition (NBFC) containing glucose as carbon source.
TL;DR: In this article, a few nickel supported platinum-rhodium (Pt-Rh) binary electrodes of varying mutual composition have been constructed by galvanostatic codeposition of Pt-Rh on Ni support from suitable precursors' solutions.