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Brazilian Journal of Microbiology :... 2016In this study a natural culture medium that mimics the synthetic yeast peptone glucose medium used for yeast fermentations was designed to screen and select yeasts...
In this study a natural culture medium that mimics the synthetic yeast peptone glucose medium used for yeast fermentations was designed to screen and select yeasts capable of producing high levels of diacetyl and acetaldehyde. The presence of whey powder and sodium citrate in the medium along with manganese and magnesium sulfate enhanced both biomass and aroma development. A total of 52 yeasts strains were cultivated in two different culture media, namely, yeast peptone glucose medium and yeast acetaldehyde-diacetyl medium. The initial screening of the strains was based on the qualitative reaction of the acetaldehyde with Schiff's reagent (violet color) and diacetyl with Brady's reagent (yellow precipitate). The fermented culture media of 10 yeast strains were subsequently analyzed by gas chromatography to quantify the concentration of acetaldehyde and diacetyl synthesized. Total titratable acidity values indicated that a total titratable acidity of 5.5°SH, implying culture medium at basic pH, was more favorable for the acetaldehyde biosynthesis using strain D15 (Candida lipolytica; 96.05mgL acetaldehyde) while a total titratable acidity value of 7°SH facilitated diacetyl flavor synthesis by strain D38 (Candida globosa; 3.58mgL diacetyl). Importantly, the results presented here suggest that this can be potentially used in the baking industry.
Topics: Acetaldehyde; Diacetyl; Energy Metabolism; Fermentation; Metabolome; Metabolomics; Yeasts
PubMed: 27528084
DOI: 10.1016/j.bjm.2016.07.005 -
Fa Yi Xue Za Zhi Oct 2019Objective To explore the change rules of blood ethanol and blood acetaldehyde concentration, the impairment of psychomotor functions of different acetaldehyde...
Objective To explore the change rules of blood ethanol and blood acetaldehyde concentration, the impairment of psychomotor functions of different acetaldehyde dehydrogenase (ALDH) 2 genotype individuals after alcohol consumption and the relationship among them. Methods The genotypes in seventy-nine healthy volunteers were obtained by SNaPshot method, then divided into (wild type) and (mutant type) group. After volunteers consumed 1.0 g/kg of alcohol, blood ethanol concentration and blood acetaldehyde concentration at a series of time points before and after alcohol consumption and psychomotor functions, such as, visual selective response time, auditory simple response time and tracking experiment were detected. Biphasic alcohol response questionnaires were collected. Results After alcohol consumption, group's blood ethanol and blood acetaldehyde concentration reached the peak earlier than group. Its blood acetaldehyde concentration was higher than that of group, 1-6 h after alcohol consumption. The psychomotor functions, such as visual selective response time and auditory simple response time in group were more significantly impaired than those in group after alcohol consumption. There was no statistical significance between the two groups in excitement or sedation reactions (>0.05). Pearson correlation coefficient test showed that blood acetaldehyde concentration was related with psychomotor function. Conclusion There are significant differences between the psychomotor function of wild type and mutant type individuals after alcohol consumption estimated to be related to the difference in blood acetaldehyde concentration after alcohol consumption.
Topics: Acetaldehyde; Alcohol Drinking; Aldehyde Dehydrogenase; Aldehyde Dehydrogenase, Mitochondrial; Aldehyde Oxidoreductases; Ethanol; Genotype; Humans; Polymorphism, Genetic; Psychomotor Performance
PubMed: 31833292
DOI: 10.12116/j.issn.1004-5619.2019.05.012 -
Nucleic Acids Research Jul 2022Acetaldehyde (AA), a by-product of ethanol metabolism, is acutely toxic due to its ability to react with various biological molecules including DNA and proteins, which...
Acetaldehyde (AA), a by-product of ethanol metabolism, is acutely toxic due to its ability to react with various biological molecules including DNA and proteins, which can greatly impede key processes such as replication and transcription and lead to DNA damage. As such AA is classified as a group 1 carcinogen by the International Agency for Research on Cancer (IARC). Previous in vitro studies have shown that AA generates bulky adducts on DNA, with signature guanine-centered (GG→TT) mutations. However, due to its weak mutagenicity, short chemical half-life, and the absence of powerful genetic assays, there is considerable variability in reporting the mutagenic effects of AA in vivo. Here, we used an established yeast genetic reporter system and demonstrate that AA treatment is highly mutagenic to cells and leads to strand-biased mutations on guanines (G→T) at a high frequency on single stranded DNA (ssDNA). We further demonstrate that AA-derived mutations occur through lesion bypass on ssDNA by the translesion polymerase Polζ. Finally, we describe a unique mutation signature for AA, which we then identify in several whole-genome and -exome sequenced cancers, particularly those associated with alcohol consumption. Our study proposes a key mechanism underlying carcinogenesis by acetaldehyde-mutagenesis of single-stranded DNA.
Topics: Acetaldehyde; DNA; DNA Adducts; DNA Damage; DNA Replication; DNA, Single-Stranded; Guanine; Mutagenesis; Mutagens; Mutation
PubMed: 35776120
DOI: 10.1093/nar/gkac570 -
Alcoholism, Clinical and Experimental... Jun 2019We previously developed enzyme nanoparticles (ENP) of alcohol metabolism. This study was to evaluate protective effects of facilitated removal of blood alcohol and/or... (Comparative Study)
Comparative Study
BACKGROUND
We previously developed enzyme nanoparticles (ENP) of alcohol metabolism. This study was to evaluate protective effects of facilitated removal of blood alcohol and/or acetaldehyde on anti-HIV drugs and alcohol-induced liver injuries.
METHODS
ENP were prepared for degrading alcohol completely (ENP1) or partially into acetaldehyde (ENP2), which were applied to mice of acute binge or chronic-binge alcohol feeding in the presence of antivirals (ritonavir and lopinavir). Liver pathologies were examined to assess the protective effects of ENP.
RESULTS
In the acute model, ENP1 and ENP2 reduced the blood alcohol concentration (BAC) by 41 and 32%, respectively, within 4 hr, whereas in control without ENP, BAC was reduced only by 15%. Blood acetaldehyde concentration (BADC) was increased by 39% in alcohol-fed mice treated with ENP2 comparing to control. No significant effects of the anti-HIV drugs on BAC or BADC were observed. Plasma alanine aminotransferase (ALT) and expression of liver TNF-α were both significantly increased in the alcohol-fed mice, which were normalized by ENP1. In the presence of the antivirals, ALT was partially reduced by ENP1 or ENP2. In the chronic model, inflammation, fatty liver, and ALT were increased, which were deteriorated by the antivirals. ENP1 partially reduced BAC, BADC, ALT, and expression of inflammation markers of TNF-α, F4/80, and IL-6 and lipogenic factors of ACC, LXRα, and SREBP1. ENP2 reduced BAC without significant effects on ALT, inflammation, or lipogenesis. Antivirals and alcohol synergistically increased expression of organelle stress markers of CHOP, sXBP-1, ATF6, and GCP60. ENP1 reduced BAC, CHOP, and sXbp-1. However, no effects of ENP1 were found on ATF6 or GCP60.
CONCLUSIONS
Removal of blood alcohol and acetaldehyde by the ENP protects the liver against alcoholic injuries, and the protection is less effective in chronic alcohol and antiviral feeding due to additional drug-induced organelle stresses.
Topics: Acetaldehyde; Alcohol Oxidoreductases; Aldehyde Dehydrogenase; Animals; Anti-HIV Agents; Catalase; Drug Evaluation, Preclinical; Ethanol; Liver Diseases, Alcoholic; Male; Mice, Inbred C57BL; Nanoparticles
PubMed: 30908665
DOI: 10.1111/acer.14034 -
Molecules (Basel, Switzerland) Apr 2022Acetaldehyde is a critical reactant on modifying the phenolic profile during red wine aging, suggesting that the acetaldehyde-mediated condensation can be responsible...
Acetaldehyde is a critical reactant on modifying the phenolic profile during red wine aging, suggesting that the acetaldehyde-mediated condensation can be responsible for the variation of antioxidant activity during the aging of this beverage. The present study employs exogenous acetaldehyde at six levels of treatment (7.86 ± 0.10-259.02 ± 4.95 mg/L) before the bottle aging of Merlot wines to encourage phenolic modification. Acetaldehyde and antioxidant activity of wine were evaluated at 0, 15, 30, 45, 60 and 75 days of storage, while monomeric and polymeric phenolics were analyzed at 0, 30 and 75 days of storage. The loss of acetaldehyde was fitted to a first-order reaction model, the rate constant (k) demonstrated that different chemical reaction happened in wines containing a different initial acetaldehyde. The disappearance of monomeric phenolics and the formation of polymeric phenolics induced by acetaldehyde could be divided into two phases, the antioxidant activity of wine did not alter significantly in the first phase, although most monomeric phenolics vanished, but the second phase would dramatically reduce the antioxidant activity of wine. Furthermore, a higher level of acetaldehyde could shorten the reaction time of the first phase. These results indicate that careful vinification handling aiming at controlling the acetaldehyde allows one to maintain prolonged biological activity during wine aging.
Topics: Acetaldehyde; Anthocyanins; Antioxidants; Phenols; Vitis; Wine
PubMed: 35565959
DOI: 10.3390/molecules27092608 -
G3 (Bethesda, Md.) Nov 2022Formaldehyde and acetaldehyde are reactive small molecules produced endogenously in cells as well as being environmental contaminants. Both of these small aldehydes are...
Formaldehyde and acetaldehyde are reactive small molecules produced endogenously in cells as well as being environmental contaminants. Both of these small aldehydes are classified as human carcinogens, since they are known to damage DNA and exposure is linked to cancer incidence. However, the mutagenic properties of formaldehyde and acetaldehyde remain incompletely understood, at least in part because they are relatively weak mutagens. Here, we use a highly sensitive yeast genetic reporter system featuring controlled generation of long single-stranded DNA regions to show that both small aldehydes induced mutational patterns characterized by predominantly C/G → A/T, C/G → T/A, and T/A → C/G substitutions, each in similar proportions. We observed an excess of C/G → A/T transversions when compared to mock-treated controls. Many of these C/G → A/T transversions occurred at TC/GA motifs. Interestingly, the formaldehyde mutational pattern resembles single base substitution signature 40 from the Catalog of Somatic Mutations in Cancer. Single base substitution signature 40 is a mutational signature of unknown etiology. We also noted that acetaldehyde treatment caused an excess of deletion events longer than 4 bases while formaldehyde did not. This latter result could be another distinguishing feature between the mutational patterns of these simple aldehydes. These findings shed new light on the characteristics of 2 important, commonly occurring mutagens.
Topics: Humans; Acetaldehyde; DNA Mutational Analysis; Formaldehyde; Mutagens; Mutation; Neoplasms; Yeasts
PubMed: 36073936
DOI: 10.1093/g3journal/jkac238 -
PLoS Computational Biology Aug 2021Ethanol is one of the most widely used recreational substances in the world and due to its ubiquitous use, ethanol abuse has been the cause of over 3.3 million deaths...
Integration of a physiologically-based pharmacokinetic model with a whole-body, organ-resolved genome-scale model for characterization of ethanol and acetaldehyde metabolism.
Ethanol is one of the most widely used recreational substances in the world and due to its ubiquitous use, ethanol abuse has been the cause of over 3.3 million deaths each year. In addition to its effects, ethanol's primary metabolite, acetaldehyde, is a carcinogen that can cause symptoms of facial flushing, headaches, and nausea. How strongly ethanol or acetaldehyde affects an individual depends highly on the genetic polymorphisms of certain genes. In particular, the genetic polymorphisms of mitochondrial aldehyde dehydrogenase, ALDH2, play a large role in the metabolism of acetaldehyde. Thus, it is important to characterize how genetic variations can lead to different exposures and responses to ethanol and acetaldehyde. While the pharmacokinetics of ethanol metabolism through alcohol dehydrogenase have been thoroughly explored in previous studies, in this paper, we combined a base physiologically-based pharmacokinetic (PBPK) model with a whole-body genome-scale model (WBM) to gain further insight into the effect of other less explored processes and genetic variations on ethanol metabolism. This combined model was fit to clinical data and used to show the effect of alcohol concentrations, organ damage, ALDH2 enzyme polymorphisms, and ALDH2-inhibiting drug disulfiram on ethanol and acetaldehyde exposure. Through estimating the reaction rates of auxiliary processes with dynamic Flux Balance Analysis, The PBPK-WBM was able to navigate around a lack of kinetic constants traditionally associated with PK modelling and demonstrate the compensatory effects of the body in response to decreased liver enzyme expression. Additionally, the model demonstrated that acetaldehyde exposure increased with higher dosages of disulfiram and decreased ALDH2 efficiency, and that moderate consumption rates of ethanol could lead to unexpected accumulations in acetaldehyde. This modelling framework combines the comprehensive steady-state analyses from genome-scale models with the dynamics of traditional PK models to create a highly personalized form of PBPK modelling that can push the boundaries of precision medicine.
Topics: Acetaldehyde; Acetaldehyde Dehydrogenase Inhibitors; Alcohol Deterrents; Alcoholism; Aldehyde Dehydrogenase, Mitochondrial; Computational Biology; Computer Simulation; Disulfiram; Ethanol; Humans; Intestinal Absorption; Kinetics; Liver; Male; Models, Biological; Tissue Distribution
PubMed: 34351898
DOI: 10.1371/journal.pcbi.1009110 -
Journal of the Air & Waste Management... Dec 2020In the 2014 National Air Toxics Assessment (NATA), the carbonyl compounds formaldehyde and acetaldehyde were identified as key cancer risk drivers and acrolein was...
In the 2014 National Air Toxics Assessment (NATA), the carbonyl compounds formaldehyde and acetaldehyde were identified as key cancer risk drivers and acrolein was identified as one of the three air toxics that drive most of the noncancer risk. In this assessment, averaged across the Continental United States, about 75% of ambient formaldehyde and acetaldehyde, and about 18% of acrolein, is formed secondarily. This study was conducted to estimate the potential contribution to these secondarily formed carbonyl compounds from mobile sources. To develop such estimates, we conducted several CMAQ runs, where emissions are set to zero for different mobile source sectors, to determine their potential contribution. Although zeroing out emissions from an individual sector can offer only a rough approximation of how the sector might contribute to overall secondary concentrations, our results suggest that across the U. S., mobile sources contribute about 6-18% to secondary formaldehyde, 0-10% to secondary acetaldehyde, and 0-70% to secondary acrolein, depending on location. : Photochemical modeling of carbonyl compounds was conducted with emissions set to zero for various mobile source sectors to determine their contribution to secondary concentrations. Results indicated mobile sources contributed to total and secondary concentrations of formaldehyde, acetaldehyde, and acrolein in many locations across the U.S. with acrolein the dominant contributor in some locations. However, biogenic sources dominated secondary formaldehyde and acetaldehyde, and fires dominated secondary acrolein.
Topics: Acetaldehyde; Acrolein; Air Pollutants; Formaldehyde; Models, Theoretical; United States
PubMed: 32841108
DOI: 10.1080/10962247.2020.1813839 -
Journal of Applied Oral Science :... 2015Acetaldehyde is the first metabolite of ethanol and is produced in the epithelium by mucosal ALDH, while higher levels are derived from microbial oxidation of ethanol by...
OBJECTIVE
Acetaldehyde is the first metabolite of ethanol and is produced in the epithelium by mucosal ALDH, while higher levels are derived from microbial oxidation of ethanol by oral microflora such as Candida species. However, it is uncertain whether acetaldehyde concentration in human breath is related to oral condition or local production of acetaldehyde by oral microflora. The aim of this pilot study was to investigate the relationship between physiological acetaldehyde concentration and oral condition in healthy volunteers.
MATERIAL AND METHODS
Sixty-five volunteers (51 males and 14 females, aged from 20 to 87 years old) participated in the present study. Acetaldehyde concentration in mouth air was measured using a portable monitor. Oral examination, detection of oral Candida species and assessment of alcohol sensitivity were performed.
RESULTS
Acetaldehyde concentration [median (25%, 75%)] in mouth air was 170.7 (73.5, 306.3) ppb. Acetaldehyde concentration in participants with a tongue coating status score of 3 was significantly higher than in those with a score of 1 (p<0.017). After removing tongue coating, acetaldehyde concentration decreased significantly (p<0.05). Acetaldehyde concentration was not correlated with other clinical parameters, presence of Candida species, smoking status or alcohol sensitivity.
CONCLUSION
Physiological acetaldehyde concentration in mouth air was associated with tongue coating volume.
Topics: Acetaldehyde; Adult; Aged; Aged, 80 and over; Candida albicans; Cross-Sectional Studies; Ethanol; Female; Humans; Male; Microbiota; Middle Aged; Mouth; Mouth Breathing; Reference Values; Sex Factors; Statistics, Nonparametric; Surveys and Questionnaires; Time Factors; Tongue; Young Adult
PubMed: 25760268
DOI: 10.1590/1678-775720140223 -
Regulatory Toxicology and Pharmacology... Jun 2017Humans are cumulatively exposed to acetaldehyde from various sources including alcoholic beverages, tobacco smoke, foods and beverages. The genetic-epidemiologic and...
Humans are cumulatively exposed to acetaldehyde from various sources including alcoholic beverages, tobacco smoke, foods and beverages. The genetic-epidemiologic and biochemical evidence in ALDH2-deficient humans provides strong evidence for the causal relationship between acetaldehyde-exposure due to alcohol consumption and cancer of the upper digestive tract. The risk assessment has so far relied on thresholds based on animal toxicology with lower one-sided confidence limit of the benchmark dose values (BMDL) typically ranging between 11 and 63 mg/kg bodyweight (bw)/day dependent on species and endpoint. The animal data is problematic for regulatory toxicology for various reasons (lack in study quality, problems in animal models and appropriateness of endpoints - especially cancer - for transfer to humans). In this study, data from genetic epidemiologic and biochemical studies are reviewed. The increase in the daily exposure dose to acetaldehyde in alcohol-consuming ALDH2-deficients vs. ALDH2-actives was about twofold. The acetaldehyde increase due to ALDH2 inactivity was calculated to be 6.7 μg/kg bw/day for heavy drinkers, which is associated with odds ratios of up to 7 for head and neck as well as oesophageal cancer. Previous animal toxicology based risk assessments may have underestimated the risk of acetaldehyde. Risk assessments of acetaldehyde need to be revised using this updated evidence.
Topics: Acetaldehyde; Alcohol Drinking; Aldehyde Dehydrogenase, Mitochondrial; Animals; Carcinogens; Ethanol; Humans; Saliva
PubMed: 28257851
DOI: 10.1016/j.yrtph.2017.02.024