Blood and Urinary Levels of Ethanol, Acetaldehyde, and C4 Compounds Such as Diacetyl, Acetoin, and 2,3-Butanediol in Normal Male Students After Ethanol Ingestion

Otsuka, Masato; Harada, Naoto; Itabashi, Toshie; Ohmori, Shinji

doi:10.1016/s0741-8329(98)00042-1

Cited by 45 publications

(44 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The protein encoded by ALDH2*2 has a Glu to Lys substitution at residue 487, resulting in an inactive subunit and the inability to metabolize acetaldehyde. The ALDH2*2 allele is rare in Western populations but prevalent in East Asian populations including Chinese, Korean, Thai, and Japanese populations (250,251) ALDH2*2/*2 homozygotes have serum acetaldehyde levels that are 13 times higher and heterozygotes have levels 4 times higher than those in *1*1 homozygotes (252). ALDH2*2/*2 homozygotes are characterized by a facial flushing response after alcohol consumption with nausea, drowsiness, headache and other unpleasant symptoms.…”

Section: Alcohol Metabolic Enzymesmentioning

confidence: 99%

Genetic polymorphisms and head and neck cancer risk (Review)

Hiyama¹,

Yoshihara²,

Tanaka³

et al. 2008

Int J Oncol

View full text Add to dashboard Cite

Abstract. The aim of this report is to review and evaluate, in a comprehensive manner, the published data regarding the contribution of genetic polymorphisms to risk of head and neck cancer (HNC). All relevant studies available in MEDLINE and published before July 2007 were identified. Studies carried out in humans that compared HNC patients with at least 1 standard control group were considered for analysis. Two hundred and eighteen publications and 3 published metaanalyses were identified. Seventy-five (34%) studies were conducted in Asian, 72 (33%) in American, and 68 (31%) in European countries. The most widely studied gene was GSTM1 (58 studies), followed by GSTT1 (42 studies), GSTP1 (codon 105, 22 studies) and p53 (codon 72, 20 studies). GSTM1, GSTT1, GSTP1, XRCC1 codons 194 and 399, and CYP1A1 codon 462 were examined by meta-analyses, and significant relations were found between the GSTM1-null genotype and an increased risk for HNC. In addition, increased risk for HNC was associated consistently with the ALDH2*1/*2, p53 codon 72 Pro/Pro and EPHX1 codon 113 Tyr/His and His/His genotypes. Cohort studies that simultaneously consider multiple genetic and environmental factors possibly involved in carcinogenesis of the head and neck are needed to ascertain not only the relative contribution of these factors to tumor development but also the contributions of their putative interactions. IntroductionHead and neck cancers (HNCs), including cancers of the oral cavity, pharynx and larynx, represent the 6 most frequent cancers and the seventh leading cause of cancer-related death worldwide. There are approximately 540,000 new cases and 271,000 deaths annually worldwide for a mortality of approximately 50% (1). HNCs represent approximately 3% of all cancers in the United States whereas these cancers are much more prevalent in other areas of the world, such as India, Thailand and Brazil (1,2). Standard therapeutic approaches, which focus on surgery, irradiation and chemotherapy (alone or in combination), have been modified over the last 30 years; however, the overall survival of HNC patients has not improved substantially. For patients affected by early-stage cancers with a high disease-specific survival rate, secondary tumors represent the most common cause of death (3). Furthermore, patients with advanced cancers have a high risk of primary treatment failure and death.Development of HNC is a multifactorial process associated with a variety of risk factors. Major risk factors in developed countries include smoking tobacco and drinking alcohol, and chewing betel quid (4,5). For tobacco smoking, a dose-response trend has been reported. Relative risks of developing laryngeal and oropharyngeal cancers are 1.8 and 1.3, respectively, for persons who smoke ≤30 cigarettes per day and 7.7 and 2.9, respectively, for persons who smoke >30 cigarettes per day compared with non-smokers (6). Alcohol consumption is also linked to increased risk of HNCs. For persons who consume >4 drinks (=47.5 g of pure ethanol) per day, the relati...

show abstract

Section: Alcohol Metabolic Enzymesmentioning

confidence: 99%

Genetic polymorphisms and head and neck cancer risk (Review)

Hiyama¹,

Yoshihara²,

Tanaka³

et al. 2008

Int J Oncol

View full text Add to dashboard Cite

show abstract

“…Otsuka et al (34) evaluated diacetyl concentration in the plasma of volunteer male students who had ingested ethanol as ranging from 0.25 to 0.75 µM, whereas that of acetoin was about 2.2 µM. Interestingly, 2,3-butanediol raised from 10 to 50 µM in the plasma and from 50 to 300 µM in the urine of an aldehyde dehydrogenase 2 defective student, 3 h after ethanol ingestion.…”

Section: Introductionmentioning

confidence: 99%

Radical Acetylation of 2′-Deoxyguanosine and l-Histidine Coupled to the Reaction of Diacetyl with Peroxynitrite in Aerated Medium

Massari

Fujiy

Dutra

et al. 2008

Chem. Res. Toxicol.

View full text Add to dashboard Cite

Diacetyl, like other alpha-dicarbonyl compounds, is reportedly cytotoxic and genotoxic. A food and cigarette contaminant, it is related with alcohol hepatotoxicity and lung disease. Peroxynitrite is a potent oxidant formed in vivo by the diffusion-controlled reaction of the superoxide radical anion with nitric oxide, which is able to form adducts with carbon dioxide and carbonyl compounds. Here, we investigate the nucleophilic addition of peroxynitrite to diacetyl forming acetyl radicals, whose reaction with molecular oxygen leads to acetate. Peroxynitrite is shown to react with diacetyl in phosphate buffer (bell-shaped pH profile with maximum at 7.2) at a very high rate constant ( k 2 = 1.0 x 10 (4) M (-1) s (-1)) when compared with monocarbonyl substrates ( k 2 < 10 (3) M (-1) s (-1)). Phosphate ions (100-500 mM) do not affect the rate of spontaneous peroxynitrite decay, but the H 2PO 4 (-) anion catalyzes the nucleophilic addition of the peroxynitrite anion to diacetyl. The intermediacy of acetyl radicals is suggested by a three-line spectrum ( a N = a H = 0.83 mT) obtained by EPR spin trapping of the reaction mixture with 2-methyl-2-nitrosopropane. The peroxynitrite reaction is accompanied by concentration-dependent oxygen uptake. Stoichiometric amounts of acetate from millimolar amounts of peroxynitrite and diacetyl were obtained under nonlimiting conditions of dissolved oxygen. In the presence of either l-histidine or 2'-deoxyguanosine, the peroxynitrite/diacetyl system afforded the corresponding acetylated molecules identified by HPLC-MS ( n ). These studies provide evidence that the peroxynitrite/diacetyl reaction yields acetyl radicals and raise the hypothesis that protein and DNA nonenzymatic acetylation may occur in cells and be implicated in aging and metabolic disorders in which oxygen and nitrogen reactive species are putatively involved.

show abstract

“…The half-life of methyl ethyl ketone in serum was 270 minutes, and the clearance time of butane-2,3-diol was 16 hours (DiVincenzo et al, 1976). A proposed pathway of butane-2,3-diol elimination is as 2,3-butanediol betaglucuronide after coupling with UDP-glucuronyltransferase (Otsuka et al, 1999). 4-Hydroxy-4-methylpentan-2-one and 4-methyl-2-pentanol were detected in serum after i.p.…”

Section: Iii3 Studies On Candidate Substancesmentioning

confidence: 99%

Scientific Opinion on Flavouring Group Evaluation 11, Revision 2 (FGE.11Rev2): Aliphatic dialcohols, diketones, and hydroxyketones from chemical groups 8 and 10

Publication¹

2011

EFS2

View full text Add to dashboard Cite

Blood and Urinary Levels of Ethanol, Acetaldehyde, and C4 Compounds Such as Diacetyl, Acetoin, and 2,3-Butanediol in Normal Male Students After Ethanol Ingestion

Cited by 45 publications

References 22 publications

Genetic polymorphisms and head and neck cancer risk (Review)

Genetic polymorphisms and head and neck cancer risk (Review)

Radical Acetylation of 2′-Deoxyguanosine and l-Histidine Coupled to the Reaction of Diacetyl with Peroxynitrite in Aerated Medium

Scientific Opinion on Flavouring Group Evaluation 11, Revision 2 (FGE.11Rev2): Aliphatic dialcohols, diketones, and hydroxyketones from chemical groups 8 and 10

Contact Info

Product

Resources

About