Eriksson C J Peter
National Public Health Institute, Department of Mental Health and Alcohol Research, Helsinki, Finland.
Novartis Found Symp. 2007;285:247-55; discussion 256-60. doi: 10.1002/9780470511848.ch18.
The aim of the present paper is to update the status regarding human acetaldehyde levels in blood, breath and saliva during normal ethanol oxidation, i.e. without deficiency in, or inhibition of, aldehyde dehydrogenase activity. The previous conclusion according to which no detectable (<0.5 microM), adequately determined 'free and/or loosely bound' acetaldehyde has not yet been found in venous blood, more or less, still holds. The only new findings within this context consist of low venous blood acetaldehyde levels (1-3 microM on average) observed in some women during the use of oral contraceptives or during the high oestradiol phases of normal menstrual cycle. Breath acetaldehyde levels are about 10-20 and 20-40nM at blood ethanol concentrations of about 10 and 20mM, respectively. Theoretically calculated corresponding blood acetaldehyde levels in pulmonary blood would be about 2-4 and 4-8 microM. The acetaldehyde in the breath most likely reflects pulmonary blood acetaldehyde, microbial and tissue acetaldehyde production in the aerodigestive tract. As well as with breath acetaldehyde, salivary acetaldehyde levels also correlate positively with the blood ethanol concentrations. At blood ethanol concentrations of about 10 and 20 mM the average acetaldehyde concentration in saliva is about 15-25 and 20-40 microM, respectively. Saliva acetaldehyde represents mostly microbial acetaldehyde formation in the oral cavity, but also, to some extent, ethanol oxidation in nearby tissues. More studies are still needed to clarify the proportion of the underlying sources for blood, breath and salivary acetaldehyde at different ethanol concentrations. The problem with rapid acetaldehyde oxidation, which may markedly affect the recovery of low acetaldehyde levels, also needs to be solved.
本文的目的是更新关于正常乙醇氧化过程中人体血液、呼出气体和唾液中乙醛水平的现状,即不存在乙醛脱氢酶活性缺乏或抑制的情况。之前得出的结论是,在静脉血中尚未发现可检测到的(<0.5微摩尔)、充分测定的“游离和/或松散结合”的乙醛,或多或少,这一结论仍然成立。在此背景下,唯一的新发现是,一些女性在使用口服避孕药期间或正常月经周期的高雌二醇阶段,观察到静脉血中乙醛水平较低(平均为1 - 3微摩尔)。当血液乙醇浓度分别约为10和20毫摩尔时,呼出气体中的乙醛水平分别约为10 - 20纳摩尔和20 - 40纳摩尔。理论计算得出的肺血中相应的乙醛水平约为2 - 4微摩尔和4 - 8微摩尔。呼出气体中的乙醛很可能反映了肺血中的乙醛、呼吸道微生物和组织产生的乙醛。与呼出气体中的乙醛一样,唾液中的乙醛水平也与血液乙醇浓度呈正相关。当血液乙醇浓度约为10和20毫摩尔时,唾液中乙醛的平均浓度分别约为15 - 25微摩尔和20 - 40微摩尔。唾液中的乙醛主要代表口腔中微生物产生的乙醛,但在一定程度上也代表附近组织中的乙醇氧化。仍需要更多研究来阐明在不同乙醇浓度下,血液、呼出气体和唾液中乙醛潜在来源的比例。快速乙醛氧化的问题可能会显著影响低乙醛水平的恢复,这一问题也需要解决。