Jones A W
Department of Alcohol Toxicology, National Laboratory of Forensic Chemistry, Linköping, Sweden.
Alcohol Alcohol. 1995 May;30(3):271-85.
Most of the acetaldehyde generated during the metabolism of ethanol becomes tightly bound to endogenous molecules such as haemoglobin, amino acids and certain phospholipids. Free acetaldehyde passes the blood-brain barrier and traces of this toxic metabolite are excreted through the lungs and can be detected in the expired air. The blood/air partition coefficient of acetaldehyde at 34 degrees C, the average temperature of end-expired air, is about 190:1. Because of various problems associated with measuring acetaldehyde in blood samples, several research groups have instead investigated the analysis of acetaldehyde in breath which offers an indirect and alternative approach for clinical and research purposes. However, care is needed when interpreting the results of breath acetaldehyde measurements, because of the possibility of local formation from microflora inhabiting the upper airways and mouth. The concentration of acetaldehyde exhaled in breath after drinking alcohol demonstrates large inter-individual differences depending on various genetic (racial) and environmental factors. Moreover, acetaldehyde is an endogenous metabolite and even without drinking any alcohol the concentrations expelled in breath span from 0.2 to 0.6 nmol/l, with higher levels observed in smokers and abstinent alcoholics. Breath acetaldehyde concentration reached between 5 and 50 nmol/l in European subjects who drank a moderate dose of ethanol (0.4-0.8 g/kg), with the highest values seen in smokers. The concentration of breath acetaldehyde in Japanese subjects after drinking alcohol reached between 200 and 500 nmol/l at the peak. These much higher levels follow because a large proportion of Orientals (40-50%) inherit an inactive form of the low Km mitochondrial isoenzyme of aldehyde dehydrogenase (ALDH2). The highest concentration of breath acetaldehyde were seen in healthy Caucasians who drank a small dose of alcohol (0.25 g/kg) after taking the alcohol-sensitizing drug calcium carbimide, which blocks the action of ALDH isozymes. During the most intense acetaldehyde-flush reaction, breath acetaldehyde reached between 200 and 1300 nmol/l, but even these abnormally high concentrations did not interfere with the analysis of ethanol in breath by means of non-specific infrared analysers currently used in many countries for testing drinking drivers.
乙醇代谢过程中产生的大部分乙醛会与血红蛋白、氨基酸和某些磷脂等内源性分子紧密结合。游离的乙醛可穿过血脑屏障，这种有毒代谢物的微量成分会通过肺部排出，并可在呼出的气体中检测到。在呼出气体的平均温度34摄氏度下，乙醛的血/气分配系数约为190:1。由于在血液样本中测量乙醛存在各种问题，几个研究小组转而研究了呼气中乙醛的分析，这为临床和研究目的提供了一种间接的替代方法。然而，在解释呼气乙醛测量结果时需要谨慎，因为上呼吸道和口腔中的微生物群落可能会在局部形成乙醛。饮酒后呼出气体中的乙醛浓度因各种遗传（种族）和环境因素而存在很大的个体差异。此外，乙醛是一种内源性代谢物，即使不饮酒，呼出气体中的乙醛浓度范围也在0.2至0.6纳摩尔/升之间，吸烟者和戒酒的酗酒者中观察到的水平更高。在饮用中等剂量乙醇（0.4 - 0.8克/千克）的欧洲受试者中，呼气乙醛浓度达到5至50纳摩尔/升，吸烟者中的值最高。日本受试者饮酒后呼气乙醛浓度在峰值时达到200至500纳摩尔/升。这些水平高得多是因为很大一部分东方人（40 - 50%）继承了一种无活性形式的低Km线粒体醛脱氢酶（ALDH2）同工酶。在服用酒精敏感药物卡马西平后饮用少量酒精（0.25克/千克）的健康白种人中，观察到呼气乙醛浓度最高。在最强烈的乙醛潮红反应期间，呼气乙醛浓度达到200至1300纳摩尔/升，但即使是这些异常高的浓度也不会干扰目前许多国家用于检测酒驾司机的非特异性红外分析仪对呼气中乙醇的分析。
