Contribution of oropharynx microflora and of lung microsomes to acetaldehyde in expired air after alcohol ingestion
Pikkarainen, P.H.; Baraona, E.; Jauhonen, P.; Seitz, H.K.; Lieber, C.S.
Journal of Laboratory and Clinical Medicine 97(5): 631-636
1981
ISSN/ISBN: 0022-2143 PMID: 7194361 Document Number: 171044
After ethanol administration acetaldehyde is found in expired air. Breath ethanol and acetaldehyde are thought to originate from blood. The ratio of acetaldehyde to ethanol was higher in dead space than in alveolar air, suggesting formation of acetaldehyde in the airways. To study this, normal subjects washed their mouth with 5 mM ethanol in saline or with saline alone. The washings with ethanol (but not with saline) produced acetaldehyde (5.1 .+-. 1.3 nmol/ml per min). Saline mouthwashings incubated with ethanol produced acetaldehyde in vitro. The reaction had an apparent Km for ethanol of 1.0 mM and a Vmax of 1.27 .+-. 0.34 nmol acetaldehyde/ml per min and was inhibited 75% by 1 mM pyrazole. This acetaldehyde production could be prevented by boiling or by microfiltration of the washings. The in vitro production of acetaldehyde increased after a 24 h culture of oropharynx flora, suggesting that it was due to microbial enzyme. The possibility of pulmonary production of acetaldehyde was studied in rats. Rat lung slices released 1.32 .+-. 0.19 nmol acetaldehyde/g lung wet wt per min into the media when incubated with 50 mM ethanol. Rat lung microsomes produced acetaldehyde from ethanol, which was enhanced by chronic alcohol consumption (2.06 .+-. 0.21 vs. 1.62 .+-. 0.23 nmol acetaldehyde/mg microsomal protein per min in alcohol-fed and controls, respectively; P < 0.005). Breath acetaldehyde originated in part from microbial oxidation of ethanol in oropharynx. This contribution was minimized by taking end-expiratory samples. End-expiratory air could be contaminated by acetaldehyde formed in lung microsomes, an effect that was enhanced by chronic alcohol consumption.