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Background  Aldehyde dehydrogenases (ALDHs) play a major role in detoxification of aldehydes. High expression of ALDHs is a marker for stem cells of many organs including the lungs. A common polymorphism in  ALDH2  gene ( ALDH2*2 ) results in inactivation of the enzyme and is associated with alcohol flushing syndrome and increased risk for cardiovascular and Alzheimer’s diseases and some cancers. The effect of this  ALDH2  polymorphism on the lung and its stem cells has not been thoroughly examined.    Methods  We examined the association between the  ALDH2*2  allele and lung function parameters in a population of healthy individuals. We also examined its association with the incidence of asthma and COPD in patient cohorts. We used the in vitro colony forming assay to detect the effect of the polymorphism on lung epithelial stem cells from both primary human surgical samples and  Aldh2*2  transgenic (Tg) and  Aldh2   −/−  mice. Response to acute and chronic lung injuries was compared between wild type (WT),  Aldh2*2  Tg and  Aldh2   −/−  mice.    Results  In humans, the  ALDH2*2  allele was associated with lower FEV1/FVC in the general population, but not with the development of asthma or COPD. Both the bronchial and lung epithelium carrying the  ALDH2*2  allele showed a tendency for lower colony forming efficiency (CFE) compared to  ALDH2  allele. In mice, the tracheal epithelial thickness, nuclear density, and number of basal stem cells were significantly lower in  Aldh2    −/−   and  Aldh2*2  Tg adult mice than in WT. Electron microscopy showed significantly increased number of morphologically abnormal mitochondria in the trachea of  Aldh2   −/−  mice.  Aldh2   −/−  tracheal and lung cells showed higher ROS levels and fewer functional mitochondria than those from WT mice. No significant differences were detected when tracheal and lung epithelial stem cells were examined for their in vitro CFE. When exposed to chronic cigarette smoke,  Aldh2*2  Tg mice were resistant to emphysema development, whereas influenza infection caused more epithelial damage in  Aldh2   −/−  mice than in WT mice.    Conclusions    ALDH2  polymorphism has several subtle effects on the lungs, some of which are similar to changes observed during normal aging, suggesting a “premature lung aging” effect.

Effects of the common polymorphism in the human aldehyde dehydrogenase 2 (ALDH2) gene on the lung