High and complementary expression patterns of alcohol and aldehyde dehydrogenases in the gastrointestinal tract: implications for Parkinson's disease.
High and complementary expression patterns of alcohol and aldehyde dehydrogenases in the gastrointestinal tract: implications for Parkinson's disease.
复制标题
胃肠道中乙醇和乙醛脱氢酶的高且互补的表达模式：对帕金森病的影响。
DOI：
10.1111/j.1742-4658.2007.05665.x
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发表时间：
2007
期刊：
影响因子：
--
通讯作者：
Galter,Dagmar
中科院分区：
文献类型：
--
作者：
Westerlund,Marie;Belin,AndreaCarmine;Felder,MichaelR;Olson,Lars;Galter,Dagmar
Parkinson's disease (PD) is a heterogeneous movement disorder characterized by progressive degeneration of dopamine neurons in substantia nigra. We have previously presented genetic evidence for the possible involvement of alcohol and aldehyde dehydrogenases (ADH; ALDH) by identifying genetic variants in ADH1C and ADH4 that associate with PD. The absence of the corresponding mRNA species in the brain led us to the hypothesis that one cause of PD could be defects in the defense systems against toxic aldehydes in the gastrointestinal tract. We investigated cellular expression ofAdh1,Adh3,Adh4andAldh1mRNA along the rodent GI tract. Using oligonucleotidein situhybridization probes, we were able to resolve the specific distribution patterns of closely related members of the ADH family. In both mice and rats,Adh4is transcribed in the epithelium of tongue, esophagus and stomach, whereasAdh1was active from stomach to rectum in mice, and in duodenum, colon and rectum in rats.Adh1andAdh4mRNAs were present in the mouse gastric mucosa in nonoverlapping patterns, withAdh1in the gastric glands andAdh4in the gastric pits.Aldh1was found in epithelial cells from tongue to jejunum in rats and from esophagus to colon in mice.Adh3hybridization revealed low mRNA levels in all tissues investigated. The distribution and known physiological functions of the investigated ADHs andAldh1are compatible with a role in a defense system, protecting against alcohols, aldehydes and formaldehydes as well as being involved in retinoid metabolism.
