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Extra info for Acetaldehyde-Related Pathology: Bridging the Trans-Disciplinary Divide (Novartis Foundation Symposium 285)
There are no other findings that have been reproduced in other laboratories and with other populations. He kids that I did well to stop working in this area because he has been frustrated by the inability to identify stronger correlations. He has one of the best databases of patients who have been well-characterized for alcoholic liver disease without hepatitis C. I believe one comes close to having a ACETALDEHYDE GENERATING ENZYME SYSTEMS 19 genetic risk factor if you combine several studies from Japan.
The authors proposed an interesting hypothesis to explain this finding. ‘ALDH2 is the key enzyme for detoxifying the various aldehydes such as, not only acetaldehyde, but also 4-hydroxy-2-nonenal (4-HNE). 4-HNE is the by-product of lipid peroxidation. Therefore, in a chronic situation of diabetes (in the mother), increased tissue levels of 4-HNE could result from inactive ALDH2. Because 4-HNE reacts preferentially with sulfhydryl (SH)-containing molecules, the mitochondrial inner membrane is easily adducted with 4-HNE.
A deficiency of ALDH2 in Asian populations is protective against development of alcoholism (Goedde et al 1992, Harada et al 1999, Xiao et al 1996, Yamamoto et al 2000) and perhaps carotid atherosclerosis (Narita et al 2003). However, this deficiency also has potentially severe consequences for those individuals who continue to consume ethanol and possibly in those that do not consume ethanol at all. There is a comprehensive analysis of the relationship between ADH1 and ALDH2 genotypes and head and neck cancer (Brennan et al 2004).