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Acetaldehyde-Related Pathology: Bridging the by Novartis Foundation

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Extra info for Acetaldehyde-Related Pathology: Bridging the Trans-Disciplinary Divide (Novartis Foundation Symposium 285)

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By learning that HeLa cells seem to be making acetaldehyde, we now have to double check what we are thinking when we say that if a certain phenomenon occurs in hepatoma cells but doesn’t occur in HeLa cells, that the explanation is that the phenomenon must be due to alcohol metabolism. We may have been misled. Eriksson: It is difficult to extrapolate to in vivo when we go to purer in vitro systems. You can see the difficulty. Based on enzyme kinetics in isolated pure systems the hepatic ratio between acetaldehyde and alcohol is surprisingly high to enable efficient alcohol oxidation.

It has been shown that the pancreas can metabolize alcohol. It has ADH. Interestingly, the kinetics of ADH in the acinar cells of the pancreas seems to match most closely to ADH5. It has a very high Km. In the cells I am interested in, the stellate cells which produce fibrosis, we think we have found ADH1. The problem I have with alcohol and acetaldehyde experiments is that when I read the literature I can’t work out whether people are using the concentrations of either ethanol or acetaldehyde that the cells may actually be exposed to in vivo.

Of course, the various regions of the brain vary in their metabolic capacity. Conventional wisdom is that brain has two to three orders less ethanol metabolic capacity than the liver. We have been measuring some adducts in alcoholic cerebellar degeneration. We are finding a lot more than one would expect. Is there another metabolizing system lurking in the brain that we are not seeing? Crabb: The compiled data in those Unigene sets will just say ‘brain’ without any further anatomical division. I don’t know whether it was libraries made from different regions all combined together, or whether it was whole brain.

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