When you cut onions they make you "cry." Why? Is it making YOU cry (a defensive measure against herbivores) or the lachrymatory (tear-producing) effect is purely coincidental
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It should not, directly. Ethanol is metabolized in five ways, three oxidative and two nonoxidative. Alcohol (ADH) and aldehyde dehydrogenases (ALDH)s, cytochromes P450, catalases and phosphlipases should not be affected directly. I think people use raw onions mainly to mask the unpleasant taste of poor quality alcohol. In principle, also, the byproduct of thiopropanal S-oxide is the propanal, which may prime the ALDHs. This is something that my father taught me; you may profit from this bit of biochemistry, too. The dynamics of alcohol metabolism is such that if you drink a lot there is a lag after ADH converts ethanol to ethanal and ALDH converts the latter to acetate: making ALDH2 takes time. So if you drink 50-100 g of alcohol 3-4 hours before going to a party then you'd have elevated concentration of ALDH during serious drinking, the acetylaldehyde is more rapidly removed, and poisoning is minimized. Another reason pre-drinking works might be that it activates cytochrome P450 isozyme in the brain, which is deficient in the ADHs. Given that ethanal binds to cystein, in principle, it is possible that S-containing compounds in onion/garlic that bind stronger can inhibit some of acetylaldehyde poisoning, though only part of it (acetaldehyde mainly binds to lysine rather than the cystein). The lysine residues in the plasma membrane proteins are the prime target. The weird thing is that these adducts are completely harmless. The problem is that the antibodies recognize them as alien proteins and start to destroy the hepatocytes in the liver. Another problem is that the cytochromes produce superoxide radicals (that may be the main mechanism for cirrhosis - the exact one is not known, as far as I know). Antioxidants help there (vitamin C, folic, N-acetyl cystein). So apples (vitamin C) and onions (cystein-related molecules) make a lot of sense as ways to minimize oxidative damage (lipid peroxidation). You should understand that very little is known how alcohol/acetaldehyde hurts us at the molecular level. If you are interested, here is a primer on alcohol biochemistry, http://pubs.niaaa.nih.gov/publications/arh294/245-255.pdf http://www.medigraphic.com/pdfs/hepato/ah-2003/ah032b.pdf here is a different take (acetaldehyde-acetate runaway imbalance in the mitochondria) http://www.elmhurst.edu/~chm/vchembook/642alcoholmet.html The bottom line is that nobody knows exactly why and how oxidative metabolism of ethanol is harming the body. That makes answering your question a hand waving affair. Depending on the mechanism, it may or may not play some role (antioxidants, Cys-binding).
http://pubs.niaaa.nih.gov/publications/arh294/245-255.pdf
http://www.medigraphic.com/pdfs/hepato/ah-2003/ah032b.pdf
here is a different take (acetaldehyde-acetate runaway imbalance in the mitochondria)
http://www.elmhurst.edu/~chm/vchembook/642alcoholmet.html
The bottom line is that nobody knows exactly why and how oxidative metabolism of ethanol is harming the body. That makes answering your question a hand waving affair. Depending on the mechanism, it may or may not play some role (antioxidants, Cys-binding).
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