Re: Detoxifying acetaldahyde

Since aldehydes are so reactive and potentially damaging to cellular structures it would be surprising if the body did not have multiple techniques for dealing with them. The dipeptide carnosine which is highly concentrated in muscle and brain tissues has the ability to scavenge aldehydes formed from the peroxidation of cell membrane fatty acids during oxidative stress. Carnosine can be manufactured in the body by carnosine synthase from L-histidine and beta-alanine with meat (beef/lamb) being its main dietary source.



The noticeable difference between carnosine and previous acetaldehyde scavengers discussed in this chain is that there are no sulfur atoms in its structure. However, it does have a long "tail" connected to the imidazole ring. One of the proposed structures for the method of aldehyde scavenging is the incorporation of the reactive carbonyl carbon into an additional ring structure formed by the combination of this tail and the aldehyde group via non-enzymatic folding of the tail back onto the original ring. Although acetaldehyde is a much smaller entity than a peroxidized fatty acid, presumably carnosine would react with it as well in a similar manner.



The reactive carbon (shown as *C) from acetaldehyde has been "herded into a paddock" and is no longer a threat to other molecular structures In the body.

See http://www.sciencedirect.com/science/article/pii/S1357272598000600

Since carnosine has been reported to have beneficial effects in numerous apparently unrelated conditions (autism, epilepsy, Parkinson's, schizophrenia) and since carnosine is a naturally occurring aldehyde scavenger in the body, this adds credence to the premise being explored in this series of posts -- namely that acetaldehyde being emitted from budding yeast (Candida Albicans) metabolism is the underlying driving force in a wide variety of disease processes. It also suggests that the normal aldehyde scavenging and detoxifying mechanisms are overloaded because of acetaldehyde levels far in excess of the body's ability to cope.

Again, however, just because a substance can scavenge or detoxify acetaldehyde does not necessarily mean that it is without possible side effects of its own. Normally the body self-regulates the concentration of carnosine with the enzyme carnosinase that splits the dipeptide back into its amino acid constituents. There is a rare autosomal recessive metabolic disorder, carnosinemia, that occurs when there is a deficiency of this enzyme. Severe and potentially debilitating neurological symptoms occur when carnosine levels are too high. The risk associated with excessive carnosine supplementation is that side effects similar to this genetic disorder may be provoked.

A less risk-prone strategy, assuming that acetaldehyde scavenging is the reason for the beneficial effects of supplemental carnosine, would be to reduce the levels of acetaldehyde at its source of production via yeast abatement.
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