Acetaldehyde and quinones by #147951 Blog entry

Blog: Minimalist Yeast Abatement Protocol
by #147951

Acetaldehyde and quinones

Explores the interaction between acetaldehyde and quinones (CoQ10, Vitamin K, Lapachol)

Date: 9/27/2012 3:32:44 PM ( 12 y ) ... viewed 5369 times

When the hydrogen atom joined to a carbonyl (C=O), something that is the distinguishing feature of an aldehyde, is another carbon-containing side group instead, then the structure is known as a ketone. A quinone contains a pair of ketones on a cyclic ring. Quinones are particularly interesting from an acetaldehyde perspective because they occur frequently in nature and in vital body nutrients.

One of the simplest quinone structures is 1,4-benzoquinone:

In the case of a quinone undergoing an acylation with acetaldehyde, the acetyl group can add either to one of the carbonyl oxygens [1] or to a carbon beside this group [2]:

Quinone derivatives have been shown to lower blood and liver acetaldehyde levels suggesting that some type of acylation of this nature may be favorable in the body [3]. With quinone structures being a potential acetaldehyde sink, then it might be expected that critical substances that are based upon quinone backbones may be subject to interference from yeast-released acetaldehyde.

Coenzyme Q10 (ubiquinone) is a vital part of the body's energy metabolism at the aerobic cellular respiration level:

Its function is coupled to the energy storing molecule ATP (Adenosine-5'-triphosphate) with the most energy-demanding organs (heart, liver, and kidney) having commensurately high CoQ10 concentrations. Acetaldehyde interference with the quinone carbonyls of CoQ10 could introduce a significant deficit in the body's energy metabolism with chronic fatigue the result.

Although CoQ10 can be biosynthesized in the body, it requires sufficient acetyl-CoA, something whose production depends upon an enzyme-bound acetaldehyde to lipoic acid interaction that may also be subject to rogue acetaldehyde interference:

See "Acetaldehyde + Acetyl-CoA Production" http://curezone.com/forums/fm.asp?i=1955511

The body's CoQ10 status can also be impacted by statin-type drugs that block HMG Co-A reductase in the mevalonate pathway shared by both CoQ10 and cholesterol synthesis. Interestingly, although not a quinone, lovastatin, has carbonyl esters that may provide binding sites for acetaldehyde:

Since there are several possible pathways for acetaldehyde interference with cholesterol levels:

See "Acetaldehyde + LDL Receptors" http://curezone.com/forums/fm.asp?i=1961332

See "Acetaldehyde + Cholesterol" http://curezone.com/forums/fm.asp?i=1961488

See "Acetaldehyde + Cholesterol Sulfate" http://curezone.com/forums/fm.asp?i=1969857

the acetaldehyde scavenging potential of a statin could in part be an "off-label" reason why statins appear to normalize cholesterol metabolism. Unfortunately, statins carry a heavy burden of side effects, either because of, or in addition to, their impact on CoQ10 production [4].

All of the structurally similar, fat-soluble vitamins known as vitamin K are derivatives of a quinone ring structure. Vitamin K is utilized in the blood coagulation process as well as for maintenance of bone and other tissue.

Menadione (vitamin K3) is a synthetic compound that has vitamin K activity:

The naturally occurring forms, phylloquinone (vitamin K1) and menaquinone (vitamin K2) have longer side-chain tails than the synthetic form.

The potential effectiveness of supplemental phylloquinone and menaquinone in the treatment of osteoporosis and arterial calcification [5] suggest that acetaldehyde disruption of these essential quinones may play a causal role in these disease conditions. Synthetic menadione has a higher toxicity profile [6] than its counterparts with their long lipophilic tails.

Lapachol from Pau D'arco used to make Taheebo tea is a quinone:

Some of its effectiveness in treating a variety of disease states, including yeast infections, may result from its acetaldehyde scavenging ability. Short side-chain quinones, however, as noted previously for menadione (vitamin K3), have a toxicity profile that makes them unfavorable for supplementation [7].

[1] Molina MT et al., "N-Heterocyclic Carbene-Catalyzed Monoacylation of 1,4-Naphthoquinones with Aldehydes", J. Org. Chem., 2009, 74 (24), pp 9573–9575
http://pubs.acs.org/doi/abs/10.1021/jo902235h

[2] Waske PA et al.,"Photoacylations of 2-substituted 1,4-naphthoquinones: a concise access to biologically active quinonoid compounds", Tetrahedron Letters Vol 47 Issue 8, 20 February 2006, Pages 1329–1332
http://www.sciencedirect.com/science/article/pii/S0040403905027292

[3] Hobara N et al., "Quinone derivatives lower blood and liver acetaldehyde but not ethanol concentrations following ethanol loading to rats.", Pharmacology. 1988;37(4):264-7.
http://www.ncbi.nlm.nih.gov/pubmed/2848265

[4] Golomb BA et al., "Statin adverse effects : a review of the literature and evidence for a mitochondrial mechanism." Am J Cardiovas Drugs 2008;8(6):373-418.
http://www.ncbi.nlm.nih.gov/pubmed/19159124

[5] Adams J et al., "Vitamin K in the treatment and prevention of osteoporosis and arterial calcification.", Am J Health Syst Pharm. 2005 Aug 1;62(15):1574-81.
http://www.ncbi.nlm.nih.gov/pubmed/16030366

[6] Tzeng WF et al., "The role of lipid peroxidation in menadione-mediated toxicity in cardiomyocytes.", J Mol Cell Cardiol. 1995 Sep;27(9):1999-2008.
http://www.ncbi.nlm.nih.gov/pubmed/8523459

[7] Felicio AC et al., "Fetal growth in rats treated with lapachol.", Contraception. 2002 Oct;66(4):289-93.
http://www.ncbi.nlm.nih.gov/pubmed/12413627