by baumgrenze » Mon Sep 22, 2008 12:25 am
I opened this thread by chance this afternoon. I hope that the rest of you have it marked as something to follow; I have another reference I think is germane.
As a result of some previous searching, I searched Google for these terms: Stocker Bowry Frei ubiquinol
*http://www.google.com/search?hl=en&q=Stocker+bowry+frei+ubiquinol+scholar&btnG=Google+Search&aq=f&oq=
1: Proc Natl Acad Sci U S A. 1991 Mar 1;88(5):1646-50.
Ubiquinol-10 protects human low density lipoprotein more efficiently against lipid peroxidation than does alpha-tocopherol.
Stocker R, Bowry VW, Frei B.
Heart Research Institute, Sydney, New South Wales, Australia.
The temporal disappearance of natural antioxidants associated with human low density lipoprotein (LDL) in relation to the appearance of various classes of lipid hydroperoxides was investigated under three types of oxidizing conditions. Freshly isolated LDL from plasma of healthy subjects was free of detectable amounts of lipid hydroperoxides as measured by HPLC postcolumn chemiluminescence detection. Exposure of such LDL to a mild, constant flux of aqueous peroxyl radicals led to rapid and complete oxidation of ubiquinol-10, followed by slower partial depletion of lycopene, beta-carotene, and alpha-tocopherol. After an initial lag period of complete inhibition of detectable lipid peroxidation, formation of hydroperoxides of cholesterol esters, triglycerides, and phospholipids was observed. The onset of detectable lipid peroxidation corresponded closely with the completion of ubiquinol-10 consumption. However, small amounts of ascorbate, present as a contaminant in the LDL preparation, rather than ubiquinol-10 itself were responsible for the initial lag period. Thus, complete consumption of ubiquinol-10 was preceded by that of ascorbate, and exposure of ascorbate-free LDL to aqueous peroxyl radicals resulted in immediate formation of detectable amounts of lipid hydroperoxides. The rate of radical-mediated formation of lipid hydroperoxides in ascorbate-free LDL was low as long as ubiquinol-10 was present, but increased rapidly after its consumption, even though more than 80% and 95% of endogenous carotenoids and alpha-tocopherol, respectively, were still present. Qualitatively similar results were obtained when peroxyl radicals were generated within LDL or when the lipoprotein was exposed to oxidants produced by activated human polymorphonuclear leukocytes. LDL oxidation was reduced significantly by supplementing the lipoprotein preparation with physiological amounts of either ascorbate or ubiquinol-10. Our data show that ubiquinol-10 is much more efficient in inhibiting LDL oxidation than either lycopene, beta-carotene, or alpha-tocopherol.
PMID: 2000375 [PubMed - indexed for MEDLINE]
Google Scholar tells us that this paper is SIGNIFICANT! It has been cited 290 times since its publication.
*http://scholar.google.com/scholar?hl=en&lr=&cites=13737431661660486891&um=1&ie=UTF-8&sa=X&oi=science_links&resnum=1&ct=sl-citedby
No, I've not read all 290 papers, not even all 290 abstracts.
What got my attention is that vitamin E is a less effective antioxidant. If you provide the LDL with a huge serum concentration of vitamin E it out-competes the ubiquinone (..ol) for the binding site on the LDL.
Co-Q10 is a fascinating topic. I only wish it was easier to find unbiased information on the uptake of the available supplemental forms in the market. Just as I do not trust Pfizer researchers to tell me the 'whole story' about lipitor, I'm uncomfortable accepting publications from researchers reporting on their firm's new Co-Q10 formulation.
Has anyone found any reliable dose/response, ideally dose/serum titer publications? My initial hypothesis is that the oil/gelcaps rely on mass action for uptake. Is this the case?
It would also be useful to know about its metabolism (pharmacokinetics and pharmacodynamics) and whether or not there is significant variability among individuals. This publication from 2007 suggests a 33 hour half-life.
*http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1852397
That suggests to me that a once a day input of the optimal dose might be more effective than smaller doses 3-4 times during the day. Has anyone seen a scientific rationale for multiple smaller doses?
Trying to balance my soluble dietary fiber intake as part of an overall strategy to control my serum cholesterol level is yet another topic I need to research in greater depth. It is my current understanding that in addition to sweeping up serum cholersterol, it also removes lipophilic vitamins like B12, A, D, and E, and most certainly also Co-Q10. Has anyone worked on balancing this cholesterol management question?
baumgrenze