Doing some self-education this morning about chemical analysis for CoQ10H2, the chemically reduced form (Ubiquinol) of CoQ10 (the chemically oxidized form, Ubiquinone). This all got started again when I tried to verify if a national biomedical diagnostics lab in USA (Quest Diagnostics) actually measured CoQ10H2 instead of simply CoQ10. Answer relayed to me from chem tech doing analysis was "CoQ10", Ubiquinone, so I cancelled the analysis.
I am supplimenting with CoQ10H2 because of its much greater bioavailability. I want to know just how much this is increasing concentration of CoQ10H2 in my blood plasma. This would have been the first of a series of measurements of CoQ10H2. For me, ALL other forms of CoQ10 have essentially no dectectable effect of my physical abilities (stamina, exercise tolerance).
Use of CoQ10H2 was pioneered by cardiologists Per and Peter Långsjöen in Midland, TX, USA. They worked with Kaneka, LTD in Japan to develop a chemically stable formulation of CoQ10H2 that could be marketed.
Here is a really good reference about measurement of CoQ10 and CoQ10H2 in blood plasma of humans
http://www.clinchem.org/cgi/content/full/47/2/256 Beware that this is primarily an article for analytical chemists. However, there are some really nice "summary" paragraphs scattered throughout the article about the biochemistry of CoQ10H2 and CoQ10 in human body, all well referenced to various medical and biochemical journal articles.
Here is C&P of first paragraph in INTRODUCTION
Coenzyme Q10 is an essential cofactor in the mitochondrial respiratory chain responsible for oxidative phosphorylation (1). Furthermore, coenzyme Q10 has a primary function as an antioxidant and is carried mainly by lipoproteins in the circulation (2). Approximately 60% of coenzyme Q10 is associated with LDL, 25% with HDL, and 15% with other lipoproteins (2). When LDL is subjected to oxidative stress in vivo (3), the reduced form of CoQ10 (CoQ10H2)1 functions as an antioxidant. It has been postulated that CoQ10H2 prevents lipid peroxidation in plasma lipoproteins and biological membranes (4). The antioxidative activity of CoQ10H2 depends not only on its concentration, but also on its redox status. Recent reports (5)(6)(7)(8)(9)(10)(11)(12)(13)(14) have suggested that the percentage of CoQ10H2 in total CoQ10 (CoQ10H2:TQ10) may be lower in patients with certain conditions, including Parkinson disease (5), prematurity (6), hemodialysis (7), chronic active hepatitis (8), liver cirrhosis (8), hepatocellular carcinoma (8), hyperlipidemia (9)(10), heart disease (11)(12), ß-thalassemia (13), and DNA damage (14). Therefore, CoQ10H2 may be a useful marker of oxidative stress, and the measurement and function of CoQ10H2 are of considerable interest.
Here is another informative paragraph of interest to us.
Accurate determination of CoQ10H2 makes it a possible marker for assessing the presence of oxidative stress in many pathologic states. Although significant differences in the plasma CoQ10H2:TQ10 ratio between controls and patients with atherosclerosis, coronary artery disease, and Alzheimer disease have not been observed by some investigators (10)(28), other researchers have reported decreased CoQ10H2 concentrations associated with certain disease processes. Hara et al. (6) suggested that the CoQ10H2:TQ10 ratio is a good marker of oxidative stress in infants with asphyxia (6). Hemodialysis patients have also been found to have significantly lower concentrations of plasma CoQ10H2 than healthy controls (7). According to one report (7), a single hemodialysis session causes a 30% decrease in mean plasma CoQ10H2 concentrations. Plasma CoQ10H2 was also found to be significantly lower in hyperlipidemic patients and in patients with liver disease (10). In 64 patients with chronic active hepatitis, liver cirrhosis, and hepatocellular carcinoma, significantly increased CoQ10 and decreased CoQ10H2 were observed (8). Palomäki et al. (12) observed that lovastatin treatment diminishes the CoQ10H2 concentration in the LDL of hypercholesterolemic patients with coronary heart disease. There are also concerns that patients could experience deleterious effects as a result of long-term therapy with hydroxymethylglutaryl-CoA reductase inhibitors or "statin" therapy. Monitoring of the effects of statin therapy on CoQ10H2 may be useful for diagnosing CoQ10H2 deficiency in many patient populations. These are but a few of a growing numbers of studies that suggest that CoQ10H2 deficiency may be related to pathophysiologic mechanisms.
Enjoy --- and please don't drown in all the chemistry.
Lars