Other Diseases

Plasma levels of ubiquinol-10 have been measured in several other diseases and pathological conditions. Significantly lower values of plasma ubiquinol-10 (compared to controls), have been reported for adult respiratory distress syndrome56 and infant asphyxia.57 Both these conditions are related to highly increased oxidative stress. This implies that plasma ubiquinol-10 can be decreased as a result of a massive and acute oxidative stress when antioxidant defense systems of the body are overcome. It seems that in order to cause a detectable decrease in plasma ubiquinol-10, oxidative stress must be extensive, as is the case for the pathologies mentioned above. This is in line with the observation that plasma ubiquinol-10 is not reduced in smoking, i.e., under conditions of milder and chronic oxidative stress.22

Taken together, currently available data indicate that decreased levels of ubiquinol-10 in human plasma may have two major causes: the presence of liver dysfunction (hepatitis, cirrhosis, hepatoma) and/or highly increased systemic oxidative stress (adult respiratory distress syndrome, infant asphyxia). Low plasma ubiquinol-10 levels might also reflect less pronounced oxidative stress in hyperlipidemia and diabetes. However, they may also (at least partly) be related to confounding liver dysfunction known to occur in hyperlipidemia58 and frequently present in diabetes. The latter explanation seems to be more probable, since comparable oxidative stress chronically present in atherosclerosis or neurological diseases such as Alzheimer's or Parkinson's disease, is unable to cause a decrease in plasma ubiquinol-10.

Ubiquinol-10 synthesis by the liver and its consumption by oxidative processes accordingly represent the major determinants of its plasma level (Figure 16.1). Typically, liver synthesis seems to be more important, and efficient recycling of ubiquinol-10 by this organ appears to outweigh its increased consumption by oxidants under conditions of relatively mild and chronic oxidative stress. It seems that the human body can efficiently maintain ubiquinol-10 levels in the absence of liver dysfunction. Conditions of acute oxidative stress are likely to be the only exception, when the efficiency of the ubiquinol-synthesizing systems of the liver is not sufficient to compensate for its consumption and to maintain its plasma level.

This suggests that measurement of plasma ubiquinol-10 can be diagnostically used to assess the function of the liver. It remains to be shown whether measuring ubiquinol-10 can provide additional information in comparison with established liver markers. In the absence of liver dysfunction, low plasma ubiquinol-10 might be a marker for a massive and acute oxidative stress. In contrast, plasma level of ubiquinol-10 is not indicative of the presence of cardiovascular and neurological diseases related to milder and chronic oxidative conditions, such as atherosclerosis, Alzheimer's, or Parkinson's disease.

Finally, it must be emphasized that the way that the plasma level of ubiquinol-10 is expressed is critically important for its value as a disease marker. Plasma level of ubiquinol-10 can be expressed

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