14.1 Introduction 219
14.2 Coenzyme Q Deficiency in Tissues and Plasma 219
14.3 Coenzyme Q Administration and Peroxidation Products 221
14.3.1 CoQ1() Administration and Oxidative Stress at the Myocardial Level 222
14.3.2 CoQ10 Effect on the Senescent Myocardium 223
14.3.3 CoQ10 Treatment and Ischemic Brain Lesions 223
14.3.4 Effect of Chronic CoQ10 Supplementation on Plasma
Lipoprotein Peroxidation 223
The bioenergetic role of coenzyme Q (CoQ) in mitochondria as well as its essential role in other redox chains is well accepted. What is more often debated is its antioxidant function and the rationale leading to clinical administration. In spite of the suggestion that CoQ in mitochondria may be involved in oxygen free radical generation,1 evidence has been found that CoQ acts as an antioxidant both in vitro1,2,3,4,4* and in vivo.5 Thus, the reasons justifying the use of CoQ in different clinical conditions may arise both from improvement of cellular bioenergetics and antioxidant protection3,6 and we shall try to critically discuss whether its therapeutic effect can reasonably be ascribed to the former or the latter of its features.
The first studies evidencing a certain degree of CoQ deficiency in myocardial tissue date to the first half of the 1970s78 and show that 75% of patients undergoing cardiac surgery were affected by this deficiency. This finding was obtained through the enzymatic assay of succinate dehydro-genase-CoQ reductase of mitochondria prepared by intraoperatory biopsies. Thanks to the same technique, similar results were concomitantly obtained in the heart muscle of rabbits fed with a vitamin E deficient diet,9 in the heart muscle of mice affected by hereditary muscle dystrophy,10 in human gingiva of subjects affected by periodontal disease,11 and in human muscle of patients affected by muscular dystrophy.12 Later in 1984, it was found, through HPLC analysis conducted on endomyocardial biopsies, that patients in NYHA classes III and IV had lower cardiac CoQ concentration
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