Coenzyme Q10 Supplementation for the Reduction of Oxidative Stress: Clinical Implications in the Treatment of Chronic Diseases

Abstract

Apart from its main function in the mitochondria as a key element in electron transport, Coenzyme Q10 (CoQ10) has been described as having multiple functions, such as oxidant action in the generation of signals and the control of membrane structure and phospholipid and cellular redox status. Among these, the most relevant and most frequently studied function is the potent antioxidant capability of its coexistent redox forms. Different clinical trials have investigated the effect of CoQ10 supplementation and its ability to reduce oxidative stress. In this review, we focused on recent advances in CoQ10 supplementation, its role as an antioxidant, and the clinical implications that this entails in the treatment of chronic diseases, in particular cardiovascular diseases, kidney disease, chronic obstructive pulmonary disease, non-alcoholic fatty liver disease, and neurodegenerative diseases. As an antioxidant, CoQ10 has proved to be of potential use as a treatment in diseases in which oxidative stress is a hallmark, and beneficial effects of CoQ10 have been reported in the treatment of chronic diseases. However, it is crucial to reach a consensus on the optimal dose and the use of different formulations, which vary from ubiquinol or ubiquinone Ubisol-Q10 or Qter®, to new analogues such as MitoQ, before we can draw a clear conclusion about its clinical use. In addition, a major effort must be made to demonstrate its beneficial effects in clinical trials, with a view to making the implementation of CoQ10 possible in clinical practice.

The Relationship between Mitochondrial Reactive Oxygen Species Production and Mitochondrial Energetics in Rat Tissues with Different Contents of Reduced Coenzyme Q

“…Thus, the observed differences in the size of the reduced Q pool (Q9 + Q10) reflect different levels of ROS production and hence may reflect different demands for reduced Qs as antioxidants at both the tissue and mitochondrial levels. It is well accepted that in their reduced form Qs have antioxidant activity, as scavengers of ROS or lipid radicals and regenerators of α-tocopherol from the α-tocopheroxyl radical [ 3 , 4 , 5 ]. Obviously, at the tissue level, the larger total and reduced Q pools are also related to the number of mitochondria in a given tissue.…”

“…Importantly, mQ is also involved in the formation of O 2 •− from semiubiquinone radicals at the Q-binding sites of complexes I and III [ 1 ]. However, Q is not only involved in mROS production through the mitochondrial respiratory chain, but also an important antioxidant in mitochondria and the entire cell [ 2 , 3 , 4 , 5 ]. Reduced Q (ubiquinol) recycles other antioxidants such as vitamin E or vitamin C, and directly acts on free radicals or oxidants, reducing and neutralizing them.…”

“…Reduced Q via binding free radicals inhibits lipid peroxidation and prevents oxidative modifications of DNA and proteins. Moreover, the Q redox state may be a useful marker of cellular oxidative stress [ 4 ].…”

Cell Death via Lipid Peroxidation and Protein Aggregation Diseases

“…CoQ10 is a lipid-soluble antioxidant that has been clinically used in the treatment of various human disorders, such as metabolic syndrome, type 2 diabetes, cardiovascular diseases, and neurodegenerative diseases [ 136 ] As described above, CoQ10 inhibits ferroptosis, and there have been various reports on neurodegenerative diseases [ 75 , 137 , 138 ].…”

Associations between Coenzyme Q10 Status, Oxidative Stress, and Muscle Strength and Endurance in Patients with Osteoarthritis

“…Aging decreased cellular bioenergy capacity and may result in a depletion of coenzyme Q10 levels [ 13 ]. It is well known that chronic diseases such as cardiac diseases, diabetes, and neurodegenerative diseases may influence the coenzyme Q10 status [ 14 , 15 , 16 , 17 ]. To date, no clinical study has investigated the level of coenzyme Q10 in patients with OA.…”