Abstract
Coenzyme Q10 (CoQ10) is an essential component of the mitochondrial electron transport chain. It is also an antioxidant in cellular membranes and lipoproteins. All cells produce CoQ10 by a specialized cytoplasmatic-mitochondrial pathway. CoQ10 deficiency can result from genetic failure or ageing. Some drugs including statins, widely used by inter alia elderly, may inhibit endogenous CoQ10 synthesis. There are also chronic diseases with lower levels of CoQ10 in tissues and organs. High doses of CoQ10 may increase both circulating and intracellular levels, but there are conflicting results regarding bioavailability. Here, we review the current knowledge of CoQ10 biosynthesis and primary and acquired CoQ10 deficiency, and results from clinical trials based on CoQ10 supplementation. There are indications that supplementation positively affects mitochondrial deficiency syndrome and some of the symptoms of ageing. Cardiovascular disease and inflammation appear to be alleviated by the antioxidant effect of CoQ10. There is a need for further studies and well-designed clinical trials, with CoQ10 in a formulation of proven bioavailability, involving a greater number of participants undergoing longer treatments in order to assess the benefits of CoQ10 treatment in neurodegenerative disorders, as well as in metabolic syndrome and its complications.
Highlights
Coenzyme Q (CoQ) is a lipid-soluble antioxidant that is produced de novo in animal cells (Laredj et al, 2014) (Fig. 1)
Injury to mitochondrial DNA impairs the function of the respiratory chain resulting in additional reactive oxygen species (ROS) formation and DNA lesions and acceleration of cellular ageing (Poulose and Raju, 2014), whereas maintenance of adequate CoQ10H2-levels appears to induce reparations of oxidative damage through direct interaction with DNA repair enzymes (Schniertshauer et al, 2020)
The use of some of these agents may cause side effects like muscle pain, general discomfort, and even osteonecrosis in some few cases. These side effects might be precipitated by the ability of high-dosed bisphosphonates to reduce the levels of Coenzyme Q10 (CoQ10) by inhibiting farnesyl pyrophosphate synthase, an enzyme that catalyzes a crucial step in the synthesis of CoQ10 (Tricarico et al, 2015)
Summary
Coenzyme Q (CoQ) is a lipid-soluble antioxidant that is produced de novo in animal cells (Laredj et al, 2014) (Fig. 1). Injury to mitochondrial DNA impairs the function of the respiratory chain resulting in additional ROS formation and DNA lesions and acceleration of cellular ageing (Poulose and Raju, 2014), whereas maintenance of adequate CoQ10H2-levels appears to induce reparations of oxidative damage through direct interaction with DNA repair enzymes (Schniertshauer et al, 2020). In addition to inborn errors in CoQ10 synthesis (Fig. 1), the level of CoQ10 declines with age, and food supplements are marketed with claims to restore the levels and improve health (Mantle and Dybring, 2020). The aim of this this paper is to review the role of CoQ10 for human health with a specific focus on ageing and diseases related to ageing and possible clinical benefits of supplementation
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