CoQ10 and Aging

Abstract

The aging process includes impairment in mitochondrial function, a reduction in anti-oxidant activity, and an increase in oxidative stress, marked by an increase in reactive oxygen species (ROS) production. Oxidative damage to macromolecules including DNA and electron transport proteins likely increases ROS production resulting in further damage. This oxidative theory of cell aging is supported by the fact that diseases associated with the aging process are marked by increased oxidative stress. Coenzyme Q10 (CoQ10) levels fall with aging in the human but this is not seen in all species or all tissues. It is unknown whether lower CoQ10 levels have a part to play in aging and disease or whether it is an inconsequential cellular response to aging. Despite the current lay public interest in supplementing with CoQ10, there is currently not enough evidence to recommend CoQ10 supplementation as an anti-aging anti-oxidant therapy.

Coenzyme Q10: Clinical Applications in Cardiovascular Diseases

“…Moreover, CoQ10 is able to accept electrons from fatty acyl-coenzyme A (acyl-CoA) dehydrogenases and it is an obligatory factor in proton transport by uncoupling proteins (UCPs), thus regulating the opening of mitochondrial permeability transition pores [8]. Other functions of CoQ10 in the cell membrane include stabilization of calcium-dependent channels, metabolic regulation, cell signaling, and cell growth through local regulation of cytosolic redox intermediates such as dihydronicotinamide-adenine dinucleotide phosphate (NADPH) [6].…”

“…In fact, in the respiratory chain, CoQ 10 transfers electrons from complex I (nicotinamide-adenine dinucleotide (NADH)-coenzyme Q reductase) or complex II (succinate-coenzyme Q reductase) to complex III (cytochrome c reductase), and it is also a structural component of both CI and CIII, reducing the production of reactive oxygen species (ROS) [6,7]. Moreover, CoQ 10 is able to accept electrons from fatty acyl-coenzyme A (acyl-CoA) dehydrogenases and it is an obligatory factor in proton transport by uncoupling proteins (UCPs), thus regulating the opening of mitochondrial permeability transition pores [8]. Other functions of CoQ 10 in the cell membrane include stabilization of calcium-dependent channels, metabolic regulation, cell signaling, and cell growth through local regulation of cytosolic redox intermediates such as dihydronicotinamide-adenine dinucleotide phosphate (NADPH) [6].…”

COVID-19 and Crosstalk between the Hallmarks of Aging

“…ROS is a normal part of bodily defense mechanisms, but during stress, high amounts are damaging. Detoxifying systems, including catalase, superoxide dismutase, glutathione peroxidase and glutathione reductase with selenium and magnesium as their cofactors (62), vitamin E and C, and coenzyme Q10 (which decreases with aging), help to minimize ROS-induced tissue damage (61,63). Virus infection, including coronaviruses, can induce ROS production and apoptosis (64).…”

Aging-Related Disorders and Mitochondrial Dysfunction: A Critical Review for Prospect Mitoprotective Strategies Based on Mitochondrial Nutrient Mixtures

“…This background knowledge has led to the awareness of the key roles of mitochondrial cofactors in aging and in ARD. Further studies were focused on an extensive number of dysmetabolic and inborn disorders [ 4 , 5 , 6 , 7 , 8 , 9 , 10 , 11 , 12 ], also including the group of mitochondrial diseases dating back to the initial definition of “mitochondrial medicine” by Luft (1994) [ 6 ]. In turn, this awareness has generated a body of experimental and clinical studies targeted to the potential use of these mitochondrial cofactors, termed as “mitochondrial nutrients” (MNs) [ 13 , 14 , 15 , 16 , 17 ].…”