If you have been following the development of mitochondrially targeted antioxidants as a potential therapy to modestly slow aging, you might find this open access paper interesting. MitoQ is one of the readily available compounds, with SkQ1 as the other. My impression from the papers is that SkQ1 and closely related plastoquinones have a larger effect size on life span in animal studies, but it still isn't more than a fraction of that produced by calorie restriction.
Mitochondrially targeted antioxidants appear to function by improving mitochondrial metabolism, but the most medically relevant effect observed so far is their ability to dampen the consequences of inflammation, particularly in inflammatory eye conditions. Inflammation and excessive levels of oxidative molecules go hand in hand. This same underlying mechanism may allow these compounds to reduce stiffness of blood vessels in older individuals, by reducing the impact of inflammation and the aged tissue environment on smooth muscle cells responsible for contraction and dilation. A human trial of MitoQ produced interesting data on this front. The paper here looks at a broader range of biomarkers and outcomes.
The postulated relationship between cellular decline and reactive oxygen species (ROS) has been well explored in the free radical theory of aging, which suggests that human lifespan and degenerative disease are tied to the adverse effects of ROS on cell structure and function. Once produced, ROS react with lipids, proteins, and nucleic acids causing oxidative damage to these macromolecules, over time contributing to the aging process.
Mitochondria are among the most metabolically active organelles in the body and are a primary source of energy production and oxidative phosphorylation. Oxidative phosphorylation, a process in energy production, results in the production of ROS. As both the major producer and primary target of ROS, mitochondria are thought to play an important role in aging.
Generally speaking, decreasing the concentration of ROS and thereby potential damaging capabilities, it is hypothesised that the aging process can be delayed. This concept has inspired a host of nutraceuticals aimed at alleviating oxidative damage, particularly in the mitochondria. To decrease mitochondrial oxidative damage, a number of mitochondria-targeted antioxidants have been developed. One such mitochondria-targeted antioxidant is MitoQ.
This review has examined the effect of MitoQ on oxidative stress markers related to the aging process. Our findings indicate that MitoQ has a statistically significant reduction in concentrations of 3-NT, a biomarker of protein oxidation produced upon the nitration of protein residues, which alters protein structure and function. This is of interest as nitration of protein residues has been shown to inhibit enzyme catalytics, and so MitoQ may promote efficiency of cellular processes as well as help decrease the concentration of reactive oxygen species.
Mitochondrial membrane potential has been shown to significantly increase upon administration of MitoQ, suggesting an upregulation in the functioning capacity of mitochondria with supplementation. Mitochondrial membrane potential is commonly used as an indication of functional status. While decreased membrane potential (depolarization) indicates damaged, dysfunctional mitochondria that cannot meet cellular energy demands, increased membrane potential (hyperpolarization) suggests increased functional capacity and work conducted.