Experimental MitoQ Treatment Fails Prevention of Age-Related Muscle Mass, Function Loss in Mice

Alice Melão avatar

by Alice Melão |

Share this article:

Share article via email
Leigh syndrome hypoxia

Researchers used a long-term treatment approach of MitoQ (mitoquinone mesylate) in aging experimental mice, but the treatment had no beneficial effects on mitochondrial function or on muscle mass and function.

The study, “Long-term administration of the mitochondria-targeted antioxidant mitoquinone mesylate fails to attenuate age-related oxidative damage or rescue the loss of muscle mass and function associated with aging of skeletal muscle,” was published in the FASEB Journal.

Loss of muscle mass and function because of aging is the major contributor of physical disability and loss of independence among the elderly population.

Studies have shown that mitochondrial dysfunction can have an active role in the aging process. The aging of muscles responsible for body movements (skeletal muscle) has long been associated with impaired mitochondrial function. Some of the changes have been linked to accumulation of oxidative stress damage induced by aging.

In order to gain a better grasp on how age-related muscle atrophy and mitochondrial dysfunction could be due mitochondrial oxidative changes, the researchers administrated MitoQ – a mitochondria-targeted antioxidant – to experimental animal models. They then determined age-related loss of muscle mass and function, and mitochondrial organelle integrity and function.

After treating older mice for 15 weeks with MitoQ, the researchers found that the treatment did not prevent age-dependent loss of skeletal muscle mass. The animals still presented signs of sarcopenia, defined by the reduction of muscle strength and overall muscle atrophy.

The authors showed that long-term administration of MitoQ showed a tendency to negatively affect mitochondrial function and to induce a decline in muscle strength, although neither of these findings reached statistical significance. In general, MitoQ treatment could not reduce the mitochondrial oxidative stress or improve the global oxidative status in the muscles.

According to the report, information collected in the study showed that long-term administration of MitoQ to specifically target mitochondria failed to decrease age-related oxidative damage in skeletal muscle and to provide any protective effect to skeletal muscles during aging in experimental animals.