Mitochondrially Targeted Antioxidant Delays Age-Related Structural Changes in Mitochondria

Mitochondrial damage is a contributing cause of aging. It happens as a natural side-effect of mitochondrial operation because mitochondria generate a flow of damaging reactive oxygen species (ROS) in the course of creating chemical energy stores to power the cell. The most likely target for these ROS? The mitochondria themselves.

Mitochondrial repair technologies and the SENS approach of creating backup mitochondrial genes in the cell nucleus are promising approaches to removing this contribution to aging. A less promising approach is to target engineered antioxidant compounds to the mitochondria to augment natural antioxidants and soak up some of those ROS before they cause harm. This is less promising because it can only slow down the process.

Here is the latest from one of the various programs of development for mitochondrially targeted antioxidants:

Sarcopenia, the gradual loss of muscle mass and function, is a common feature of human aging. The molecular mechanisms leading to sarcopenia are not completely identified, but the retardation [of] oxidative damage entailed with an age-linked mitochondrial dysfunction occurring in the muscle cells looks as promising approach to treat this disease.

Our study of skeletal muscles [of] Wistar rats have revealed age-related changes in the amount of mitochondria, forms of mitochondrial profiles and ultrastructure. The treatment of animals with a mitochondria-targeted antioxidant SkQ1 retarded development of age-related destructive pathological changes in mitochondria of both Wistar and OXYS rats. Again, this is true for the amount of mitochondria, the development of mitochondrial reticulum and ultrastructure of the mitochondrial cristae.

Accumulating evidence supports the existence of a close relationship between declining anabolic hormones, such as growth hormone (GH) and insulin-like growth factor-1 (IGF-1) levels and age-related changes in body composition and function. Therefore, the age-dependent decline of GH and IGF-1 serum levels might promote the loss of muscle mass and strength. We recently measured the levels of these hormones in the SkQ1-treated animals. It was found that an SkQ1 treatment between the ages of 19 and 23 months increased the blood levels of GH and IGF-I in the Wistar and the OXYS rats above those found in the 19 month-old animals. These results suggest that the effect of the SkQ1 against sarcopenia may be partially mediated by an activation of somatotropic (GH/IGF-1) signaling which is reduced in OXYS rats since a young age.



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