Here, researchers report on a recent study of the ability of mitochondrially targeted antioxidants to modestly increase healthy life span in lower animals such as the flies used here. Mitochondria are important in the progression of aging for a number of reasons, all of which seem to be very connected to the reactive oxygen species (ROS) they produce in the course of generating chemical energy stores to power the cell. ROS can damage mitochondrial structures, and that can lead to mutant mitochondria that take over and cripple cells, causing harm to surrounding tissues. ROS are also used as signals in many fundamental cellular processes, such as the response to exercise and triggering of cellular maintenance in response to stresses. Thus antioxidants targeted specifically to the interior of mitochondria have the ability to influence these processes, where other types of antioxidant cannot:
Mitochondria play an important role in aging. Strongly reduced function of the mitochondria shortens life span, whereas moderate reduction prolongs life span, with reactive oxygen species production being the major factor contributing to life span changes. Previously, picomolar concentrations of the mitochondria-targeted antioxidant SkQ1 were shown to increase the life span of Drosophila by approximately 10%. In this article, we demonstrate that SkQ1 elevates locomotion, which is often considered a marker of health and age. We also show that mating frequency and fecundity may be slightly increased in SkQ1-treated flies. These results indicate that SkQ1 not only prolongs life span but also improves health and vigor.
An important property of any potential therapeutic is the stability of its effects in an uncontrolled and changing environment as well as on individuals with various genetic constitutions. In this article, we present data on SkQ1 effects on Drosophila longevity in extreme environments (low temperatures and starvation) and on individuals with severe genetic alterations in the mitochondrial systems responsible for production and detoxification of reactive oxygen species. We hypothesize that in vivo SkQ1 is capable of alleviating the probable negative effects of increased mitochondrial reactive oxygen species production on longevity but is not effective when reactive oxygen species production is already reduced by other means.