Reactive oxygen species (ROS) are damaging molecules that can rip up important cellular machinery; all machinery in a cell is an arrangement of atoms, and promiscuously reactive molecules can gum up the works, pull out important parts of the machinery, and otherwise cause all sorts of issues. In discussions of our biology, the term free radical is often used interchangeably to refer to these reactive molecules. They are produced within our cells as a byproduct of some of the most important mechanisms of metabolism, a fact shared by the vast majority of species, dating back far into evolutionary time. As for all aspects of cellular chemistry with such deep origins, evolution has has a very long time indeed in which to build feedback loops and interlaced machinery that depend upon the existence of ROS, co-opting these molecules for diverse purposes in signaling and regulating the operation of cells and tissues.

Thus ROS generation and damage is not just a harmful side-effect of being alive and having cells that are churning away, but it is also fundamental to the complex processes by which our metabolism maintains cellular homeostasis in the face of day to day challenges. Here are a couple of open access papers that summarize what is known about the more important roles of ROS in the body - in the first paper, section 6 is where you'll find the focus on aging, while the second paper looks at the intersection of muscle, ROS, and exercise.

Mitochondria-Ros Crosstalk in the Control of Cell Death and Aging

ROS are a normal side product of the respiration process, and they react with lipids, protein, and DNA, generating oxidative damage. Indeed, mitochondria are the major site of ROS production, but also the major targets of their detrimental effects, representing the trigger for several mitochondrial dysfunctions. In this review, we will focus on this deadly liaison, with particular attention on ROS production, mitochondrial ROS targets, and their role in apoptosis, autophagy, and aging. ... At physiological levels, ROS function as 'redox messengers' in intracellular signalling and regulation, whereas excess ROS induce cell death by promoting the intrinsic apoptotic pathway. Recent work has pointed to a further role of ROS in activation of autophagy and their importance in the regulation of aging. This review will focus on mitochondria as producers and targets of ROS and will summarize different proteins that modulate the redox state of the cell. Moreover, the involvement of ROS and mitochondria in different molecular pathways controlling lifespan will be reported, pointing out the role of ROS as a 'balance of power,' directing the cell towards life or death.

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The decline associated with aging is caused by the accumulation of ROS, as supported by cellular and biological data from different model systems and organisms. Indeed defects in antioxidant defense mechanisms fail to protect against oxidative damage, reducing lifespan and causing cardiomyopathy, neurodegeneration, and cancer. ... The relationship between mitochondria dysfunctions observed during aging and ROS production is still debated. However, it is clear that the decline of the integrity of mitochondria as a function of age is implicated in aging and age-related diseases.
Given this wide scientific evidence, many studies were aimed to identify the molecular mechanisms responsible for ROS deleterious effects on the aging process.

Reactive Oxygen Species in Skeletal Muscle Signaling

Up to the 1990s of the past century, ROS have been solely considered as toxic species resulting in oxidative stress, pathogenesis and aging. However, there is now clear evidence that ROS are not merely toxic species but also - within certain concentrations - useful signaling molecules regulating physiological processes. During intense skeletal muscle contractile activity myotubes' mitochondria generate high ROS flows: this renders skeletal muscle a tissue where ROS hold a particular relevance. According to their hormetic nature, in muscles ROS may trigger different signaling pathways leading to diverging responses, from adaptation to cell death.

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As an example, many studies have concluded that inactivity-induced ROS production in skeletal muscle contributes to disuse muscle atrophy. On the contrary, growing evidence also suggests that intracellular ROS production is a required signal for the normal remodelling that occurs in skeletal muscle in response to repeated bouts of endurance exercise. How can the same trigger promote such opposite effects? Based upon current knowledge, it appears that the mode and the situation characterizing skeletal muscle cells exposure to ROS may account, at least in part, for this apparent paradox. Transiently increased, moderate levels of oxidative stress might represent a potentially health-promoting process, whereas its uncontrolled persistence and/or propagation might result in overwhelming cell damage thus turning into a pathological event: for instance, the role of ROS in inflammation fits well with this model.

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Supplementation with exogenous antioxidants is being widely studied to attain and maintain an 'ideal titration' of ROS within skeletal muscle: unfortunately, at the present, no clear indication of the benefits arising from supplemental antioxidant intake emerges from literature.

The evolution of knowledge regarding ROS in human metabolism, and the parallel evolution of the market for dietary antioxidant supplements, should be taken as a cautionary tale. Metabolism is complicated, and trying to alter its operation through the use of such blunt tools is probably not the most efficient way to use science to extend human life.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm