The presence of oxidative molecules in our biochemistry rises with aging, and cells react to this in many different ways. Internally to cells, this sort of damage can be rapidly repaired and brief bursts of oxidative molecule creation even serve as a signal for many necessary processes, such as the beneficial reactions to the stresses of exercise. Chronic oxidative stress produces dysfunction, however, whether that is via the production of toxic oxidized lipids or through through more direct means of causing cells to act in a harmful manner.
Chronic inflammation and mitochondrial dysfunction are two of the upstream causes of increased numbers of oxidative molecules. Among the downstream consequences can be found all sorts of detrimental cellular reactions, many of which are only poorly explored at best. The open access paper here is an example of the type. The best solution to this class of age-related problem is to go after the upstream causes, though mitochondrially targeted antioxidants appear to provide a beneficial suppression of oxidative stress in at least some situations.
The production of reactive oxygen species (ROS) is progressively increased in aging and is one of the
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