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Inflammation and Aging

By: Marie Alice Dibon, PharmD
Posted: March 7, 2011, from the March 2011 issue of GCI Magazine.

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As you age, there is also a lack in the elimination of oxidated proteins, due to the decay of the proteasome. These proteins will in turn transfer reactive oxygen species (or ROS—highly reactive molecules, such as free radicals, that can damage cellular components) to the cells, further adding to the oxidative damage triggering the inflammation.

In a recent article, a team of Italian scientists1 summarized state-of-the-art research on inflamm-aging and reviewed new hypotheses on the role of mitochondria. The data favored the hypothesis that pro-inflammatory cytokines play an important role in aging and longevity.

The Energy Theory of Aging

The role played by the loss of efficiency in mitochondrial activity and most particularly by the progressive deterioration of the electron transport chain during the generation of energy—producing more and more free radicals for less and less energy—is one of the most promising avenues of research around inflamm-aging.

Production of adenosine triphosphate (ATP)—a nucleotide that is the basic unit of energy that cells use—is reduced, and the generation of ROS (in particular, the hydroxyl radical) increases. These are generated inside the very cell and close the mitochondrial and nuclear DNA, imparting an even more damaging effect than exogenous ROS. These endogenous damages then add onto t

he exogenous damages created by the chronic inflammation triggered by pollutants and other environmental factors.

Oxidized Proteins