Hormesis Produces Benefits via Altered Mitochondrial Activity
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Small, short doses of damaging cellular stress, such as that achieved through the application of heat, toxins, lack of nutrients, or raised levels of oxidative molecules, produce a net benefit to cell and tissue function. This is called hormesis. It occurs because cells react to short periods of stress with a lasting upregulation of maintenance activities and other altered behavior. Hormetic behaviors are the basis for many of the benefits of exercise, calorie restriction, and other related interventions shown to slow aging to some degree in animal studies.

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In the research noted here, scientists report on an investigation into the way in which mitochondrial activity changes in response to cellular stress. Mitochondria are the power plants of the cell, and their function is central to cellular health. With age, mitochondria become dysfunctional in a number of different ways. Periodic hormetic stress may slow down or attenuate this progressive decline by, for example, increasing the housekeeping processes of mitophagy, responsible for recycling damaged mitochondria. Other signaling processes that more directly determine mitochondrial function are also likely involved, however.

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Researchers report that brief exposures to stressors can be beneficial by prompting the cell to trigger sustained production of antioxidants, molecules

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