Stress Tolerance

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Stress Tolerance

Stress tolerance is the ability of organism to eliminate any consequences caused by stressors. Continuous exposure to environmental and intrinsic stress results in cumulative damage in macromolecules. The ‘‘stress resistance’’ theory covers stress from intrinsic and extrinsic (environmental) sources, and hypothesizes that increased stress resistance leads to prolonged life span.

An increase in stress resistance at a cellular and organismal level would not only result in augmented resistance to environmental toxins, but also enhanced protection against inflammation, neurodegeneration and cancer, diseases that are often associated with aging. Increased toxin resistance may also contribute to a more stable proteome and genome, thereby retarding senescence and aging. Oxidative stress-associated cellular damage has a fundamental role in the initiation and development of many diseases, including age-associated diseases such as diabetes, cardiovascular disease, and cancer. Antioxidant enzymes provide an important cellular defense against oxidative stress by removing reactive oxygen species (ROS), such as superoxide and hydrogen peroxide, before they cause oxidative damage. Alterations in the activity of signaling pathways that result in increased levels of antioxidant enzymes are also frequently associated with increased oxidative stress resistance and longevity.

Species differences in resistance to oxidative and other endogenous and/or environmental stressors correlate with maximum species lifespan potential. For example, a targeted mutation of the mouse p66shc gene confers resistance to oxidative stress (paraquat) and also appears to prolong life by 30%. Enhanced stress resistance has been shown in skin fibroblasts from multiple long-lived species after a variety of toxic insults, including heavy metals, DNA-damaging agents, heat and dietary interventions. This type of cytoprotection moves beyond neutralization of oxidative stress but also encompasses other exogenous chemical stressors and supports the premise that the degree of endogenous oxidative stress is not a determinant of species longevity. Rather, longevity is influenced by how the species responds to mitigate the impact of that particular stressor. Considerable evidence has now accumulated showing that cytoprotection and stress resistance may be a significant contributing factor to a positive healthspan and extended lifespan.