Thoughts on Macromolecular Damage and Human Life Span

Macromolecules are parts in our cellular machinery, themselves large and complex arrangements of atoms. Some of these macromolecules are short lived and rapidly recycled, but many are not. They are vulnerable to damage in ways that can significantly alter their behavior - such as by reacting with free radicals generated by mitochondria, or being glued together into advanced glycation end-products. Here is a paper offering some thoughts on what that means for human aging: "A number of tissues and organs in the human body contain abundant proteins that are long-lived. This includes the heart, lung, brain, bone and connective tissues. It is proposed that the accumulation of modifications to such long-lived proteins over a period of decades alters the properties of the organs and tissues in which they reside. Such insidious processes may affect human health, fitness and ultimately may limit our lifespan. The human lens, which contains proteins that do not turnover, is used to illustrate the impact of these gradual deleterious modifications. On the basis of data derived from the lens, it is postulated that the intrinsic instability of certain amino acid residues, which leads to truncation, racemisation and deamidation, is primarily responsible for the age-related deterioration of such proteins. Since these post-translational modifications accumulate over a period of many years, they can only be studied using organisms that have lifespans measured in decades. One conclusion is that there may be important aspects of human aging that can be studied only using long-lived animals." With or without further study, researchers know that these forms of damage exist and know how best to proceed to fix them - it's just a matter of funding and the will to proceed.



Agreed, enough studies! Who cares how the damage comes about, just fix it!!

Posted by: Will Nelson at February 1st, 2011 8:48 AM

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