A couple more interesting items from sci.life-extension to brighten up your day.
It has been proposed that somatic mutations make major contributions to aging. The first paper, based on a gene knock-in mouse, supports a contributory role for mutation in [mitochondrial DNA] (mtDNA) in aging, but does not support a damaged-mtDNA-producing-more-damaged-mtDNA hypothesis. The second paper indicates some GC-rich sequences in the nuclear DNA are more sensitive to oxidative damage than mtDNA. As a result, key genes involved in brain function and mitochondrial function are progressively inactivated with age. Failure in these nucleus-encoded mitochondrial genes may be a primary reason for mitochondrial failure in old age.
In other words, these researchers suggest that there is no feedback mechanism associated with ongoing damage in mitochondrial DNA, the cellular powerhouses, and reduction in mitochondrial function with age is caused by changes in cell nucleus DNA.
Nanobiology implies application of the engineering concepts of nanotechnology to biological systems, providing novel opportunities to intervene in the pathology of disease. Here, we have merged nanoscale engineering with cell biology to intervene in a common biomedical pathology, that being aging and free radical-induced cell dysfunction.
We hypothesize that the unique valence structure of cerium oxide, in the nanoparticle form, promotes cell longevity and protects against free radical-mediated injury by acting as a regenerative free radical scavenger.
The search for ever better antioxidants (free radical scavengers) has been going on for quite some time, ever since the free radical theory of aging was first developed. It remains to be seen whether current nanoscale materials science can do significantly better than the antioxidants already sold by the supplement industry.