Compared to other elderly, membranes from centenarians (> 100 yrs) showed:
1) decreased lipid peroxide levels and reduced susceptibility to peroxidation
2) increased unsaturated/saturated fatty acid ratio
3) higher levels of EPA and DHA, reduced LA and AA
4) higher fluidity
Membranes from centenarians show some distinct features in comparison with elderly subjects that might act in a protective way against injuries
-http://www.waiworld.com/waitalk/phpBB3/viewtopic.php?f=20&t=3385
The above is from a thread where the topic of membrane composition, peroxidation and lifespan is covered
I was reading the book Neurons and the DHA Principle, and it seems that neuron's have substantial polyunsaturated fat content in membranes but can overcome this by antioxidant defenses. Given these are the longest lived cells in the body and can function for over 120 years(oldest human is said to've been free from dementia), it suggests to me that if some lipid soluble antioxidant was found that didn't turn pro-oxidant nor significantly interfered with ROS signalling it could be an overall positive.
The accumulation of lipofuscin-like material may be the result of an imbalance between formation and disposal mechanisms: Such accumulation can be induced in rats by administering a protease inhibitor (leupeptin); after a period of three months, the levels of the lipofuscin-like material return to normal, indicating the action of a significant disposal mechanism.[3] However, this result is controversial, as it is questionable if the leupeptin-induced material is true lipofuscin.[4][5] There exists evidence that "true lipofuscin" is not degradable in vitro;[6][7][8] whether this holds in vivoover longer time periods is not clear.-link
Assuming the cells can't actually digest it, all that would be necessary is some mechanism to export the waste and discard it elsewhere. Whether such a mechanism exists is a good question, but I think it is likely.
We report that long-term overexpression of
Parkin can eliminate mitochondria with deleterious COXI mutations
in heteroplasmic cybrid cells, thereby enriching cells for wild-type
mtDNA and restoring cytochrome coxidase activity.-link
Emerging data indicate that selective mitochondrial degradation through autophagy (mitophagy) plays a critical role in mitochondrial quality control. Inhibition of mammalian target of rapamycin (mTOR) kinase activity can activate mitophagy. To test the hypothesis that enhancing mitophagy would drive selection against dysfunctional mitochondria harboring higher levels of mutations, thereby decreasing mutation levels over time-link
The mitochondria has its own dna, it codes for vital functions not redundantly covered in the nucleus. It is subject to direct exposure to damaging reactive species, so it can become dysfunctional much more easily than the dna in the nucleus. An obvious question was how can such an organelle subject to far more mutational damage not lead to extinction of most any species. A method of quality control has been found in female reproductive systems, iirc at the level of discarding cells, again iirc. But it opened the question as to whether an intracellular method of quality control might also exist(after all neurons last for over a century of high metabolic activity and they don't divide). As the above two links show it seems very likely there is a method of quality control that can preserve mitochondrial quality.
