Targeted Chelation Versus Lipofuscin Buildup?

In a similar fashion to the way in which antioxidants change from dubious to demonstrably beneficial for lifespan when targeted to mitochondria, it is proposed that chelation targeted to the cell's lysosomes can slow the accumulation of lipofuscin in your cells. You might recall that lipofuscin buildup with age contributes to age-related degeneration by eventually destroying the ability of cells to function. "Since the sensitivity of lysosomes to oxidative stress can be manipulated by altering the intralysosomal level of redox-active iron, it follows that lipofuscin formation might also be influenced. It is suggested that pulse doses of iron chelators that easily penetrate membranes could be used to diminish lipofuscinogenesis." But don't run out to buy chelation products - ingesting that stuff won't send it anywhere near your lysosomes, just as swallowing antioxidant products won't affect your mitochondria. More engineering is needed, and in this case a technology demonstration to confirm the proposal.


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