Mitohormesis is a process by which a low dose of some toxic substance or environmental effect causes mitochondria in cells to emit a little more in the way of damaging reactive oxygen species, which in turn causes cellular maintenance mechanisms to ramp up their efforts. The end result is a net gain in health and longevity:
Arsenite is one of the most toxic chemical substances known and is assumed to exert detrimental effects on viability even at lowest concentrations. By contrast and unlike higher concentrations, we here find that exposure to low-dose arsenite promotes growth of cultured mammalian cells. In the nematode C. elegans, low-dose arsenite promotes resistance against thermal and chemical stressors, and extends lifespan of this metazoan, whereas higher concentrations reduce longevity.
While arsenite causes a transient increase in reactive oxygen species (ROS) levels in C. elegans, co-exposure to ROS scavengers prevents the lifespan-extending capabilities of arsenite, indicating that transiently increased ROS levels act as transducers of arsenite effects on lifespan, a process known as mitohormesis. This requires two transcription factors, namely DAF-16 and SKN-1, which employ the metallothionein MTL-2 as well as the mitochondrial transporter TIN-9.1 to extend life span. Taken together, low-dose arsenite extends lifespan, providing evidence for non-linear dose-response characteristics of toxin-mediated stress resistance and longevity in a multicellular organism.
SKN-1 and DAF-16 are already well known as longevity-related genes in nematodes - more data for the importance of mitochondria in aging.