New paper by Ristow group on mitochondrial hormesis

Mitochondrial hormesis links low-dose arsenite exposure to lifespan extension.

Schmeisser S, Schmeisser K, Weimer S, Groth M, Priebe S, Fazius E, Kuhlow D, Pick D, Einax JW, Guthke R, Platzer M, Zarse K, Ristow M.
Source
Department of Human Nutrition, Institute of Nutrition, University of Jena, D-07743, Jena, Germany; Leibniz Graduate School of Aging, Leibniz Institute for Age Research, Fritz-Lipmann-Institute, D-07745, Jena, Germany.

Abstract
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 lifespan. Taken together, low-dose arsenite extends lifespan, providing evidence for nonlinear dose-response characteristics of toxin-mediated stress resistance and longevity in a multicellular organism.

Mithridates was on to something.

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The military school of health and long life - Rogue Health and Fitness says February 2, 2015

[…] which the body acts to defend itself. This is even the case with frankly poisonous substances, like arsenite. In effect, what doesn’t kill the body makes it stronger. As Nietzsche called this aphorism, […]

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