Open AccessMitochondrial hormesis links low‐dose arsenite exposure to lifespan extension
Author(s) -
Schmeisser Sebastian,
Schmeisser Kathrin,
Weimer Sandra,
Groth Marco,
Priebe Steffen,
Fazius Eugen,
Kuhlow Doreen,
Pick Denis,
Einax Jürgen W.,
Guthke Reinhard,
Platzer Matthias,
Zarse Kim,
Ristow Michael
Publication year - 2013
Publication title -
aging cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.103
H-Index - 140
eISSN - 1474-9726
pISSN - 1474-9718
DOI - 10.1111/acel.12076
Subject(s) - hormesis , arsenite , biology , metallothionein , reactive oxygen species , longevity , microbiology and biotechnology , oxidative stress , genetics , biochemistry , arsenic , chemistry , gene , organic chemistry
Summary 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.