Hormesis, cell death and aging Review uri icon

Overview

MeSH Major

  • Aging
  • Cell Death
  • Hormesis

abstract

  • Frequently, low doses of toxins and other stressors not only are harmless but also activate an adaptive stress response that raise the resistance of the organism against high doses of the same agent. This phenomenon, which is known as "hormesis", is best represented by ischemic preconditioning, the situation in which short ischemic episodes protect the brain and the heart against prolonged shortage of oxygen and nutrients. Many molecules that cause cell death also elicit autophagy, a cytoprotective mechanism relying on the digestion of potentially harmful intracellular structures, notably mitochondria. When high doses of these agents are employed, cells undergo mitochondrial outer membrane permeabilization and die. In contrast, low doses of such cytotoxic agents can activate hormesis in several paradigms, and this may explain the lifespan-prolonging potential of autophagy inducers including resveratrol and caloric restriction.

publication date

  • September 2011

Research

keywords

  • Review

Identity

Language

  • eng

PubMed Central ID

  • PMC3227447

PubMed ID

  • 21931183

Additional Document Info

start page

  • 821

end page

  • 8

volume

  • 3

number

  • 9