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Aging augments mitochondrial susceptibility to heat stress
Journal article   Open access   Peer reviewed

Aging augments mitochondrial susceptibility to heat stress

Jodie L Haak, Garry R Buettner, Douglas R Spitz and Kevin C Kregel
American journal of physiology. Regulatory, integrative and comparative physiology, Vol.296(3), pp.R812-R820
03/2009
DOI: 10.1152/ajpregu.90708.2008
PMCID: PMC2665848
PMID: 19144753
url
https://doi.org/10.1152/ajpregu.90708.2008View
Published (Version of record) Open Access

Abstract

The pathophysiology of aging is accompanied by a decline in tolerance to environmental stress. While mitochondria are primary suspects in the etiology of aging, little is known about their ability to tolerate perturbations to homeostasis in older organisms. To investigate the role of mitochondria in the increased susceptibility to heat stress that accompanies aging, young and old Fischer 344 rats underwent a heat stress protocol known to elicit exaggerated cellular damage with aging. At either 2 or 24 h after heat stress, livers were removed from animals, and hepatic mitochondria were isolated. Electron microscopy revealed extensive morphological damage to mitochondria from young and, to a greater extent, old rats after heat stress. There was also a significant loss of cytochrome c from old, but not young, mitochondria and a persistent increase in 4-hydroxynonenal-modified proteins in old vs. young mitochondria exposed to heat stress. Electron paramagnetic resonance measurements of superoxide indicate greater superoxide production from mitochondria of old compared with young animals and suggest that mitochondrial integrity was altered during heat stress. The mitochondrial stress response, which functions to correct stress-induced damage to mitochondrial proteins, was also blunted in old rats. Delayed and reduced levels of heat shock protein 60 (Hsp60), the main inducible mitochondrial stress protein, were observed in old compared with young mitochondria after heat stress. Additionally, the amount of Hsp10 protein increased in young, but not old, rat liver mitochondria after hyperthermic challenge. Taken together, these data suggest that mitochondria in old animals are more vulnerable to incurring and less able to repair oxidative damage that occurs in response to a physiologically relevant heat stress.
 stress response cytochrome c liver mitochondria Environmental Physiology ROS

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