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Journal article
Aging augments mitochondrial susceptibility to heat stress
American journal of physiology. Regulatory, integrative and comparative physiology, v 296(3), pp R812-R820
01 Mar 2009
PMID: 19144753
Featured in Collection : UN Sustainable Development Goals @ Drexel
Abstract
Haak JL, Buettner GR, Spitz DR, Kregel KC. Aging augments mitochondrial susceptibility to heat stress. Am J Physiol Regul Integr Comp Physiol 296: R812-R820, 2009. First published January 14, 2009; doi:10.1152/ajpregu.90708.2008.-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.
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Details
- Title
- Aging augments mitochondrial susceptibility to heat stress
- Creators
- Jodie L. Haak - University of IowaGarry R. Buettner - University of IowaDouglas R. Spitz - University of IowaKevin C. Kregel - University of Iowa
- Publication Details
- American journal of physiology. Regulatory, integrative and comparative physiology, v 296(3), pp R812-R820
- Publisher
- Amer Physiological Soc
- Number of pages
- 9
- Grant note
- R01 AG-12350; RO1 CA-100045; P30 CA-086862 / National Institutes of Health; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA P30CA086862 / NATIONAL CANCER INSTITUTE; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Cancer Institute (NCI) University of Iowa College of Medicine ESR R01AG012350 / NATIONAL INSTITUTE ON AGING; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Institute on Aging (NIA)
- Resource Type
- Journal article
- Language
- English
- Academic Unit
- Health Sciences
- Web of Science ID
- WOS:000263745200038
- Scopus ID
- 2-s2.0-64149116643
- Other Identifier
- 991021889038204721
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- Web of Science research areas
- Physiology