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JHC exPRESS: First Published March 31, 2008. doi:10.1369/jhc.2008.950873
Copyright © Histochemical Society, Inc.

A more recent version of this article appeared on June 1, 2008.
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Articles

Aging Results in Increased Autophagy of Mitochondria and Protein Nitration in Rat Hepatocytes Following Heat Stress

Terry D. Oberley 1*, Jamie M. Swanlund 1, Hannah J. Zhang 1 and Kevin C. Kregel 1

1 Department of Integrative Physiology and Free Radical and Radiation Biology Program, Department of Radiation Oncology, The University of Iowa, Iowa City, Iowa (KCK,HJZ); Department of Pathology and Laboratory Medicine, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin (TDO); and Department of Pathology and Laboratory Medicine, William S. Middleton Memorial Veterans Hospital, Madison, Wisconsin (TDO,JMS)

* To whom correspondence should be addressed. E-mail: toberley{at}wisc.edu.

Submitted on January 15, 2008
Accepted on 12 March 2008


  Abstract
The natural breakdown of cells, tissues, and organ systems is a significant consequence of aging and is at least partially due to a decreased ability to tolerate environmental stressors. Based on quantitative ultrastructural analysis using transmission electron microscopy (EM) and computer imaging, we show significant differences in hepatocyte morphology between young and old rats during a 48 h recovery period following a two-day heat stress protocol. Mitochondrial injury was greater overall in old compared to young rats. Autophagy was observed in both young and old rats, with autophagy greater overall in old compared to young hepatocytes. Lipid peroxidation and protein nitration were evaluated by localization and quantification of 4-hydroxy-2-nonenal (4-HNE)-modified protein adducts and 3-nitrotyrosine (3-NT) levels, respectively. Levels of 3-NT but not 4-HNE-protein adducts were significantly elevated in hepatocytes of old rats in comparison to young at 90 min post heat stress, suggesting a major role for reactive nitrogen species (RNS) in pathology observed at this time point. These results demonstrate a differential response of hepatocyte mitochondria to heat stress with aging, as well as greater levels of both autophagic and nitrative damage in old versus young hepatocytes. This manuscript contains online supplemental material at http://www.jhc.org. Please visit this article online to view these materials.

Key Words: mitochondria, 3-nitrotyrosine, autophagy, heat stress, oxidative stress


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