Journals of Gerontology Series A: Biological Sciences and Medical Sciences Large Type Edition
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The Journals of Gerontology Series A: Biological Sciences and Medical Sciences 63:813-822 (2008)
© 2008 The Gerontological Society of America

Reduction of Age-Associated Pathology in Old Mice by Overexpression of Catalase in Mitochondria

Piper M. Treuting, Nancy J. Linford, Sue E. Knoblaugh, M. J. Emond, John F. Morton, George M. Martin, Peter S. Rabinovitch and Warren C. Ladiges

Departments of 1 Comparative Medicine, 2 Pathology, and 4 Biostatistics, University of Washington, Seattle.
3 Fred Hutchinson Cancer Research Center, Seattle, Washington.

Address correspondence to Piper M. Treuting, DVM, T140 Health Sciences Center, Box 357190, Seattle, WA, 98195-7190. E-mail: treuting{at}u.washington.edu

We describe the effects of mitochondrially targeted catalase (MCAT) expression on end-of-life pathology in mice using detailed semiquantitative histopathological evaluation. We previously reported that the median and maximum life spans of MCAT mice were extended relative to those of wild-type littermates. We now report that MCAT expression is associated with reduced malignant nonhematopoietic tumor burden, reduced cardiac lesions, and a trend toward reduced systemic inflammation, with no effect on hematopoietic neoplasia or glomerulonephropathy. Combined disease burden and comorbidity are also reduced, and MCAT expression is not associated with any detrimental clinical effects. The results suggest that oxidative damage is involved in aging of C57BL/6J mice via modulation of a subset of age-associated lesions. Antioxidant interventions targeting mitochondria may therefore be a viable strategy for prevention or postponement of some age-associated diseases. The variability of the MCAT effect across tissues, however, illustrates the importance of developing semiquantitative histopathology for assessment of comorbidity in life-span studies.

Key Words: Pathology • Free radicals • Oxidative stress






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