CHANGES IN CATHEPSIN-B AND LIPOFUSCIN DURING DEVELOPMENT AND AGING INRAT-BRAIN AND HEART

Citation
E. Porta et al., CHANGES IN CATHEPSIN-B AND LIPOFUSCIN DURING DEVELOPMENT AND AGING INRAT-BRAIN AND HEART, Gerontology, 41, 1995, pp. 81-89
Citations number
28
Categorie Soggetti
Geiatric & Gerontology
Journal title
ISSN journal
0304324X
Volume
41
Year of publication
1995
Supplement
2
Pages
81 - 89
Database
ISI
SICI code
0304-324X(1995)41:<81:CICALD>2.0.ZU;2-O
Abstract
While results with inhibitors of thiol proteases have led to the sugge stion that the progressive increase with age of lipofuscin in post-mit otic and some stable cells may be due to an age-related decline in the activity of these enzymes (Ivy et al., 1989), no direct evidence has been yet presented to support this hypothesis. In this study Wistar fe male rats were killed at age of 5, 14, and 24 months and the amounts o f lipofuscin were histologically quantitated in neurons of the left ce rebral parietal cortex and in cardiac myocytes of left ventricle. The sites of cathepsin B activity histochemically detected were quantitate d in sections from left cerebral parietal cortex and left ventricle, a nd the activity of this enzyme was also measured biochemically in brai n and heart homogenates. In line with previous findings, the amounts o f lipofuscin in neurons and cardiac myocytes increased linearly during development and aging (from 5 to 14 and from 14 to 24 mo.). The sites of cathepsin B activity histochemically detected in sections from cer ebral cortex significantly increased from 5 to 14 mo., but remained un changed from 14 to 24 mo, while in sections from the left cardiac vent ricle these sites of activity remained unchanged during development, a nd significantly increased during aging. On the other hand the biochem ically determined activities of cathepsin B in brain and heart homogen ates remained unchanged from 5 to 14 mo., but significantly decreased from 14 to 24 mo. These results suggest that the increase in lipofusci n with age may not be due to an age-wise decline in cathepsin B activi ty.