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.