1980 Volume 17 Issue 6 Pages 601-617
In order to investigate the correlation i) between the accumulation of lipofuscin and aging or other factors, ii) among the accumulation of lipofuscin in the heart, liver and adrenal cortex and iii) between the accumulation of lipofuscin in the different sites within these three organs, the grade of accumulation of this pigment was examined by its occupied area and density in the cells. Histological sections were obtained from the cases of 109 pathological autopsies (0-84 years old), 28 legal autopsies and 34 liver biopsies. Other factors except the aging were as follows: 1) presence or absence of severe morphological lesion in each organ, 2) difference of disease in autopsy diagnosis, 3) the duration of clinical history, 4) sex difference and 5) atomic bomb survivors or non-exposed patients. Quantitative analysis was made statistically.
Significant correlation was noted between the aging and the accumulation of lipofuscin in cardiac, adrenal and hepatic cells. However, only the accumulation of lipofuscin in cardiac muscle cell seems to be applicable to the criteria for a basic biological aging process. In the cases with severe morphological lesion in these organs, the correlation rate was decreased in adrenal and cardiac cells compared with normal organs. The same tendency was noted in each group of disease except the cases of cardiovascular disease and legal autopsy.
The cases with severe morphological lesion in the liver or hepatic disease, in which regeneration and proliferation of hepatocyte was increased, revealed no correlation between the accumulation of lipofuscin in hepatocyte and aging, but the accumulation of lipofuscin in these cases was significantly lower than that of normal hepatocyte. The accumulation of lipofuscin was larger in the central zone than in the peripheral zone of liver with or without severe morphological lesion. This seems to be interesting in association with the contrary localization of reductase in the liver.
The above-mentioned results suggest that the accumulation of lipofuscin is not only regulated with linear rates of increase with aging, but also it is modified by the kinds of organ and its sites.
No correlation was noted between the duration of clinical history and the accumulation of lipofuscin in any factors and decades. The ratio of accumulation of lipofuscin in the cardiac, adrenal and hepatic cells showed 3:2:1. The organ correlation was higher between cardiac and adrenal cell and lower between the hepatic and adrenal cell. In atomic bomb survivors, the accumulation of lipofuscin was not different from that of non-exposed patients.