Abstract

The recognition of the lysosome as a distinct intracellular structure has been followed by several attempts to elucidate the possible role of this organelle in the production or exacerbation of cellular radiation damage. The lysosome is a natural subject for such investigations, since it is essentially a depot of hydrolytic enzymes segregated from the rest of the cell by a single bounding membrane. The properties of lysosomes have been recently reviewed (1). Studies of the lysosomal enzyme acid phosphatase in cells collected from the peritoneal cavity of rats bearing induced peritoneal exudates 1 to 10.5 hours after whole-body X-irradiation (800 R) indicated an increase in the amount of this enzyme and suggested the possibility of lysosomal damage. Other cells and tissues of irradiated animals have also been found to possess slightly increased or labilized lysosomal enzyme content (2-9). The interpretation of these results is often complicated, however; there is evidence that the apparent increase in enzyme activity observed after whole-body irradiation may be the result of changes in cell population within certain tissues (10), destruction of lymphatic tissues (9), or increased endocrine activity (7). In the case of the peritoneal cell study cited above, the analysis is further complicated by the occurrence of early postirradiation changes in the net permeability of blood vessels in or bordering on the peritoneal cavity.2 Investigations of isolated lysosomes have not provided a complete answer to the question of the extent of lysosomal involvement in cellular radiation effects. Although high doses are usually required to elicit release of hydrolytic enzymes in vitro (11), lysosomes isolated from different tissues respond differently to ionizing radiation. Lysosomes isolated from rat liver showed increased reaction with enzyme

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