Abstract

The location of the initial lesions produced by ionizing radiations in living systems has been investigated by many radiobiologists. One result of radiation injury is the increase in enzymic activities frequently observed in irradiated organisms. Bacq and Alexander (1) suggested that this effect could be explained on the basis that radiations break down internal barriers by altering the cellular and intracellular membranes with consequent release of enzymes. Recently it has been shown (2) that membrane-bound organelles containing hydrolytic enzymes are found in the cytoplasm of cells in many tissues: these particles have been named lysosomes. According to the enzyme release theory, if an ionizing radiation produces damage to the intracellular membranes, and therefore also to the membranes of these lysosomes, a release of the lysosomal enzymes should be expected after irradiation. This hypothesis seems to be supported by some experimental evidence. An increase of acid DNase (deoxyribonucleate 3'-nucleotidohydrolase, E.C. 3.1.4.6) (lysosomal enzyme) has been reported, for instance, a few hours after irradiation in the serum and in the urine of animals treated with X-rays (3, 4). Furthermore, this nuclease and the acid RNase (polyribonucleotide 2-oligonucleotide-transferase (cyclizing), E.C. 2.7.7.16), which is also a lysosomal enzyme, appear to be increased in the soluble fraction of homogenates of tissues derived from animals treated with X-rays (5, 6). Zeman et al. (7) have also demonstrated, by histochemical reactions, that, in mice brain irradiated with microbeams of accelerated deuterons, lysosomal enzymes such as acid phosphatase (o-phosphoric monoester phosphohydrolase, E.C. 3.1.3.2), B3-glucuronidase (3-D-glucuronide glucuronohydrolase, E.C. 3.2.1.31), and cathepsin c (E.C. 3.4.4.9) become evident. The positive histochemical reaction appears along the path of the ionizing particles.

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