HISTOCHEMISTRY OF PARTICLE MICROBEAM LESIONS IN THE BRAIN OF THE MOUSE*

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Abstract
This investigation was undetaken to obtain some histochemical data on brain tissue tolerance to particle microbeam irradiation by comparing early and delayed neuronal and vascular damage in sequential and concurrent time relations during pathogenesis. It was found that: Non-significant changes in alkaline phosphatase activity in brain tissue irradiated with slit microbeams suggested that vascular disturbances may play a relatively minor role in the early and delayed cell necrosis in such microbeam lesions. In contrast, lesions produced by 1 mm beams were characterized by decreased alkaline phosphatase activity which preceded cell necrosis. Early direct cellular damage was identified by a conglomeration of particles rich in acid phosphatase and cathepsin Type-C esterase. Both reactions decreased subsequent to cellular autolysis. At later postirradiation stages, an increase in glial acid phosphatase activity was observable in the irradiated white matter suggesting repair of damaged interstitial glial and endothelial elements as demonstrated by uptake of injected H3-thymidine. The severity of early and delayed vascular damage was related to beam diameter, volume of irradiated tissue, and caliber of blood vessels. In general, increasing beam diameters produced increasing circulatory damage and greater latency as well as variability in both cellular and vascular radiation injury. Histochemically, the irradiated vessels developed hyalinization, became PAS positive and were characterized by a deposition of PAS positive globules in the perivascular regions.

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