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Experimental alterations of the bound state of cerebral lysosomal enzymes

I N IIIS LYSOSOMAL HYPOTHESIS of cell injury, de Duvel proposed that the acid hydrolases, ordinarily bound within the lysosomes, might be released into the cell sap and surrounding tissues under various injurious conditions, resulting in local destruction of cellular components and adjacent tissue. Leighty and coworkers,2 using canine heart muscle, and de Duve and Beaufay,3 with rat liver, have presented evidence that this may occur as a result of anoxia. Excess vitamin A was employed by Weissmann and Thomas4 and Dingle5 to obtain similar results in rabbit cartilage and rat liver. Abraham et a1.6 have recently presented histochemical evidence that oxygen toxicity may also produce an alteration in the permeability of rat liver lysosomal membranes. Their work complemented the biochemical evidence This study was undertaken to evaluate the effects of these labilizers upon lysosomal enzyme distribution in brain and to assess the possible role of hydrolase release in the pathogenesis of experimental brain injury. The study utilized the techniques of enzyme latency measurements and nonsedimentable fraction determinations, and many of the results were compared with parallel studies on rat liver.