The effect of anoxia on cerebral acid hydrolases in the five-day-old rat.

1. Five-day-old anaesthetized rats subjected to slow, prolonged asphyxia (50-55 min) were either allowed to die or resuscitated when at the point of death. Activities of various cerebral acid hydrolases known to be associated with lysosomes were determined in these animals and in littermate controls. 2. Asphyxia to death resulted in a significant increase in the activities of acid phosphatase, cathepsin (pH5.0) and beta-glucuronidase in whole-brain homogenates. 3. The effect of asphyxia on beta-glucuronidase activity was not apparent when the assay was performed in the presence of Triton X-100 (0.1%, v/v). 4. In resuscitated animals whole-brain-homogenate beta-glucuronidase activity showed the greatest increase (31%) 15 min after recovery. After a 60 min recovery period differences between control and asphyxiated animals were no longer apparent. 5. In animals anoxiated to death activities of acid phosphatase and beta-N-acetylglucosaminidase in brain high-speed supernatants were significantly higher than in controls. Acid phosphatase activity was similarly increased in asphyxiated animals resuscitated for 5 or 60 min. 6. It is suggested that the response of the immature rat brain to asphyxia involves a disruption or increased fragility of lysosomal particles.