抄録
Superoxide dismutase (S. O. D.) is the enzyme to protect from destructive effect of superoxide (O2-) produced in many metabolic pathways related to oxygen. The purpose of this study was to investigate the possibility that S. O. D. may play an important role in the platelet function.
The cytoplasmic and mitochondrial S. O. D. has been investigated spectrophotometrically and gel electrophoretically in human platelets from eleven patients of chronic myelogenous leukemia (CML) and three patients of primary thrombocythemia (P. Th.). Neither deficiency nor abnormality of cytoplasmic and mitochondria. S. O. D. has been found electrophoretically in any case compared to normal platelets. However, the total activity from three of the CML patients and one of the P. Th. patients were above 3 unit/mg platelet protein (normal subjects: 2.11-2.70 unit/mg protein), suggesting the possibility either that more O2- production occurs in the platelets or that rather little O2- production due to much O2- deprivation by the increased S. O. D.. The platelets from two CML patients and those from one P. Th. were separated into three different platelet density fractions. The cytoplasmic S. O. D. from two of the three patients was different in each three fractions, while that from normal subjects was almost equal, suggesting the qualitative heterogeniety in the platelets from these patients.
The S. O. D. activity of human platelets has been also investigated in several conditions, where much O2- generation might occur in platelets. Sodium fluoride (2mM), which increases platelet O2- production about 3 fold, had no effect on platelet S. O. D. The aggregated platelets induced by ADP (10-5M), epinephrine (50μg/ml), ristocetin (1.5mg/ml) or collagen (1-20μg/ml) had no increase of S. O. D. activity compared to that from non aggregated platelets. X-ray irradiation (1, 000-20, 000R) had not induced its activity increase or decrease. These findings indicated the induction of platelet S. O. D. was not brought about under these conditions.
