抄録
Thrombin-induced thiobarbituric-acid reactive substance (Th-TBARS) formation by platelets was investigated under various experimental conditions. When aspirinized-platelets were incubated with thrombin, Th-TBARS was not detected under any experimental conditions examined. Therefore, thiobarbituric-acid reactive substance (TBARS) formation from endogenous arachidonic acid (AA) was shown not to contain TBARS via the lipoxygenase (PLO) pathway but to be derived from the cyclooxygenase (PCO) pathway. The estimations of PCO and PLO pathway by the measurement of exogenous AA-induced TBARS, the measurement of Th-TBARS and platelet aggregation study by the Born's method were performed in the patients with diabetes mellitus (DM, n=22). Th-TBARS was significantly increased in DM patients (p<0.001) as compared with normal control (n=23). Neither PCO nor PLO activity of diabetic patients was significantly different from normal controls. These data suggest that the mechanism of increase in Th-TBARS formation in DM patients could be ascribed to the increased AA liberation from the platelet membrane. There were no specific relationships between any two of the presence of retinopathy, the increased platelet aggregation and the increased Th-TBARS formation in DM patients.
