AIM: To assess the levels of antioxidant capacity and oxidative damage in blood of chronic pancreatitis (CP) patients in comparison with those in healthy control sub- jects, by using several different analytical techn...AIM: To assess the levels of antioxidant capacity and oxidative damage in blood of chronic pancreatitis (CP) patients in comparison with those in healthy control sub- jects, by using several different analytical techniques. METHODS: Thirty-five CP patients and 35 healthy con- trol subjects were investigated prospectively with re- spect to plasma levels of thiols, ferric reducing ability of plasma (FRAP, i.e. antioxidant capacity), levels of protein carbonyls and thiobarbituric acid reactive substances (TBARS). Additionally, we evaluated the production of reactive oxygen species (ROS) in whole blood. RESULTS: The antioxidative thiols including cysteine, cysteinylglycine and glutathione were significantly lower in CP patients. In addition, the non-enzymatic antioxi- dant capacity was significantly lower in CP patients, which correlated with the amount of oxidative protein (protein carbonyls) and the extent of lipid damage (TBARS), both were significantly higher in CP patients. The ROS production in whole blood after stimulation with phorbol 12-myritate 13-acetaat, demonstrated a strong tendency to produce more ROS in CP patients. CONCLUSION: Oxidative stress may contribute to the pathogenesis of chronic pancreatitis by decreasing anti- oxidant capacity and increasing oxidative damage in CP patients may be a rationale for intervention with antioxi- dant therapy.展开更多
基金Supported by a grant from the Dutch Foundation of Digestive Diseases
文摘AIM: To assess the levels of antioxidant capacity and oxidative damage in blood of chronic pancreatitis (CP) patients in comparison with those in healthy control sub- jects, by using several different analytical techniques. METHODS: Thirty-five CP patients and 35 healthy con- trol subjects were investigated prospectively with re- spect to plasma levels of thiols, ferric reducing ability of plasma (FRAP, i.e. antioxidant capacity), levels of protein carbonyls and thiobarbituric acid reactive substances (TBARS). Additionally, we evaluated the production of reactive oxygen species (ROS) in whole blood. RESULTS: The antioxidative thiols including cysteine, cysteinylglycine and glutathione were significantly lower in CP patients. In addition, the non-enzymatic antioxi- dant capacity was significantly lower in CP patients, which correlated with the amount of oxidative protein (protein carbonyls) and the extent of lipid damage (TBARS), both were significantly higher in CP patients. The ROS production in whole blood after stimulation with phorbol 12-myritate 13-acetaat, demonstrated a strong tendency to produce more ROS in CP patients. CONCLUSION: Oxidative stress may contribute to the pathogenesis of chronic pancreatitis by decreasing anti- oxidant capacity and increasing oxidative damage in CP patients may be a rationale for intervention with antioxi- dant therapy.
