Plasma myeloperoxidase is related to the severity of coronary artery disease.

OBJECTIVE: It has been shown that the main apolipoprotein of HDL, Apo A-1, is subjected to nitration by myeloperoxidase (MPO) and this oxidative modification renders HDL proatherogenic. The aim of this study is to evaluate the relationship between plasma MPO levels, and the severity of coronary artery disease. METHODS AND RESULTS: Forty-eight patients with coronary artery narrowing and 30 control subjects were enrolled in this study. The severity of the disease was assessed by Gensini scoring after angiography. MPO concentrations were determined by using an enzyme immunoassay. A subgroup of 30 patients underwent computerized tomography to determine the calcium load of coronary arteries. Plasma MPO levels were found significantly higher in patients with coronary artery disease than controls (4.27 [1.60 to 42.43] ng/mL vs. 2.93 [1.00 to 9.25] ng/mL, P = 0.002). MPO was positively correlated with both Gensini (r = 0.228, P = 0.044) and coronary calcium scores (r = 0.433, P = 0.017). The atherosclerotic burden was more strongly correlated with MPO levels than the traditional markers such as total cholesterol and HDL. CONCLUSIONS: We found that MPO levels were elevated in patients with coronary artery disease and this increase correlated with the extent and severity of atherosclerosis. Although it is a preliminary study with a relatively small group of subjects, we suggest that MPO might be evaluated as a new marker indicating the presence and severity of coronary artery disease.

Effect of fludarabine on leukocyte functions.

BACKGROUND: Fludarabine induces leukemic cell apoptosis and is highly efficient in chronic lymphocytic leukemia. However, fludarabine therapy causes severe leukopenia. Leukocyte myeloperoxidase (MPO) catalyzes the formation of HOCl, and this is the main microbicidal function in phagocytes. The aim of our study was to evaluate the effect of fludarabine on leukocytes, i.e. their degranulation capacity, MPO activity and HOCl production. METHODS: Peripheral blood leukocytes were incubated for 48 h with fludarabine. Degranulation was measured using a flow-cytometric method. MPO activity and HOCl production were measured spectrophotometrically. RESULTS: The degranulation capacity of fludarabine-treated leukocytes was significantly elevated compared to untreated controls. MPO activity and HOCl production were also increased in parallel. A possible direct activating effect of fludarabine was tested on the MPO activity of HL60 cells. Fludarabine did not affect MPO activity at concentrations ranging from 10 microM to 2 mM. CONCLUSION: Fludarabine had no inhibitory effect on the microbial killing of leukocytes.