dinoprost and Precursor-Cell-Lymphoblastic-Leukemia-Lymphoma

In this study the authors addressed the question whether neurotoxicity due to the chemotherapy of acute lymphoblastic leukemia (ALL) is associated with cerebrospinal fluid (CSF) oxidative stress. Examination of 38 ALL patients revealed significant increases in 8-isoprostane concentration and important decreases in total antioxidative capacity of CSF during therapy. The mean 8-isoprostane level at diagnosis was 9.05 +/- 1.62 pg/mL, and no correlations with initial leukocytosis, organomegaly, and lactate dehydrogenase levels were noted. 8-Isoprostane concentrations were increased on the 59th day of treatment (mean level: 24.85 +/- 7.59 pg/mL [P < .01]) and remained elevated at 4 points of the consolidation phase (17.28 +/- 2.16 pg/mL [P < .05]; 22.72 +/- 6.04 pg/mL [P < .05]; 24.92 +/- 6.31 pg/mL [P < .01]; 32.32 +/- 7.94 pg/mL [P < .01]) as compared to their level at diagnosis. The mean total antioxidative capacity at diagnosis was 203.08 +/- 6.17 mumol/L and was remarkably decreased on the 59th day of treatment (189.76 +/- 1.9 mumol/L [P < .05]) and at one point of the consolidation phase (188.29 +/- 3.46 mumol/L [P < .05]) as compared to the level at diagnosis. This study indicates that neurotoxicity of standard ALL treatment may be related to oxidative stress.

Topics: Adolescent; Antineoplastic Combined Chemotherapy Protocols; Antioxidants; Child; Child, Preschool; Dinoprost; Female; Humans; Male; Oxidative Stress; Precursor Cell Lymphoblastic Leukemia-Lymphoma