Zima T, Spicka I, Stípek S, Crkovská J, Pláteník J, Merta M, Tesar V
1st Institute of Medical Chemistry and Biochemistry, First Faculty of Medicine, Charles University, Prague, Czech Republic.
Neoplasma. 1996;43(2):69-73.
Reactive oxygen species and other free radicals are known to be the mediators of phenotypic and genotypic changes that lead from mutation to neoplasia. The imbalance in tumor cell antioxidant defense mechanism can influence also the sensitivity to cytoreductive therapy. In erythrocytes it can result to hemolysis which is one of the pathogenetic mechanisms of anemia in cancer patients. Parameters of lipid peroxidation (malondialdehyde-MDA) and antioxidant enzymes here represented by superoxide dismutase (SOD) and glutathione peroxidase (GPx) in multiple myeloma (MM) have been investigated. Nine patients of various clinical stages and activities of the disease were studied. Significantly higher concentrations of total MDA in plasma (1.20 +/- 0.24 mumol/l vs. 0.64 +/- 0.22 mumol/l, p < 0.0001) as well as in erythrocytes (2.72 +/- 0.81 mumol/l vs. 1.03 +/- 0.44 mumol/l, p < 0.0001) were found comparing to the control group. The levels of free MDA in plasma (0.31 +/- 0.09 mumol/l vs. 0.49 +/- 0.17 mumol/l, p < 0.05) and in erythrocytes (0.29 +/- 0.20 mumol/l vs. 0.59 +/- 0.22 mumol/l, p < 0.001) were decreased in myeloma patients. Significantly lower activities of GPx (19.17 +/- 4.07 U/g Hb vs. 23.26 +/- 3.61 U/g Hb, p < 0.05) and SOD (1882.46 +/- 181.73 U/g Hb vs. 2347.13 +/- 502.51 U/g Hb, p < 0.05) in erythrocytes were found. We did not observe evident relationship between the concentration of MDA or the activities of SOD and GPx and either the stage of the disease, or the level and the type of paraprotein. These results propose possible role of free radicals with reduced antioxidant activities of SOD and GPx in multiple myeloma.
已知活性氧和其他自由基是导致从突变到肿瘤形成的表型和基因型变化的介质。肿瘤细胞抗氧化防御机制的失衡也会影响对减瘤治疗的敏感性。在红细胞中，这可能导致溶血，这是癌症患者贫血的发病机制之一。研究了多发性骨髓瘤（MM）中脂质过氧化参数（丙二醛-MDA）以及以超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GPx）为代表的抗氧化酶。研究了9例处于不同临床阶段和疾病活动度的患者。与对照组相比，血浆中总MDA浓度显著更高（1.20±0.24μmol/l对0.64±0.22μmol/l，p<0.0001），红细胞中也是如此（2.72±0.81μmol/l对1.03±0.44μmol/l，p<0.0001）。骨髓瘤患者血浆中游离MDA水平（0.31±0.09μmol/l对0.49±0.17μmol/l，p<0.05）和红细胞中游离MDA水平（0.29±0.20μmol/l对0.59±0.22μmol/l，p<0.001）降低。红细胞中GPx（19.17±4.07U/g Hb对23.26±3.61U/g Hb，p<0.05）和SOD（1882.46±181.73U/g Hb对2347.13±502.51U/g Hb，p<0.05）的活性显著降低。我们未观察到MDA浓度或SOD和GPx活性与疾病阶段、副蛋白水平及类型之间存在明显关系。这些结果提示自由基以及SOD和GPx抗氧化活性降低在多发性骨髓瘤中可能发挥作用。
