Zima T, Spicka I, Stípek S, Crkovská J, Pláteník J, Merta M, Nĕmecek K, Tesar V
I. ústav lékarské chemie a biochemie 1. LF UK, Praha.
Cas Lek Cesk. 1996 Jan 4;135(1):14-7.
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 results to hemolysis which is one of pathogenetic mechanisms of anemia in cancer patients.
We investigated the parameters of lipid peroxidation (malondialdehyde-MDA) and antioxidant enzymes here represented by superoxide dismutase (SOD) and glutathione peroxidase (GPx) in multiple myeloma. Nine patients of various clinical stage and activity of disease were studied. A significant higher concentration of total MDA in plasma (1.20 +/- 0.24 mumol/l v.s. 0.64 +/- 0.22 mumol/l, p < 0.0001) as well as in erythrocytes (2.72 +/- 0.81 mumol/l v.s. 1.03 +/- 0.44 mumol/l, p < 0.0001) was found comparing to the control group. The levels of free MDA in plasma (0.31 +/- 0.09 mumol/l v.s. 0.49 +/- 0.17 mumol/l, p < 0.05) and in erythrocytes (0.29 +/- 0.20 mumol/l v.s. 0.59 +/- 0.22 mumol/l, p < 0.001) were decreased in myeloma patients. A significantly lower activity of GPx (19.17 +/- 4.07 U/g v.s. 23.26 +/- 3.61 U/g Hb, p < 0.05) and SOD (1882.46 +/- 181.73 U/g v.s. 2347.13 +/- 502.51 U/g Hb, p < 0.05) in erythrocytes were found.
We didn't observe evident relationship between the concentration of MDA or activities of SOD and GPx and either the stage of disease or level and type of paraprotein. We can conclude, that higher concentration of total MDA as a parameter of lipid peroxidation, is significantly increased in patients with multiple myeloma. It could be consequence of impaired antioxidant defence. These results propose possible role of free radicals with reduced antioxidant activity of SOD and GPx in multiple myeloma. As we can consider the role of free radicals in pathogenesis of malignant proliferation, prognostic value and the change during the course of therapy should by studied.
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细胞减灭疗法的敏感性。在红细胞中，这可能导致溶血，而溶血是癌症患者贫血的发病机制之一。
我们研究了多发性骨髓瘤中脂质过氧化参数（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例处于不同临床分期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活性（19.17±4.07U/g对23.26±3.61U/g Hb，p<0.05）和SOD活性（1882.46±181.73U/g对2347.13±502.51U/g Hb，p<0.05）显著降低。
我们未观察到MDA浓度或SOD和GPx活性与疾病分期、副蛋白水平及类型之间存在明显关系。我们可以得出结论，作为脂质过氧化参数的总MDA浓度在多发性骨髓瘤患者中显著升高。这可能是抗氧化防御受损的结果。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的作用。鉴于我们可以考虑自由基在恶性增殖发病机制中的作用，其预后价值以及治疗过程中的变化值得研究。
