Koistinen Pirjo, Ruuska Satu, Saily Marjaana, Kakko Sakari, Siitonen Pauliina, Siitonen Timo, Savolainen Markku J, Kinnula Vuokko L, Savolainen Eeva-Riitta
Department of Internal Medicine, University of Oulu, Finland.
Haematologica. 2006 Jun;91(6):829-32.
Manganese superoxide dismutase (MnSOD) protects cells against oxidative stress by eliminating superoxides. Hypothetically, decreased MnSOD levels in cancer might lead to increased oxidative stress and, thus, to increased sensitivity of cells to chemotherapy agents. Eighty-nine patients with acute myeloid leukemia (AML) were analyzed for a functional C to T polymorphism of MnSOD, which could potentially lead to decreased enzyme concentrations inside mitochondria. A significant survival advantage (p=0.02) was observed for those AML patients carrying T-containing alleles of MnSOD compared to the patients with the CC genotype. These preliminary results may indicate an important role for genetic factors regulating the cellular redox state in determining the outcome of leukemia chemotherapy.
锰超氧化物歧化酶（MnSOD）通过清除超氧化物来保护细胞免受氧化应激。据推测，癌症中MnSOD水平降低可能导致氧化应激增加，进而导致细胞对化疗药物的敏感性增加。对89例急性髓系白血病（AML）患者进行了MnSOD功能性C到T多态性分析，该多态性可能导致线粒体内酶浓度降低。与CC基因型患者相比，携带MnSOD含T等位基因的AML患者具有显著的生存优势（p=0.02）。这些初步结果可能表明，在决定白血病化疗结果方面，调节细胞氧化还原状态的遗传因素具有重要作用。
