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ABSTRACT:Objective To detect the expressions of thioredoxin (TRX1)and c-jun-activation-domain binding protein-1 (JAB1)in patients with acute myelogenous leukemia (AML)and healthy controls,and measure the TRX1 level in AML patients at different stages for evaluating its clinical significance.Methods The expressions of TRX1 and JAB1 in leukemia samples were analyzed by RT-PCR and Western blot at mRNA and protein levels, respectively.The correlation between TRX1 and JAB1,and the relationship between the gene expression and peripheral blood leukocytes count were also analyzed.Furthermore,serum TRX1 was measured by ELISA.Results TRX1 and JAB1 expressions at both mRNA and protein levels were obviously upregulated in leukemia patients (P<0.05). TRX1 was positively related to JAB1 in both newly diagnosed and recurrent AML patients.And high levels of TRX1 and JAB1 expressions were associated with white blood cell (WBC)counts in AML patients (P<0.05).Moreover, abundance of TRX1 in serum was significantly greater in AML patients,especially in the patients with recurrent AML,than in healthy donors (P<0.05).Conclusion There is a positive correlation between the expressions of TRX1 and JAB1 ,which is closely related to the occurrence and progression of AML.
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Objective To study the mechanism of oxidative stress involved in the pathogenesis and relapse of acute monocytic leukemia (M5 ).Methods We detected reactive oxide species (ROS)levels,conducted plasma analysis obtained from 76 M5 patients at diagnosis and at relapse,and observed the ultrastructure of mitochondria of mononuclear cells in peripheral blood by transmission electron microscope.Results Compared with that in the control group,the average fluorescence intensity of intracellular ROS was significantly increased in M5 groups, especially in the relapse patients (P < 0.05 ).Low total antioxidative capacity (T-AOC)and antioxidant enzyme activity were characteristic of M5 at both diagnosis and relapse. However, lactate dehydrogenase (LDH ), malondialdehyde (MDA)and 8-hydroxy-2’-deoxyguanine (8-OHdG)increased significantly at both diagnosis and relapse (P < 0.05 ).Prominent ultrastructural abnormalities (mitochondrial swelling,outer membrane blebs,and aberrant cristae disorder)were present in patients with primary M5,and they were obviously abnormal in relapsing M5 patients.Conclusion Oxidative stress is the initiating factor of M5.Mitochondria are the main intracellular location for ROS generation.To maintain the dynamic balance between ROS and antioxidant defence may be the critical factor for preventing relapse.