西安交通大学学报(医学版)
西安交通大學學報(醫學版)
서안교통대학학보(의학판)
JOURNAL OF XI'AN JIAOTONG UNIVERSITY(MEDICAL SCIENCES)
2015年
4期
501-504
,共4页
白改改%路晨阳%申秋菊%蒙珊%惠凌云%苏丹%张王刚%周芙玲
白改改%路晨暘%申鞦菊%矇珊%惠凌雲%囌丹%張王剛%週芙玲
백개개%로신양%신추국%몽산%혜릉운%소단%장왕강%주부령
急性单核细胞白血病(M5)%复发%活性氧自由基%线粒体%氧化应激%抗氧化酶
急性單覈細胞白血病(M5)%複髮%活性氧自由基%線粒體%氧化應激%抗氧化酶
급성단핵세포백혈병(M5)%복발%활성양자유기%선립체%양화응격%항양화매
acute monocytic leukemia (M5)%relapse%reactive oxide species%mitochondrion%oxidative stress%antioxidant enzyme
目的:通过检测氧化应激的相关指标来探讨氧化应激参与急性单核细胞白血病(M5)发病及复发的机制。方法检测原发、复发、化疗缓解后 M5患者细胞内活性氧的水平、外周血血浆中抗氧化酶活性、氧化损伤产物含量,并用透射电镜观察其外周血单个核细胞线粒体的超微结构。结果与正常对照组比较,原发组及复发组 M5患者细胞内活性氧的平均荧光强度均显著增高(P <0.05);原发组 M5患者血浆中抗氧化酶 T-AOC、SOD 活性降低,氧化损伤产物 LDH、MDA、8-OHdG 含量升高,复发组 T-AOC、SOD 活性显著下降,LDH、MDA、8-OHdG 含量显著升高(P <0.05),而化疗缓解组 T-AOC、SOD 活性升高,LDH、MDA、8-OHdG 含量降低;原发组 M5患者线粒体轻度肿胀、嵴间隙增宽;复发组 M5患者线粒体肿胀、畸形明显。结论氧化应激是 M5发病的始动因素。线粒体是生物氧化进行的主要场所,活性氧及其相关的抗氧化酶之间动态平衡的破坏可能是促进复发的主要原因。
目的:通過檢測氧化應激的相關指標來探討氧化應激參與急性單覈細胞白血病(M5)髮病及複髮的機製。方法檢測原髮、複髮、化療緩解後 M5患者細胞內活性氧的水平、外週血血漿中抗氧化酶活性、氧化損傷產物含量,併用透射電鏡觀察其外週血單箇覈細胞線粒體的超微結構。結果與正常對照組比較,原髮組及複髮組 M5患者細胞內活性氧的平均熒光彊度均顯著增高(P <0.05);原髮組 M5患者血漿中抗氧化酶 T-AOC、SOD 活性降低,氧化損傷產物 LDH、MDA、8-OHdG 含量升高,複髮組 T-AOC、SOD 活性顯著下降,LDH、MDA、8-OHdG 含量顯著升高(P <0.05),而化療緩解組 T-AOC、SOD 活性升高,LDH、MDA、8-OHdG 含量降低;原髮組 M5患者線粒體輕度腫脹、嵴間隙增寬;複髮組 M5患者線粒體腫脹、畸形明顯。結論氧化應激是 M5髮病的始動因素。線粒體是生物氧化進行的主要場所,活性氧及其相關的抗氧化酶之間動態平衡的破壞可能是促進複髮的主要原因。
목적:통과검측양화응격적상관지표래탐토양화응격삼여급성단핵세포백혈병(M5)발병급복발적궤제。방법검측원발、복발、화료완해후 M5환자세포내활성양적수평、외주혈혈장중항양화매활성、양화손상산물함량,병용투사전경관찰기외주혈단개핵세포선립체적초미결구。결과여정상대조조비교,원발조급복발조 M5환자세포내활성양적평균형광강도균현저증고(P <0.05);원발조 M5환자혈장중항양화매 T-AOC、SOD 활성강저,양화손상산물 LDH、MDA、8-OHdG 함량승고,복발조 T-AOC、SOD 활성현저하강,LDH、MDA、8-OHdG 함량현저승고(P <0.05),이화료완해조 T-AOC、SOD 활성승고,LDH、MDA、8-OHdG 함량강저;원발조 M5환자선립체경도종창、척간극증관;복발조 M5환자선립체종창、기형명현。결론양화응격시 M5발병적시동인소。선립체시생물양화진행적주요장소,활성양급기상관적항양화매지간동태평형적파배가능시촉진복발적주요원인。
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.