CAJ | 학술논문

目的　通过测定超氧化物歧化酶（SOD）活力变化，观察刀豆蛋白A（ConA）及与NaF对多形核中性粒细胞（PMN）超氧阴离子自由基（·O2-）释放的影响。方法　采用体外实验。结果　研究表明：①在1ml的反应体系中，37℃温育含粒细胞悬液0.5ml(终浓度1×109/L)，SOD(50NU/ml),当加入ConA后，SOD活力明显下降，即·O2-的释放量明显高于对照组，且ConA浓度为200mg/L时，SOD活力下降明显，即·O2-的释放量最大；②上述条件不变，加入ConA(200mg/L)，当加入NaF(10mg/L)，温育30s时，SOD活力下降最明显，即·O2-释放量最大；NaF达到（50.0,100.0mg/L）时，·O2-释放量不增加且趋于平稳。结论　提示：一定浓度ConA是人粒细胞产生·O2-有效诱发剂；低剂量NaF(10.0mg/L)可能是粒细胞产生活性氧自由基的耗氧性刺激剂，且在较短时间（30s）即可刺激产生大量·O2-；而高剂量NaF可能通过产生蓄积性毒性，损害PMN的结构和功能，从而影响·O2-的释放。
목적　통과측정초양화물기화 매（SOD）활력변화，관찰도두단백A（ConA）급여NaF대다형핵중성립세포（PMN）초양음리자자유기（·O2-）석방적영향。방법　채용체외실험。결과　연구표명：①재1ml적반응체계중，37℃온육함립세포현액0.5ml(종농도1×109/L)，SOD(50NU/ml),당가입ConA후，SOD활력명현하강，즉·O2-적석방량명현고우대조조，차ConA농도위200mg/L시，SOD활력하강명현，즉·O2-적석방량최대；②상술조건불변，가입ConA(200mg/L)，당가입NaF(10mg/L)，온육30s시，SOD활력하강최명현，즉·O2-석방량최대；NaF체도（50.0,100.0mg/L）시，·O2-석방량불증가차추우평은。결론　제시：일정농도ConA시인립세포산생·O2-유효유발제；저제량NaF(10.0mg/L)가능시립세포산생활성양자유기적모양성자격제，차재교단시간（30s）즉가자격산생대량·O2-；이고제량NaF가능통과산생축적성독성，손해PMN적결구화공능，종이영향·O2-적석방。
Objective　Effects of concanavalin A (ConA) and fluoride on the release of superoxide anion(·O2-) in polymorphonuclearl eukocyte (PMN) were studied by measuring the activity of superoxide diamutase (S OD).Methods　In vitro experiments were used.Results　The results as followed:①The reaction mixture in a total volume of 1ml containing 0.5ml of granulocytes suspension (1×109/L final concentration) and 50NU/ml of SOD was incubated at 37℃.When ConA was ad ded,the amount of·O2- was significantly higher than that in the con trol.When the concentration of ConA was 200 mg/L,the amount of　·O2- reached maximal level.②Under the same conditions,when 200 mg/L ConA and NaF(1 0mg/L) were added and incubated for 30 seconds,the amount of　·O2- re leas ed reached maximal level.Very little additional　·O2- occurred when t he concentration of NaF reached 50 mg/L.Conclusions　The results suggested that ConA could induce effectively the release of　·O2- in PMN.The lower concentration of NaF might be a kind of effective stimulant,while the higher concentration of NaF might affect the release of　·O2- by producing accumulative injury and injuring the structure and function.