慢性苯中毒患者骨髓细胞凋亡和增殖细胞核抗原的研究

Studies on apoptosis and proliferating cell nuclear antigen of bone marrow cells in chronic benzene intoxication patients

目的 探讨慢性苯中毒患者出现血象异常的机制。方法 采用末端脱氧核苷酸转移酶介导的脱氧三磷酸尿嘧啶末端标记法 (TUNEL法 )和免疫组化法分别对慢性苯中毒患者的骨髓标本进行凋亡细胞和增殖细胞核抗原 (PCNA)的检测 ,并分别与正常对照组比较 ,同时将慢性苯中毒患者的骨髓细胞凋亡指数 (AI)和增殖细胞核抗原指数 (PI)作直线相关分析 ,将AI值和PI值分别与所测血象中的白细胞计数、中性粒细胞计数、红细胞计数、血红蛋白量、血小板计数作直线相关分析。结果 慢性苯中毒患者的骨髓细胞AI值为 2 4 .7%± 12 .0 % ,高于正常对照组 (7.3%± 3.5 % ) ,差异有显著性 (P <0 .0 5 ) ;慢性苯中毒组PI值为 10 .7%± 7.8% ,明显低于正常对照组 (31.8%± 11.7% ) ,差异有显著性 (P <0 .0 1) ;慢性苯中毒组的AI值与PI值之间没有直线相关性 (r =0 .36 ,P >0 .0 5 ) ,这两者与血象中各项指标无直线相关性 (P >0 .0 5 )。结论 人类慢性苯中毒的发病过程可出现骨髓细胞凋亡及增殖失衡 ,与造血功能障碍有关。

Objective To explore the pathogenesis of hematologic changes in chronic benzene intoxication patients. Methods Terminal deoxynucleotidyl transferase(TdT) mediated deoxyuridine triphosphate(dUTP) nick end labelling(TUNEL) technique and immunohistochemical assay were employed respectively to detect apoptosis and proliferating cell nuclear antigen(PCNA) of human bone marrow cells in chronic benzene intoxication patients and healthy adult controls.Cell apoptosis index( AI ) and PCNA index( PI ) were calculated,and the correlation between AI and PI ,as well as the correlation between AI , PI and other hematologic indices(such as leukocyte count,neutrophil count,red cell count,hemoglobin,platelet count) were also evaluated. Results The value of AI was 24.7%±12.0% and the value of PI was 10.7%±7.8% in chronic benzene intoxication,while those in controls were 7.3%±3.5% and 31.8%±11.7% respectively.The differences of the AI and PI value between the benzene intoxication and control groups were statistically significant( P <0.05 and P <0.01 respectively).However,no linear correlation between AI and PI was found in chronic benzene intoxication( r =0.36, P >0.05).Neither AI nor PI showed linear relationship with all the other hematologic indics( P >0.05). Conclusion There is evidence on the acceleration of apoptosis and inhibition of proliferation of bone marrow cells in chronic benzene intoxication,which may be the pathogenesis of benzene induced hematopoietic damage.