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目的 观察桦木尘对小鼠肺组织脂质过氧化和氧化还原相关基因REF 1表达的影响。方法 采用桦木尘水和有机提取液 ,建立小鼠肺肿瘤短期诱发实验二阶段模型 ,将染毒小鼠处死后分为染毒正常肺组织组、肺乳头状腺瘤组织组、肺腺瘤组织组和肺混合型腺瘤组织组 ,另将溶剂组设为对照组。TBA法检测组织匀浆脂质过氧化物 ,免疫组织化学染色法检测REF 1基因的表达。结果 所有染毒组肺组织匀浆TBARS显著高于溶剂对照组 ,其中 ,肺乳头状腺瘤组、肺腺瘤组和肺混合型腺瘤组P <0 0 1 ,染毒正常肺组织组P <0 0 5 ;与染毒正常肺组织组相比 ,肺乳头状腺瘤组织和肺腺瘤组织组TBARS升高 ,P <0 0 5。溶剂对照组和染毒正常肺组织REF 1蛋白免疫组织化学染色反应为阴性 ,肺乳头状腺瘤表现为强烈的核着色 ,肺腺瘤和肺混合型腺瘤则表现为核和胞浆着色。结论 桦木尘的毒作用机制可能与其改变REF 1蛋白的氧化还原调控功能 ,扰乱机体的氧化与抗氧化平衡状态有关
Objective To observe the effect of birch dust on the expression of lipid peroxidation and redox-related gene REF 1 in lung of mice. Methods Two-stage model of mouse lung tumor was established by using birch dust and organic extract. The mice were sacrificed and divided into normal lung tissue group, pulmonary papillary adenoma group, pulmonary adenoma group Group and pulmonary mixed adenoma tissue group, the other solvent group as the control group. Tissue homogenate lipid peroxide was detected by TBA method. The expression of REF 1 gene was detected by immunohistochemical staining. Results TBARS in lung tissue homogenate was significantly higher in all the infected groups than in the solvent control group. Among them, the lung papillary adenoma group, lung adenoma group and pulmonary mixed adenoma group had P <0.01, and the normal lung tissue group P <0 0 5; Compared with normal lung tissue, the TBARS of pulmonary papillary adenoma and lung adenoma increased (P <0.05). The immunoreactivity of REF 1 protein in the solvent control group and normal lung tissue was negative. The pulmonary papillary adenoma showed strong nuclear staining. The pulmonary adenoma and pulmonary mixed adenoma showed nuclear and cytoplasmic staining. Conclusion The toxic mechanism of birch dust may be related to its function of redox regulation of REF 1 protein and disturbing the body’s oxidation and antioxidant balance