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目的研究氯化铟气管注入染毒对大鼠造成的遗传损伤和氧化损伤。方法选取32只雄性健康成年SPF级Wistar大鼠,随机分为4组[生理盐水对照组,低、中、高剂量(0.065、0.65和1.3 mg/kg)氯化铟染毒组],采用非暴露式气管内注入法染毒,HE染色法光镜下观察肺组织病理形态学变化,测定肺组织匀浆丙二醛(MDA)和超氧化物歧化酶(SOD)含量,对骨髓涂片进行嗜多染红细胞微核计数,并采用ICP-MS法检测大鼠全血和肺组织中铟的含量。结果 3个剂量组大鼠血铟、肺铟含量和骨髓嗜多染红细胞微核率均明显高于对照组(P<0.01);中、高剂量组大鼠肺组织中MDA含量亦较对照组显著增加(P<0.05),而SOD水平均显著低于对照组(P<0.05);肺组织病理观察显示氯化铟染毒后大鼠气管周围充血明显,肺泡间隔、细支气管壁增厚,肺泡腔内充满细颗粒状蛋白样物质。结论氯化铟气管注入法染毒会引起大鼠血铟、肺铟蓄积,骨髓嗜多染红细胞微核率增加,发生氧化损伤和组织病理学改变。
Objective To study the genetic damage and oxidative damage induced by injecting indium chloride in trachea in rats. Methods Thirty-two healthy adult Wistar rats were randomly divided into 4 groups (saline control group, low, medium and high dose (0.065, 0.65 and 1.3 mg / kg) Indium Chloride exposure group) Exposed to intratracheal instillation, the pathological changes of lung tissue were observed under light microscope with HE staining, and the content of malondialdehyde (MDA) and superoxide dismutase (SOD) in lung homogenates were measured. Micronucleus count of polychromatic erythrocytes, and the contents of indium in whole blood and lung tissue of rats were detected by ICP-MS method. Results The levels of blood indium, lung indium and micronuclei of bone marrow polychromatic erythrocytes were significantly higher in the three dose groups than those in the control group (P <0.01). The contents of MDA in lung tissue of middle and high dose groups were also higher than those in the control group (P <0.05), while the level of SOD was significantly lower than that of the control group (P <0.05). The pathological observation of lung tissue showed that the rats had hyperemic tracheal peritoneum after exposure to indium chloride, the alveolar septum, thickened bronchiole wall, Alveolar cavity filled with fine granular protein-like substance. Conclusion Indium chloride intratracheal instillation can induce the accumulation of blood indium, lung and indium in rat blood, increase the micronucleus rate of bone marrow polychromatic erythrocytes, and cause oxidative damage and histopathological changes.