机构地区:[1]天津市疾病预防控制中心职业健康研究所,天津300011
出 处:《公共卫生与预防医学》2024年第1期34-38,共5页Journal of Public Health and Preventive Medicine
基 金:天津市医学重点建设学科(TJYXZDXK-066B);天津市卫生健康科技项目(TJWJ2023QN088)。
摘 要:目的观察亚慢性吸入染毒甲苯二异氰酸酯(toluene diisocyanate,TDI)对大鼠肺脏组织的氧化应激损伤影响。方法无特定病原体级健康SD雄性大鼠随机分组,对照组大鼠予新鲜空气,低、中和高剂量组大鼠以动式染毒的方式暴露于TDI环境。观察大鼠肺脏组织的超微结构和组织病理学改变;采用化学比色法检测肺脏组织中丙二醛(MDA)、还原型谷胱甘肽(GSH)、谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)和过氧化氢酶(CAT)水平;采用Real-time PCR检测法检测HO-1 mRNA相对表达水平,蛋白质免疫印迹法检测HO-1蛋白表达水平。结果各剂量组大鼠体质量、肺组织质量和肺脏脏器系数均低于对照组(P<0.05),各组大鼠体质量均随染毒时间的增加而增加(P<0.05);肺组织病理学检查结果显示:TDI染毒后高剂量组大鼠肺组织见肺泡壁明显充血、水肿,肺泡壁明显增厚,肺泡腔内可见大量红细胞淤积等病理变化。肺组织超微结构检查结果显示:TDI染毒后高剂量组大鼠肺泡细胞肿胀、数量减少,细胞边界不清晰、形态不规则等。各剂量TDI染毒组大鼠肺组织中MDA水平分别高于对照组(P值均<0.05),而GSH、GSH-Px、SOD和CAT水平分别低于对照组(P<0.05);各组大鼠的HO-1基因和蛋白水平比较,差异均无统计学意义(P>0.05)。结论亚慢性TDI染毒可导致大鼠肺脏组织的病理结构和超微结构发生改变,导致肺功能代谢酶水平的异常,从而诱导肺脏发生氧化应激损伤;但HO-1在肺脏氧化应激损伤中无明显变化。Objective To investigate the effect of subchronic inhalation of toluene diisocyanate(TDI)on oxidative stress damage in rat lung tissue.Methods SPF-grade Sprague-Dawley male rats were randomly divided into 4 groups,the rats were placed in a HOPE-MED 8050A movable poison cabinet in a cage.To observe the ultrastructural and histopathology changes of lung tissue in rats.The levels of reduced glutathione(GSH),glutathione peroxidase(GSH-Px),malondialdehyde(MDA),superoxide dismutase(SOD),and catalase(CAT)in lung tissue were detected.The ultrastructural and histopathological changes were examined.The expression levels of HO-1 mRNA and protein were detected by Real-time PCR and Western Blot,respectively.Results The body mass,lung tissue mass,and lung organ coefficient of rats in each dose group were lower than those in the control group(P<0.05),and the body mass of rats in each group increased with the increase of exposure time(P<0.05);The results of lung histopathological examination showed that after TDI exposure,in the high-dose group,pulmonary alveolar wall hyperemia and edema were observed in the lung tissue of rats,alveolar wall thickening was observed,alveolar septa widening,and a large number of red blood cells were seen in the alveolar cavity.The results of ultrastructural examination of lung tissue showed that after TDI exposure,while in the high-dose group,the number of alveolar cells decreased,with unclear cell boundaries and irregular morphology.The levels of MDA in the lung tissue of rats exposed to TDI at various doses were higher than those in the control group(P<0.05),while the levels of GSH,GSH-Px,SOD,and CAT were lower than those in the control group(P<0.05);There was no significant difference in HO-1 gene and protein levels among rats in each group(P>0.05).Conclusion Subchronic inhalation of TDI can cause changes in the pathology and ultrastructure of rat lung tissue,leading to abnormal levels of metabolic enzymes in lung function,thereby inducing oxidative stress damage to the lungs.However,there was
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...