中华劳动卫生职业病杂志
中華勞動衛生職業病雜誌
중화노동위생직업병잡지
CHINESE JOURNAL OF INDUSTRIAL HYGIENE AND OCCUPATIONAL DISEASES
2011年
9期
705-706
,共2页
程宁%王秋英%李宇%王蓓%宣小强%刘静%吴喜江
程寧%王鞦英%李宇%王蓓%宣小彊%劉靜%吳喜江
정저%왕추영%리우%왕배%선소강%류정%오희강
羰基镍%肺%DNA损伤
羰基鎳%肺%DNA損傷
탄기얼%폐%DNA손상
Nickel carbonyl%Lung%DNA damage
目的 观察大鼠急性羰基镍中毒后肺细胞DNA损伤程度以及组织细胞病理变化。方法 SD大鼠静态分别吸人20、135和250 mg/m3羰基镍染毒30 min,另设250 mg/m3氯气染毒组和正常对照组在染毒后第1、2、3和7天取肺组织单细胞凝胶电泳试验检测肺细胞DNA损伤程度,同时观察大鼠肺组织病理变化和细胞超微结构改变。结果 不同浓度羰基镍染毒后不同时间,大鼠肺组织细胞均有损伤,以72 h DNA损伤最重,但损伤晚于氯气。不同浓度羰基镍染毒大鼠肺组织有炎性渗出和增生,部分细支气管破坏,黏膜坏死脱落;肺泡Ⅰ型细胞的细胞器肿胀,肺泡Ⅱ型细胞板层体减少且排空,胞质内空泡增多、线粒体肿胀,肺泡纵隔内胶原纤维增生。结论 急性羰基镍对大鼠肺组织细胞有明显的损伤作用,且存在剂量-效应关系和时间-效应关系。
目的 觀察大鼠急性羰基鎳中毒後肺細胞DNA損傷程度以及組織細胞病理變化。方法 SD大鼠靜態分彆吸人20、135和250 mg/m3羰基鎳染毒30 min,另設250 mg/m3氯氣染毒組和正常對照組在染毒後第1、2、3和7天取肺組織單細胞凝膠電泳試驗檢測肺細胞DNA損傷程度,同時觀察大鼠肺組織病理變化和細胞超微結構改變。結果 不同濃度羰基鎳染毒後不同時間,大鼠肺組織細胞均有損傷,以72 h DNA損傷最重,但損傷晚于氯氣。不同濃度羰基鎳染毒大鼠肺組織有炎性滲齣和增生,部分細支氣管破壞,黏膜壞死脫落;肺泡Ⅰ型細胞的細胞器腫脹,肺泡Ⅱ型細胞闆層體減少且排空,胞質內空泡增多、線粒體腫脹,肺泡縱隔內膠原纖維增生。結論 急性羰基鎳對大鼠肺組織細胞有明顯的損傷作用,且存在劑量-效應關繫和時間-效應關繫。
목적 관찰대서급성탄기얼중독후폐세포DNA손상정도이급조직세포병리변화。방법 SD대서정태분별흡인20、135화250 mg/m3탄기얼염독30 min,령설250 mg/m3록기염독조화정상대조조재염독후제1、2、3화7천취폐조직단세포응효전영시험검측폐세포DNA손상정도,동시관찰대서폐조직병리변화화세포초미결구개변。결과 불동농도탄기얼염독후불동시간,대서폐조직세포균유손상,이72 h DNA손상최중,단손상만우록기。불동농도탄기얼염독대서폐조직유염성삼출화증생,부분세지기관파배,점막배사탈락;폐포Ⅰ형세포적세포기종창,폐포Ⅱ형세포판층체감소차배공,포질내공포증다、선립체종창,폐포종격내효원섬유증생。결론 급성탄기얼대대서폐조직세포유명현적손상작용,차존재제량-효응관계화시간-효응관계。
Objective To observe DNA damage and morphological changes of lung cells in rats with acute carbonyl nickel poisoning. Methods SD rats were exposed to 20, 135 and 250 mg/m3 carbonyl nickel for 30 min by inhalation. On the third day and 7th day after exposure, DNA damage of lung cells were examined by single cell gel electrophoresis (SCGE) and the pathological changes in lung tissues and the changes of microstructure in lung cells were observed. Results The DNA damage of the rat lung cells were obviously found in all exposure groups at different exposure times and there was the most obvious DNA damage at 72 hour after exposure to nickel carbonyl but the damage appeared later than chlorine exposure group. The inflammatory infiltration and hyperplasia in lung tissue, bronchiolar damage and the bronchial mucosa defulvium appeared in the rats exposed to carbonyl nickel. The results of microstructure examination indicated that the organelles of type I pneumocytes was swellen, the body of type Ⅱ pneumocytes was emptied. The cytoplasm empty bubbles increased, the mitochondria was swellen, and alveolar mediastinum inside the collagen fiber in alveolar mediastinum increased. Conclusion The acute carbonyl nickel exposure could induce the injury of lung tissues and cells with dose-effect relationship and time-effect relationship.