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Subacute lung toxicity caused by repeated intratracheal exposure to cadmium nitrate in rats

机译:大鼠反复气管内暴露于硝酸镉引起的亚急性肺毒性

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Recent increase in the use of cadmium nitrate Cd(NO_(3))_(2) (CdN) in nickel cadmium (Ni-Cd) batteries means that workers at factories producing these batteries are at risk of frequent inhalation of CdN aerosols. We aimed to investigate the subacute harmful effects towards the lungs, liver, and kidneys after intermittent inhalation and biological monitoring of Cd. Aerosols were intratracheally administered to rats administered CdN and saline (control) ten times in total every other day using an aerosol generator for three weeks. Blood, bronchoalveolar lavage fluid (BALF), and lung tissues were sampled. Blood parameters indicated severe hypoxemia. Pathohistological findings of the CdN group indicated typical, though nonspecific changes such as tissue-destructive processes, occupation of the alveolar region, proliferation-associated changes, and extensive deformities of alveolar architecture. Increased LDH and SP-D in BALF were suspected to be due to injurious effects and hyperplasia, respectively, of the type-II pneumocytes. In a previous study, we defined serum levels of Cd at which no mortality and no abnormalities in the liver and kidneys were observed. Blood Cd concentrations in this study suggest that the absorbed dose was much lower than that of fatal cases following acute inhalation accidents. It is generally reported that toxicity to the respiratory system is proportional to the time and level of exposure. However, subacute lethal effects were suspected to increase despite the minimal dose used in the present study, as repeated inhalation exposure and length of contact with Cd would yield severe pathohistological changes. Morphological abnormalities could also be responsible for the significant decrease in arterial blood gas values in this study. The marked pathologic change in the lungs, diagnosed as diffuse alveolar damage, was likely caused by repeated inhalation exposure of Cd. Subacute lung damage which worsened for a few days was lethal.
机译:最近在镍镉(Ni-Cd)电池中使用硝酸镉Cd(NO_(3))_(2)(CdN)的增加意味着在生产这些电池的工厂中的工人有频繁吸入CdN气溶胶的风险。我们旨在调查间歇性吸入和Cd的生物监测后对肺,肝和肾的亚急性危害。使用气雾剂发生器,每隔一天对总共施用CdN和盐水(对照组)的大鼠气管内施用气雾剂,共三次,每次十次。抽取血液,支气管肺泡灌洗液(BALF)和肺组织。血液参数表明严重低氧血症。 CdN组的病理组织学发现显示出典型但非特异性的改变,例如组织破坏性过程,肺泡区域的占据,与增殖有关的改变以及肺泡结构的广泛畸形。怀疑BALF中LDH和SP-D升高分别是由于II型肺细胞的伤害作用和增生所致。在先前的研究中,我们定义了血清Cd水平,在该水平下未观察到死亡和肝肾均无异常。这项研究中的血液中Cd浓度表明,吸收剂量远低于急性吸入事故后致命病例的吸收剂量。通常据报道,对呼吸系统的毒性与暴露时间和暴露水平成正比。然而,尽管在本研究中使用了最小剂量,但仍怀疑亚急性致死作用会增加,因为反复吸入和接触Cd的时间会引起严重的病理组织学改变。在这项研究中,形态异常也可能是导致动脉血气值显着下降的原因。被诊断为弥漫性肺泡损伤的肺部明显病理变化可能是由于反复吸入Cd引起的。持续数天恶化的亚急性肺损伤是致命的。

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