Department of Ecology, Institute for Biological Research Sinisa Stankovic, University of Belgrade, 11000 Belgrade, Serbia.
Environ Toxicol Pharmacol. 2009 Sep;28(2):225-31. doi: 10.1016/j.etap.2009.04.008. Epub 2009 Apr 21.
Pulmonary inflammation is a biological response to cadmium entering the body via the respiratory route. Systemic administration of this metal revealed the lungs as a significant site of its disposition. In this study, the presence of basic indicators of lung inflammation (leukocyte infiltration and activity of cells recovered from lungs by enzyme digestion) was analyzed in the rat model of acute systemic cadmium intoxication. Intraperitoneal administration of both cadmium doses (0.5mg/kg and 1.0mg/kg) resulted in increased numbers of neutrophils. Signs of spontaneous activation of lung cells including the capacity of reduction of nitroblue tetrazolium (NBT), increase in myeloperoxidase (MPO) intracellular content and increase in interleukin-6 (IL-6) production were noted at both cadmium doses. Increased lung cell responsiveness to stimulation in vitro was noted at the higher cadmium dose. The presence of pulmonary inflammatory parameters in rats administered intraperitoneally with cadmium revealed the lungs as remote inflammatory targets of this metal.
肺部炎症是一种生物反应，是由于镉通过呼吸道进入体内引起的。全身给予这种金属后发现肺部是其主要分布部位。在这项研究中，在急性系统性镉中毒大鼠模型中分析了肺部炎症的基本指标（白细胞浸润和酶消化后从肺部回收的细胞活性）。腹腔内给予两种剂量的镉（0.5mg/kg 和 1.0mg/kg）均导致中性粒细胞数量增加。在两个镉剂量下均观察到自发激活肺细胞的迹象，包括还原硝基四唑蓝（NBT）的能力、髓过氧化物酶（MPO）细胞内含量增加和白细胞介素-6（IL-6）产生增加。在较高的镉剂量下，还观察到肺细胞对体外刺激的反应性增加。腹腔内给予镉的大鼠存在肺部炎症参数，表明肺部是该金属的远程炎症靶标。
