Odewumi Caroline, Latinwo Lekan M, Sinclair Andre, Badisa Veera L D, Abdullah Ahkinyala, Badisa Ramesh B
Department of Biological Sciences, Florida A&M University, Tallahassee, FL 32307, USA.
Department of Integrated Environmental Science and Natural Science, School of Science Engineering and Math, Bethune‑Cookman University, Daytona Beach, FL 32114, USA.
Mol Med Rep. 2015 Nov;12(5):6422-6. doi: 10.3892/mmr.2015.4316. Epub 2015 Sep 10.
Cadmium is an environmentally hazardous metal, which causes toxicity in humans. Inhalation of cigarette smoke and industrial fumes containing cadmium are sources of cadmium exposure. It is responsible for the malfunction of various organs, leading to disease particularly in the lungs, liver and kidneys. In the present study, the effect of cadmium chloride (CdCl2) on cell viability, and the expression levels of interleukin (IL)‑1α and IL‑10 cytokines at various concentrations and incubation durations were assessed in MRC‑9 human normal lung and A549 human lung cancer cells to elucidate the mechanism of cadmium toxicity. Cell viability was measured using a crystal violet dye binding assay. The expression levels of the cytokines were measured by cytokine specific enzyme‑linked immunosorbent assay kits. The viability assay results revealed higher sensitivity of the A549 lung cancer cells to CdCl2 compared with the normal MRC‑9 lung cells. In the normal MRC‑9 lung cells, higher expression levels of the cytokines were observed at the lowest CdCl2 concentration at a shorter exposure time compared with the lung cancer cells. Higher levels of the cytokines were observed in the A549 lung cancer cells at all other times and concentrations compared with the MRC‑9 cells, indicating higher levels of inflammation. The cytokine levels were reduced at higher CdCl2 concentrations and longer exposure durations, demonstrating the toxic effect of cadmium. The results indicated that CdCl2 affected the expression levels of the cytokines and led to cytotoxicity in human lung cells, and suggested that compounds which reduce inflammation may prevent cadmium toxicity.
镉是一种对环境有害的金属，可导致人体中毒。吸入含有镉的香烟烟雾和工业烟雾是镉暴露的来源。它会导致各种器官功能失调，尤其会引发肺部、肝脏和肾脏疾病。在本研究中，为阐明镉毒性的机制，在MRC-9人正常肺细胞和A549人肺癌细胞中评估了不同浓度和孵育时间的氯化镉（CdCl2）对细胞活力以及白细胞介素（IL）-1α和IL-10细胞因子表达水平的影响。使用结晶紫染料结合试验测量细胞活力。通过细胞因子特异性酶联免疫吸附测定试剂盒测量细胞因子的表达水平。活力测定结果显示，与正常的MRC-9肺细胞相比，A549肺癌细胞对CdCl2更敏感。在正常的MRC-9肺细胞中，与肺癌细胞相比，在最短暴露时间的最低CdCl2浓度下观察到细胞因子的表达水平更高。与MRC-9细胞相比，在所有其他时间和浓度下，A549肺癌细胞中观察到更高水平的细胞因子，表明炎症水平更高。在更高的CdCl2浓度和更长的暴露时间下，细胞因子水平降低，证明了镉的毒性作用。结果表明，CdCl2影响细胞因子的表达水平并导致人肺细胞的细胞毒性，并且表明减少炎症的化合物可能预防镉毒性。
