التفاصيل البيبلوغرافية
| العنوان: |
Toxic response of nickel nanoparticles in human lung epithelial A549 cells |
| المؤلفون: |
Ahamed, Maqusood1 maqusood@gmail.com |
| المصدر: |
Toxicology in Vitro. Jun2011, Vol. 25 Issue 4, p930-936. 7p. |
| مصطلحات موضوعية: |
*NICKEL in the body, *NANOPARTICLES, *EPITHELIAL cells, *CATALYSTS, *PULMONARY blood vessels, *ANTIOXIDANTS, *OXIDATIVE stress, *MITOCHONDRIA, *MEMBRANE lipids |
| مستخلص: |
Abstract: Nickel nanoparticle (Ni NP) is increasingly used in modern industries such as catalysts, sensors and electronic applications. Due to wide-spread industrial applications the inhalation is the primary source of exposure to Ni NPs. However, data demonstrating the effect of Ni NPs on the pulmonary system remain scarce. The present study was designed to examine the toxic effect of human lung epithelial A549 cells treated with well characterized Ni NPs at the concentrations of 0, 1, 2, 5, 10 and 25μg/ml for 24 and 48h. Mitochondrial function (MTT assay), membrane leakage of lactate dehydrogenase (LDH assay), reduced glutathione (GSH), reactive oxygen species (ROS), membrane lipid peroxidation (LPO) and caspase-3 activity were assessed as toxicity end points. Results showed that Ni NPs reduced mitochondrial function and induced the leakage of LDH in dose and time-dependent manner. Ni NPs were also found to induce oxidative stress in dose and time-dependent manner indicated by depletion of GSH and induction of ROS and LPO. Further, activity of caspase-3 enzyme, marker of apoptosis was significantly higher in treated cells with time and Ni NPs dosage. The results exhibited significant toxicity of Ni NPs in human lung epithelial A549 cells which is likely to be mediated through oxidative stress. This study warrants more careful assessment of Ni NPs before their industrial applications. [Copyright &y& Elsevier] |
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