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- W2533804945 abstract "ABSTRACTHigh levels of industrial lead (Pb) exposure have decreased in the last 10 years as an outcome of removal of the metal from gasoline and paints. However, environmental Pb exposures remain extensive and may be correlated with adverse human health outcomes. The present study was designed to examine molecular mechanisms underlying cytotoxicity of lead oxide nanoparticles (PbONPs) on human lung alveolar epithelial (A549) cells. When A549 cells were incubated with PbONPs, the production of reactive oxygen species was enhanced as observed by 2',7'-dichlorodihydrofluorescein diacetate. PbONPs significantly reduced proliferation of A549 cells and increased caspase3 activity. In addition, exposure of PbONPs decreased levels of glutathione, and increased lipid peroxide levels and activities of superoxide dismutase and catalase. Exposure of PbONPs enhanced DNA damage as evidenced by tail DNA (%) and olive tail moment. Taken together, these finding indicated that PbONPs diminished cell proliferation and incre..." @default.
- W2533804945 created "2016-10-28" @default.
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- W2533804945 date "2016-10-17" @default.
- W2533804945 modified "2023-09-24" @default.
- W2533804945 title "Involvement of mitochondrial dysfunction in nanosized lead oxide induced cellular damage in human lung alveolar epithelial cells" @default.
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- W2533804945 doi "https://doi.org/10.1080/02772248.2016.1234177" @default.
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