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Mechanisms of action of cytotoxicity of transition metal oxide nanoparticles in human lung cells
Author(s) -
Huang Yue-Wern,
Chusuei Charles C.,
Aronstam Robert S.
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1050.15
Subject(s) - oxidative stress , intracellular , cytotoxicity , biophysics , chemistry , a549 cell , programmed cell death , lipid peroxidation , apoptosis , nanotoxicology , calcium in biology , metal , dna damage , cell , calcium , nanoparticle , nanotechnology , materials science , biochemistry , dna , biology , in vitro , organic chemistry
The cytotoxicity of nano‐sized oxides of fourth period metals (Ti, Cr, Mn, Fe, Ni, Cu, and Zn), which are widely used in industry, was assessed in two human lung cell lines (A549 & BEAS‐2B). The particles were 16–82 nm in diameter. Toxicity expressed on the bases of particle mass increased with atomic number. Metal oxides altered the cellular redox state, leading to cellular injury as revealed by lipid peroxidation, DNA strand breaks, and membrane depolarization. Oxidative stress produced by exposure to metal oxide nanoparticles also perturbed certain cellular signaling pathways, induced the expression of cell death‐related genes, and compromised the ability of cells to maintain a low concentration of intracellular calcium. Synergistic interactions between intracellular [Ca 2+ ] and OS are a likely contributing factor. While [Ca 2+ ] and OS affect the activity of each other, they induce cell death by distinct pathways. We evaluated the contributions of physicochemical properties of metal oxides to the initiation of cellular oxidative stress. Particle surface charge, particle surface available binding sites, and metal dissolution highly correlated with oxidative response. Our results can inform design of safer nanomaterials for applications in biomedical science.