Oxidative Stress Induced by Zero-Valent Iron Nanoparticles and Fe(II) in Human Bronchial Epithelial Cells

Abstract

To identify the mechanism through which nanoparticulate zero-valent iron (nZVI; Fe0(s)) damages cells, a series of experiments were conducted in which nZVI in phosphate-buffered saline (PBS) was exposed to oxygen in the presence and absence of human bronchial epithelial cells. When nZVI is added to PBS, a burst of oxidants is produced as Fe0 and ferrous iron (Fe[II]) are converted to ferric iron (Fe[II]). Cytotoxicity and internal reactive oxygen species (ROS) production in cells exposed to nZVI is equivalent to the response observed when cells are exposed to the same concentration of dissolved Fe(II). Experiments conducted in the absence of cells indicate that the oxidant produced during Fe(II) oxidation reacts with methanol and dimethyl sulfoxide, but not with compounds such as tert-butanol and benzoate that react exclusively with hydroxyl radical. The role of reactive oxidants produced during Fe(II) oxidation in cytotoxicity and internal ROS production is further supported by experiments in which cell damage was limited by the addition of ligands that prevented Fe(II) oxidation and by the absence of cell damage when the nanoparticles were oxidized prior to exposure. The behavior of the oxidant produced by nZVI is consistent with an oxidant such as the ferryl ion, rather than hydroxyl radical.

Toxicity-based toxicokinetic/toxicodynamic assessment of bioaccumulation and nanotoxicity of zerovalent iron nanoparticles in <em>Caenorhabditis elegans</em>

“…However, despite the low cost and high efficiency of Fe 0 NPs in removing contaminants, [1][2][3][4][5][6] there are concerns that Fe 0 NP application contributes to long-term impacts on environmental and human health risks. [7][8][9][10][11][12][13][14][15][16][17] Moreover, the increasing use of Fe 0 NPs in in situ groundwater remediation could lead to large numbers of NPs released into the environment and is highly likely to pose potential exposure risks. 8 Several studies have indicated that Fe 0 NPs could cause cytotoxicity in human bronchial epithelial cells.…”

“…[7][8][9][10][11][12][13][14][15][16][17] Moreover, the increasing use of Fe 0 NPs in in situ groundwater remediation could lead to large numbers of NPs released into the environment and is highly likely to pose potential exposure risks. 8 Several studies have indicated that Fe 0 NPs could cause cytotoxicity in human bronchial epithelial cells. 8,18,19 Previous studies on the effects of Fe 0 NPs on microorganisms, such as Bacillus cereus, Pseudomonas stutzeri, and Escherichia coli, have revealed that Fe might be reduced from NPs to lead to stress responses.…”

“…8 Several studies have indicated that Fe 0 NPs could cause cytotoxicity in human bronchial epithelial cells. 8,18,19 Previous studies on the effects of Fe 0 NPs on microorganisms, such as Bacillus cereus, Pseudomonas stutzeri, and Escherichia coli, have revealed that Fe might be reduced from NPs to lead to stress responses. 7,17,20 Inhibition in embryo development, mortality of spermatozoa, and declines in fertilization in embryos were observed in marine microalgae in response to Fe 0 NP exposure.…”

Toxicity of Nanomaterials and Recent Developments in Lung Disease

“…One latest study showed that, after 12 weeks of inhalation tests, small TiO 2 nanoparticles 20 nm in size were characterized by a longer retention time in the lungs of rats and increased translocation to interstitial sites than larger TiO 2 nanoparticles 250 nm in size [4,[50][51][52]. Another study in healthy animals also showed that inhalation of metallic nanoparticles (less than 30 nm) into the circulatory system was much faster than that of non-metallic nanoparticles (between 4 nm and 200 nm) [53].…”

“…Longterm toxicity of nanomaterials and examination of chronic exposure must be studied in detail to understand the mechanisms involved. Even though several factors are involved in nanomaterial toxicity, more efforts and time are needed to conduct research on nanoscale products and lung and other diseases [6,50].…”