Influence of platinum, palladium and rhodium as compared with cadmium, nickel and chromium on cell viability and oxidative stress in human bronchial epithelial cells

Schmid, M.; Zimmermann, Sonja; Krug, Harald F.; Sures, Bernd

doi:10.1016/j.envint.2006.12.003

Cited by 96 publications

(54 citation statements)

References 18 publications

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“…Fluorescence increases when 2',7'-dichlorodihy-2 DCF-DA; Molecular Probes, Eugene, OR, USA) is oxidized by ROS to DCF. This assay was carried out in BEAS-2B cells as described by Hussain et al (2005) and Schmid et al (2007). The cells were harvested with 0.05% trypsin-0.53 mM EDTA·4Na (Gibco BRL, Grand Island, NY, USA) and resuspended in BEGM.…”

Section: Determination Of Ros Generationmentioning

confidence: 99%

Silver nanoparticles induce p53-mediated apoptosis in human bronchial epithelial (BEAS-2B) cells

et al. 2014

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-Deregulated apoptosis has been associated with many lung diseases. Although many studies have reported the apoptotic effects exhibited by silver nanoparticles (Ag-NPs) in various circumstances, the apoptosis mechanism of Ag-NPs is unclear. We investigated oxidative stress and apoptosis in human normal bronchial epithelial (BEAS-2B) cells to elucidate the role of p53 in apoptosis by Ag-NPs. First, dispersion and stability of Ag-NPs improved using bronchial epithelial cell growth medium with 5% fetal bovine serum. Then, we observed oxidative stress in BEAS-2B cells exposed to Ag-NPs. Second, we carried out a cell death assay to measure DNA fragmentation as a biomarker of apoptosis. BEAS--mentation. We also found that apoptosis-related genes (caspase-3, Bax, and Bcl-2) were regulated by AgNPs, which was detected by mRNA and protein levels. These results suggest that Ag-NPs induced p53-Ag-NPs in pulmonary disease. Original ArticleThe Journal of Toxicological Sciences (J. Toxicol. Sci.) Vol.39, No.3, 401-412, 2014 Vol. 39 No. 3 401 lar and DNA damage (Risom et al., 2005). DNA damage induces extracellular and intracellular signals that trigger the onset of a signaling cascade with characteristic biochemical and morphological features, including nuclear condensation, membrane blebbing, and DNA fragmentation, leading ultimately to cell death (Johnson et al., 1996). This is called apoptosis, which is essential for the normal functioning and survival of multi-cellular organisms. However, deregulated apoptosis has been associated with many lung diseases because toxic contents are released from apoptotic cells unless the cells are quickly recognized or ingested by phagocytes (Pandya et al., 2006).The p53 gene regulates the apoptosis pathway (Korsmeyer, 1995;Yang and Duerksen-Hughes, 1998) and is tightly controlled through a complex series of events including translational regulation, interaction with regu--cations including multisite phosphorylation and acetylation (Giaccia and Kastan, 1998;Meek, 1999;Prives and Hall, 1999). In particular, phosphorylation of the serine-15 (Ser-15) residue due to DNA damage plays an important role in p53-mediated apoptosis (Dumaz and Meek, 1999;Siliciano et al., 1997;Unger et al., 1999). This activation of p53 leads to expression of its downstream effectors such as Bax, Bcl-2 and caspase-3, resulting in apoptosis (Martin and Elkon, 2004).In this study, we hypothesized that Ag-NPs induce apoptosis via the p53 signaling pathway in normal human lung bronchial epithelial (BEAS-2B) cells. Although many reports have shown apoptotic effects of Ag-NPs in various circumstances (Foldbjerg et al., 2009;Li et al., 2010;Miura and Shinohara, 2009;Piao et al., 2011), the were used to elucidate the role of p53 in apoptosis by Ag--sion of TiO 2 NPs improved by adding bovine serum albumin (BSA) or fetal bovine serum (FBS) to the medium (Ji et al., 2010). Thus, Ag-NPs were dispersed in bronchial epithelial growth medium (BEGM) with 5% FBS and were characterized. Then, we observed ROS generation...

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Section: Determination Of Ros Generationmentioning

confidence: 99%

Silver nanoparticles induce p53-mediated apoptosis in human bronchial epithelial (BEAS-2B) cells

et al. 2014

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“…In general the Pt(II), Pt(V) and Pd(II) toxic effects on the cellular level are comparable to the toxic effects of Cd(II) and Cr(VI), sometimes even exceeding the damage induced by the above species of Cd and Cr [3].…”

Section: Introductionmentioning

confidence: 61%

Graphene Oxide–Antimony Nanocomposite Sensor for Analysis of Platinum Group Metals in Roadside Soil Samples

Silwana¹,

Horst²,

Iwuoha³

et al. 2017

Graphene Materials - Advanced Applications

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The present study introduced a very sensitive and low-cost analytical procedure based on voltammetry to study platinum group metals in road dust and roadside soil matrices. Cathodic stripping voltammetry in conjunction with a reduced graphene oxide-antimony nanocomposite sensor and ICP-MS analysis were used to analyse roadside soil and dust samples. The results were processed to evaluate possible pollution in order to map the distribution of the PGMs along specific roads in the Stellenbosch area, outside Cape Town. The results revealed that within each site under investigation, Pd was more abundant than Pt and Rh using both voltammetric and spectroscopic methods. The AdDPCSV results obtained showed concentrations for Pd(II) ranging between 0.92 -4.0 ng kg -1 . For Pt (II), the concentrations ranged between 0.84 -0.99 ng kg . For Rh, concentrations ranged between 0.002 -0.26 µg kg -1 . The analysis showed significant levels of all PGMs in soil and dust samples analysed. Metal concentration in dust and soil followed the trend Pd > Pt > Rh using both voltammetric and spectroscopic techniques.

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“…Pallidum results in bronchial epithelial cell death by increasing the intracellular production of ROS [30], and it is likely to be the most effective mechanism of toxicity. Production of ROS and cells detoxification via ROS degradation is continual process in cell growth cycle that results in the stabilization of the levels of ROS.…”

Section: Discussionmentioning

confidence: 99%

Palladium induced oxidative stress and cell death in normal hepatocytes

Hashemzaei¹,

Yarahmazehi²,

Tabrizian³

et al. 2016

J. Fundam and Appl Sci.

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Palladium (Pd) accumulates in many organs and renders many deleterious effects. Although the Pd toxicity has been documented, the precise mechanism of Pd toxicity still needs to be elucidated. In the current research, a hepatotoxicity mechanism of Pd has been investigated.Our findings clearly indicate that Pd induces reactive oxygen species (ROS) formation and oxidative stress, mitochondrial and lysosomal injury and finally cell death. These effects are reversed by antioxidants and ROS scavengers, mitochondrial permeability transmission [1] pore sealing agent, ATP progenitor, and lysosomotropic agent. Pretreatment of hepatocytes with ROS scavengers and MPT pore sealing agents reduced cell death which explains the role of oxidative stress and mitochondrial pathway of ROS formation in Pd hepatocytes cell toxicity. Overall, the results have distinctly determined the mechanism by which Pd-induced toxicity in the isolated rat hepatocytes.

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Influence of platinum, palladium and rhodium as compared with cadmium, nickel and chromium on cell viability and oxidative stress in human bronchial epithelial cells

Cited by 96 publications

References 18 publications

Silver nanoparticles induce p53-mediated apoptosis in human bronchial epithelial (BEAS-2B) cells

Silver nanoparticles induce p53-mediated apoptosis in human bronchial epithelial (BEAS-2B) cells

Graphene Oxide–Antimony Nanocomposite Sensor for Analysis of Platinum Group Metals in Roadside Soil Samples

Palladium induced oxidative stress and cell death in normal hepatocytes

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