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Comparison of the acute oxidative damage of transition metals on two cell lines.

Authors
Bukowski-VC; Chapman-RS; Leonard-SS
Source
Toxicologist 2009 Mar; 108(1):66
NIOSHTIC No.
20035243
Abstract
Previous research has shown chromium (Cr), cadmium (Cd) and nickel (Ni) to be carcinogenic. Cr is used in pigment production, electroplating, and stainless steel welding. Cd is used in steel electroplating, plastic pigmentation, and battery production. Ni is used in steel and alloy production, electroplating, and jewelry. Cr, Cd, and Ni all produce acute and chronic effects in various organs in the body. These effects are determined by the route of exposure and chemical composition of the metal. Our research goal was to assess the acute oxidative damage of three metal compounds; sodium dichromate (Na2Cr2O7), cadmium chloride (CdCl2) and nickel chloride (NiCl2) on RAW 264.7 mouse monocyte macrophage cells and HepG2/C3A human hepatocellular carcinoma cells. Electron spin resonance was used to analyze free radicals produced by Na2Cr2O7, CdCl2, and NiCl2 under various conditions. A Fenton-like system was used with hydrogen peroxide (H2O2) as well as exposure to RAW 264.7 cells and HepG2/C3A cells. The results showed that in a Fenton-like system only Na2Cr2O7 was able to produce measurable free radicals. This was also true when the RAW 264.7 cells were treated with the metal compounds. However, HepG2/C3A cells produced free radicals after Na2Cr2O7 and CdCl2 exposures. In addition, H2O2 and oxygen consumption were measured in the two cell lines after being treated with the metals. There was no significant increase in oxygen consumption for either cell line. A significant increase in H2O2 for both cells lines was observed when treated with Na2Cr2O7. There was little to no increase in H2O2 when the cells were treated with the other metals (CdCl2 and NiCl2). A comet assay was used to determine the DNA damage. The results showed significant DNA damage in the cells for all three metals. These results imply that Na2Cr2O7, CdCl2 and NiCl2 produce cellular oxidative damage through the use of three different mechanisms.
Keywords
Airborne-dusts; Airborne-particles; Biological-effects; Biological-function; Biological-systems; Biological-transport; Cell-biology; Cell-damage; Cell-function; Cell-metabolism; Cellular-reactions; Chemical-composition; Chemical-analysis; Chemical-hypersensitivity; Chemical-properties; Chemical-reactions; Dose-response; Dosimetry; Exposure-assessment; Exposure-levels; Exposure-methods; Genetic-disorders; Genotoxic-effects; Genotoxicity; Laboratory-animals; Metal-poisoning; Metallic-dusts; Molecular-biology; Metal-compounds; Metal-fumes; Metal-oxides; Metallic-fumes; Particle-aerodynamics; Particulate-dust; Particulates; Pulmonary-clearance; Statistical-analysis; Toxic-effects; Welding
CAS No.
7440-43-9; 7440-47-3; 7440-02-0
Publication Date
20090301
Document Type
Abstract
Fiscal Year
2009
NTIS Accession No.
NTIS Price
Issue of Publication
1
ISSN
1096-6080
NIOSH Division
HELD
Priority Area
Manufacturing
Source Name
The Toxicologist. Society of Toxicology 48th Annual Meeting and ToxExpo, March 15-19, 2009, Baltimore, Maryland
State
WV
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