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Hepatic and pulmonary differential toxicity and pathogenicity of hevavalent chromium, nickel, and cadmium.

Authors
Valerie-MC; Rebecca-CC; Hall-J; Meighan-T; Pack-D; Lewis-JA; Jackson-D; Vallyathan-V; Leonard-SS
Source
Toxicologist 2010 Mar; 114(1):463
NIOSHTIC No.
20036638
Abstract
Both civilians and military personnel can be exposed to toxic chemicals and materials from occupational sources, environmental pollution, or as the result of military activity. The goal in this first stage of our study was to measure oxidative stress markers after different transition metal exposures. We performed a toxicological study to examine these effects using rats treated through I.P. injection. Sprague- Dawley rats were dosed with NiCl2 (0.25. 0.5, 0.75 mmol/kg BW), Na2Cr2O7 (5, 10, 20 mg/kg BW) and CdCl2 (0.5, 1.25, 2.5 mg/kg BW) and humanely sacrificed 1, 3 and 7 days post exposure. Liver tissue, kidney tissue, blood and lung lavage fluid were collected and analyzed. Liver tissue showed an increase in oxidative damage, through lipid peroxidation and hydrogen peroxide production, in all metal exposures with Cr being the most dramatic and Ni showing damage at days 3 and 7. Kidney tissue demonstrated immediate damage from Cr and then showed recovery, while Cd and Ni showed effects at day 7, at the highest concentration. Electron spin resonance results showed an increase in hydroxyl radical formation in liver and kidney tissue from Cr, day 1, as well as Cd & Ni on days 3 and 7, at the highest exposure levels. Bronchiopulmonary lavage was also performed on the rats to yield macrophages and cell for differential measurements. From this a small rise in Cr exposed animals indicated a cross talk from the I.P. exposure. To summarize, Cr-induced oxidative damage at day 1 was reduced or resolved at day 7, while Cd and Ni produced more oxidative damage at days 3 and 7 at the higher exposure levels. This data will be combined with the second stage of our study which involved the analysis of blood biomarkers and gene transcripts to develop a method of identifying early biomarkers of transition metal exposure.
Keywords
Airborne-particles; Biological-effects; Cell-biology; Cellular-reactions; Chemical-hypersensitivity; Chemical-reactions; Environmental-exposure; Exposure-assessment; Exposure-levels; Exposure-methods; Genes; Genetic-factors; Hepatotoxicity; Inhalants; Inhalation-studies; Laboratory-animals; Laboratory-testing; Liver; Liver-function; Liver-microsomes; Metal-dusts; Metal-fumes; Microbiology; Microscopic-analysis; Military-personnel; Occupational-exposure; Particle-aerodynamics; Particulate-dust; Particulates; Pulmonary-system; Pulmonary-system-disorders Toxic-effects; Toxins
CAS No.
7440-47-3; 7440-02-0; 7440-43-9
Publication Date
20100301
Document Type
Abstract
Fiscal Year
2010
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 49th Annual Meeting and ToxExpo, March 7-11, 2010, Salt Lake City, Utah
State
WV; UT
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