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Oxidative injury in the lungs of neonatal rats following short-term exposure to ultrafine iron and soot particles.

Authors
Zhong-CY; ZhoYM; SmitKR; Kennedy-IM; Chen-CY; Aust-AE; Pinkerton-KE
Source
J Toxicol Environ Health, A 2010 Jan; 73(12):837-847
NIOSHTIC No.
20036717
Abstract
Greater risk of adverse effects from particulate matter (PM) has been noted in susceptible subpopulations, such as children. However, the physicochemical components responsible for these biological effects are not understood. As critical constituents of PM, transition metals were postulated to be involved in a number of pathological processes of the respiratory system through free radical-medicated damage. The purpose of this study was to examine whether oxidative injury in the lungs of neonatal rats could be induced by repeated short-term exposure to iron (Fe) and soot particles. Sprague Dawley rats 10 d of age were exposed by inhalation to two different concentrations of ultrafine iron particles (30 or 100 microg/m(3)) in combination with soot particles adjusted to maintain a total particle concentration of 250 microg/m(3). Exposure at 10 d and again at 23 d of age was for 6 h/d for 3 d. Oxidative stress was observed at both Fe concentrations in the form of significant elevations in glutathione disulfide (GSSG) and GSSG/glutathione (GSH) ratio and a reduction in ferric/reducing antioxidant power in bronchoalveolar lavage. A significant decrease in cell viability associated with significant increases in lactate dehydrogenase (LDH) activity, interleukin-1-beta (IL-1beta), and ferritin expression was noted following exposure to particles containing the highest Fe concentration. Iron from these particles was shown to be bioavailable in an in vitro assay using the physiologically relevant chelator, citrate. Data indicate that combined Fe and soot particle exposure induces oxidative injury, cytotoxicity and pro-inflammatory responses in the lungs of neonatal rats.
Keywords
Age-factors; Age-groups; Biochemical-analysis; Biochemistry; Biodynamics; Biological-effects; Biological-monitoring; Cell-damage; Cellular-reactions; Cytotoxic-effects; Exposure-assessment; Exposure-levels; Exposure-methods; Inhalation-studies; Laboratory-animals; Laboratory-testing; Lung-disorders; Lung-irritants; Metallic-dusts; Metallic-poisoning; Particulate-dust; Particulates; Pulmonary-disorders; Pulmonary-system-disorders; Respiratory-irritants; Respiratory-system-disorders; Statistical-analysis; Toxic-effects; Toxins
Contact
Dr. Kent E. Pinkerton, Center for Health and the Environment, Old Davis Road, University of California, Davis, CA 95616
CODEN
JTEHD6
CAS No.
7439-89-6
Publication Date
20100101
Document Type
Journal Article
Email Address
kepinkerton@ucdavis.edu
Funding Type
Agriculture; Cooperative Agreement
Fiscal Year
2010
NTIS Accession No.
NTIS Price
Identifying No.
Cooperative-Agreement-Number-U50-OH-007550
Issue of Publication
12
ISSN
1528-7394
Source Name
Journal of Toxicology and Environmental Health, Part A: Current Issues
State
CA
Performing Organization
University of California - Davis
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