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Vanadium-induced apoptosis and pulmonary inflammation in mice: role of reactive oxygen species.

Authors
Wang-L; Medan-D; Mercer-R; Overmiller-D; Leonard-S; Castranova-V; Shi-X; Ding-M; Huang-C; Rojanasakul-Y
Source
J Cell Physiol 2003 Apr; 195(1):99-107
NIOSHTIC No.
20022656
Abstract
Pulmonary exposure to metals and metal-containing compounds is associated with pulmonary inflammation, cell death, and tissue injury. The present study uses a mouse model to investigate vanadium-induced apoptosis and lung inflammation, and the role of reactive oxygen species (ROS) in this process. Aspiration of the pentavalent form of vanadium, V (V), caused a rapid influx of polymorphonuclear leukocytes into the pulmonary airspace with a peak inflammatory response at 6 h post-exposure and resolution by 72 h. During this period, the number of apoptotic lung cells which were predominantly neutrophils increased considerably with a peak response at 24 h accompanied by no or minimum necrosis. After 24 h when the V (V)-induced inflammation was in the resolution phase, an increased influx of macrophages and engulfment of apoptotic bodies by these phagocytes was observed, supporting the role of macrophages in apoptotic cell clearance and resolution of V (V)-induced lung inflammation. Electron spin resonance (ESR) studies using lavaged alveolar macrophages showed the formation of ROS, including O(2)(*-), H(2)O(2), and (*)OH radicals which were confirmed by inhibition with free radical scavengers. The mechanism of ROS generation induced by V (V) involved the activation of an NADPH oxidase complex and the mitochondrial electron transport chain. The ROS scavenger, catalase (H(2)O(2) scavenger), effectively inhibited both lung cell apoptosis and the inflammatory response, whereas superoxide dismutase (SOD) (O(2)(*-) scavenger) and the metal chelator, deferoxamine (inhibitor of (*)OH generation by Fenton-like reactions) had lesser effects. These results indicate that multiple oxidative species are involved in V (V)-induced lung inflammation and apoptosis, and that H(2)O(2) plays a major role in this process.
Keywords
Vanadium-compounds; Vanadium-dust; Vanadium-fumes; Pulmonary-system; Animal-studies; Animals; Laboratory-animals; Exposure-levels; Metal-compounds; Metals; Models; Leukocytes; Alveolar-cells
Contact
Liying Wang, National Institute for Occupational Safety and Health, Pathology and Physiology Research Branch, 1095 Willowdale Road, Morgantown, WV 26505
CODEN
JCLLAX
CAS No.
1314-62-1
Publication Date
20030401
Document Type
Journal Article
Email Address
lmw6@cdc.gov
Fiscal Year
2003
NTIS Accession No.
NTIS Price
Issue of Publication
1
ISSN
0021-9541
NIOSH Division
HELD
Source Name
Journal of Cellular Physiology
State
WV; NY
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