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Oxidant release from pulmonary phagocytes.

Authors
Castranova-V; Antonini-JM; Reasor-MJ; Wu-L; Dyke-K
Source
Silica and Silica-Induced Lung Diseases. Castranova V, Vallyathan V, Wallace WE, eds., Boca Raton, FL: CRC Press, 1995 Dec; :185-195
Link
NIOSHTIC No.
00238729
Abstract
This report presents in-vitro and in-vivo data indicating that silica (14808607) may be associated with the production of reactive oxygen species from pulmonary phagocytes. Studies have indicated that in-vitro exposure of alveolar macrophages to 2mg/ml silica increased oxygen consumption by 213%. Half maximal stimulation was observed at 0.56mg/ml silica. The stimulatory effect of silica on respiratory burst activity is apparent within 1 to 2 minutes of in- vitro exposure. In-vitro exposure of neutrophils to 5mg/ml silica results in a 915% increase in chemiluminescence. Silica is also an indirect stimulant of neutrophils. Alveolar macrophage interaction with inhaled silica results in infiltration of neutrophils into the airspaces. Once in the airspaces, macrophage derived platelet activating factor can direct active oxygen metabolism in these neutrophils. Evidence also indicates that in-vivo exposures of rats to silica potentiates the activity of pulmonary phagocytes. Priming of oxygen metabolism in alveolar macrophages is noted 4 days after a 6 hour inhalation of silica. Zymosan stimulated oxygen consumption is increased by 44% while zymosan stimulated hydrogen-peroxide release is elevated by 38%. In-vivo exposure to silica dust also causes an induction of NO synthase in lung cells. The authors conclude that crystalline silica is a direct stimulant of oxygen metabolism and release of reactive oxidant species by both alveolar macrophages and neutrophils in-vitro and that silica can induce the release of mediators which are chemoattractants and activators of neutrophils. They suggest that the continuously elevated production of oxidants by pulmonary phagocytes in this disease state may be sufficient to overwhelm the native antioxidant defense systems of lung cells, resulting in parenchymal damage, scarring, and fibrosis which is characteristic of silicosis.
Keywords
Cytotoxic-effects; Lung-cells; Alveolar-cells; Silica-dusts; Mineral-dusts; Dust-exposure; Dust-inhalation; Lung-disease; Respiratory-system-disorders
CAS No.
14808-60-7
Publication Date
19951220
Document Type
Book or book chapter
Editors
Castranova-V; Vallyathan-V; Wallace-WE
Fiscal Year
1996
NTIS Accession No.
NTIS Price
ISBN No.
0849347092
NIOSH Division
DRDS
Source Name
Silica and Silica-Induced Lung Diseases
State
WV
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