Hydroxyl radical production and lung injury in the rat following silica or titanium dioxide instillation in vivo.

Schapira, Ralph M.; Ghio, Andrew J.; Effros, Richard M.; Morrisey, James F; Almagro, Urias A.; Dawson, Christopher A.; Hacker, Allen D.

doi:10.1165/ajrcmb.12.2.7865220

Cited by 68 publications

(57 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Similarly, desferrioxamine decreases the ability of freshly fractured quartz to generate 'OH in aqueous media (10). Such pulmonary production of 'OH has been demonstrated in quartz-exposed rats and has been associated with lung inflammation (22). The results of the current investigation support the hypothesis (24).…”

Section: Measurement Ofthe Lung Lipid Peroxidationsupporting

confidence: 81%

Augmentation of pulmonary reactions to quartz inhalation by trace amounts of iron-containing particles.

Castranova

Vallyathan²,

Ramsey³

et al. 1997

Environ Health Perspect

View full text Add to dashboard Cite

Fracturing quartz produces silica-based radicals on the fracture planes and generates hydroxyl radicals (OH) in aqueous media. 'OH production has been shown to be directly associated with quartz-induced cell damage and phagocyte activation in vitro. This 'OH production in vitro is inhibited by desferrioxamine mesylate, an Fe chelator, indicating involvement of a Fenton-like reaction. Our objective was to determine if Fe contamination increased the ability of inhaled quartz to cause inflammation and lung injury. Male Fischer 344 rats were exposed 5 hr/day for 10 days to filtered air, 20 mg/m3 freshly milled quartz (57 ppm Fe), or 20 mg/m3 freshly milled quartz contaminated with Fe (430 ppm Fe). High Fe contamination of quartz produced approximately 57% more reactive species in water than quartz with low Fe contamination. Compared to inhalation of quartz with low Fe contamination, high Fe contamination of quartz resulted in increases in the following responses: leukocyte recruitment (537%), lavageable red blood cells (157%), macrophage production of oxygen radicals measured by electron spin resonance or chemiluminescence (32 or 90%, respectively), nitric oxide production by macrophages (71 %), and lipid peroxidation of lung tissue (38%). These results suggest that inhalation of freshly fractured quartz contaminated with trace levels of Fe may be more pathogenic than inhalation of quartz alone. Environ Health Perspect 105(Suppl 5): 1319-1324 (1997)

show abstract

Section: Measurement Ofthe Lung Lipid Peroxidationsupporting

confidence: 81%

Augmentation of pulmonary reactions to quartz inhalation by trace amounts of iron-containing particles.

Castranova

Vallyathan²,

Ramsey³

et al. 1997

Environ Health Perspect

View full text Add to dashboard Cite

show abstract

“…All of these AM responses are enhanced in the presence of freshly fractured silica [67]. HO • production in rat lung tissue following silica instillation has also been described using titanium dioxide as a negative control particle [89]. Further evidence for silica-induced ROS in rat model lungs comes from observed increases in antioxidant enzymes such as manganese superoxide dismutase (MnSOD) from type II epithelial cells [90], along with increased SOD and glutathione peroxidase mRNA in rat lungs following silica inhalation [91].…”

Section: Cell-derived Free Radicalsmentioning

confidence: 94%

Silica binding and toxicity in alveolar macrophages

Hamilton

Thakur

Holian

2008

Free Radical Biology and Medicine

333

242

View full text Add to dashboard Cite

Inhalation of the crystalline form of silica is associated with a variety of pathologies from acute lung inflammation to silicosis, in addition to autoimmune disorders and cancer. Basic science researchers looking at the mechanisms involved with the earliest initiators of disease are focused on how the alveolar macrophage (AM) interacts with the inhaled silica particle and the consequences of silicainduced toxicity on the cellular level. Based on experimental results, several rationales have been developed on exactly how crystalline silica particles are toxic to the macrophage cell that is functionally responsible for clearance of the foreign particle. For example, silica is capable of producing reactive oxygen species (ROS) either directly (on the particle surface) or indirectly (produced by the cell as a response to silica) triggering cell-signaling pathways initiating cytokine release and apoptosis. With murine macrophages, reactive nitrogen species (RNS) are produced in the initial respiratory burst in addition to ROS. An alternative explanation for silica toxicity includes lysosomal permeability, where silica disrupts the normal internalization process leading to cytokine release and cell death. Still other research has focused on the cell surface receptors (collectively known as scavenger receptors) involved in silica binding and internalization. The silica-induced cytokine release and apoptosis is described as the function of receptor-mediated signaling rather than free radical damage. Current research ideas on silica toxicity and binding in the alveolar macrophage are reviewed and discussed.

show abstract

“…Significantly increased levels of sICAM-1 were found in the BAL fluid of mice exposed to silica ( Figure 6) with times of increase (days 3, 5, and 7) parallel to increased AM-associated ICAM-1. Titanium dioxide exposure also elicited increased levels of sICAM-1, but well below that observed in silica exposed animals.…”

Section: Silica-induced Icam-1 Expresionmentioning

confidence: 95%

Localization of Intercellular Adhesion Molecule-1 (ICAM-1) in the Lungs of Silica-Exposed Mice

Nario¹,

Hubbard²

1997

Environmental Health Perspectives

View full text Add to dashboard Cite

Intercellular adhesion molecule-1 (ICAM-1) is expressed on a variety of cells including endothelial cells, alveolar epithelial cells, and alveolar macrophages. Endothelial/epithelial cell ICAM-1 participates in the migration of leukocytes out of the blood in response to pulmonary inflammation, whereas alveolar macrophage ICAM-1 may represent cell activation. Our previous studies have shown that there is increased expression of ICAM-1 in lung tissue during acute inflammation following intratracheal injection with silica particles (2 mg/mouse). This increased expression was shown to play a role, in part, in the migration of neutrophils from the circulation into the tissue parenchyma. The aim of the current work is to localize expression of ICAM-1 during acute inflammation in lungs of mice exposed to either silica or the nuisance dust, titanium dioxide. In silica-exposed mice, a significant increase in ICAM-1 was detected on day 1 and localized by immunohistochemistry to aggregates of pulmonary macrophages and to type 11 epithelial cells. Areas of the lung with increased ICAM-1 expression also showed increased tumor necrosis factor alpha expression. Immunocytochemical staining of bronchoalveolar lavage (BAL) cells demonstrated increased ICAM-1 expression associated with alveolar macrophages 3, 5, and 7 days following silica exposure. Finally, soluble ICAM-1 levels in the BAL fluid were significantly increased in mice exposed to silica on the same days. Titanium dioxide exposure elicited a minimal increase in expression of ICAM-1 in the lungs. These data demonstrate that exposure to the toxic particle silica specifically increases ICAM-1 expression localized to pulmonary macrophages and type II epithelial cells.

show abstract

Hydroxyl radical production and lung injury in the rat following silica or titanium dioxide instillation in vivo.

Cited by 68 publications

References 18 publications

Augmentation of pulmonary reactions to quartz inhalation by trace amounts of iron-containing particles.

Augmentation of pulmonary reactions to quartz inhalation by trace amounts of iron-containing particles.

Silica binding and toxicity in alveolar macrophages

Localization of Intercellular Adhesion Molecule-1 (ICAM-1) in the Lungs of Silica-Exposed Mice

Contact Info

Product

Resources

About