Changes in pulmonary surfactant and phosphatidylcholine metabolism in rats exposed to chrysotile asbestos dust

Tetley, Teresa D.; Richards, Roy J.; Harwood, John L.

doi:10.1042/bj1660323

Cited by 45 publications

(14 citation statements)

References 62 publications

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“…Early studies in animal models indicated a general increase in surfactant volume, but not composition in response to silica [12,13], which according to Muller et al, is unique to silica inhalation compared to tobacco smoke and diesel particles [14]. One study found 3-7 fold increases in PL and SP, respectively, occurring in a rat model with acid-washed silica, but not with unwashed silica [15].…”

Section: Effect Of Silica Exposure On Lung Surfactantmentioning

confidence: 99%

Silica binding and toxicity in alveolar macrophages

Hamilton

Thakur

Holian

2008

Free Radical Biology and Medicine

341

242

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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.

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Section: Effect Of Silica Exposure On Lung Surfactantmentioning

confidence: 99%

Silica binding and toxicity in alveolar macrophages

Hamilton

Thakur

Holian

2008

Free Radical Biology and Medicine

341

242

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“…Increases in extracellular surfactant in response to asbestos deposition have been reported in several studies (55)(56)(57). Crystalline silica (alpha-quartz) is perhaps the most powerful inducer of surfactant phospholipids.…”

Section: Pulmonary Surfactantmentioning

confidence: 99%

Hypertrophy and Hyperplasia of Alveolar Type II Cells in Response to Silica and Other Pulmonary Toxicants

Miller¹,

Hook²

1990

Environmental Health Perspectives

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“…Sulfuric acid fumes produced small changes in the surface activity of rat lung (353). Dusts, such as quartz, silica, and chrysotile asbestos, have been reported to increase the amount of total and surfactant phospholipid in the lung (354)(355)(356)(357)(358). Surface activity, however, was decreased on exposure to silica (359).…”

Section: Other Factors Which Influence Surfactant Production In the Fmentioning

confidence: 99%

Lung surfactant.

Rooney¹

1984

Environ Health Perspect

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Aspects of pulmonary surfactant are reviewed from a biochemical perspective. The major emphasis is on the lipid components of surfactant. Topics reviewed include surfactant composition, cellular and subcellular sites as well as pathways of biosynthesis of phosphatidylcholine, disaturated phosphatidylcholine and phosphatidylglycerol. The surfactant system in the developing fetus and neonate is considered in terms of phospholipid content and composition, rates of precursor incorporation, activities of individual enzymes of phospholipid synthesis and glycogen content and metabolism. The influence of the following hormones and other factors on lung maturation and surfactant production is discussed: glucocorticoids, thyroid hormone, estrogen, prolactin, cyclic AMP, p-adrenergic and cholinergic agonists, prostaglandins and growth factors. The influence of maternal diabetes, fetal sex, stress and labor are also considered. Nonphysiologic and toxic agents which influence surfactant in the fetus, newborn and adult are reviewed.

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Changes in pulmonary surfactant and phosphatidylcholine metabolism in rats exposed to chrysotile asbestos dust

Cited by 45 publications

References 62 publications

Silica binding and toxicity in alveolar macrophages

Silica binding and toxicity in alveolar macrophages

Hypertrophy and Hyperplasia of Alveolar Type II Cells in Response to Silica and Other Pulmonary Toxicants

Lung surfactant.

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