Response of alveolar macrophages to in vitro exposure to freshly fractured versus aged silica dust: The ability of prosil 28, an organosilane material, to coat silica and reduce its biological reactivity

Vallyathan, Val; Kang, Ji-Hee; Dyke, Knox Van; Dalal, N. S.; Castranova, Vincent

doi:10.1080/15287399109531529

Cited by 65 publications

(45 citation statements)

References 18 publications

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“…•− , H 2 O 2 [72,87], and increased NO • synthesis, in addition to nitric oxide synthase [88]. All of these AM responses are enhanced in the presence of freshly fractured silica [67].…”

Section: Cell-derived Free Radicalsmentioning

confidence: 89%

“…The most compelling evidence for oxygen radicals causing silica toxicity is based on the observation that freshly fractured silica particles are more toxic in vitro [70][71][72], and more inflammatory [73], and fibrogenic in vivo [74] when compared to aged silica. This obviously has relevance to occupational exposure, because in most situations workers will inhale freshly fractured silica dusts.…”

Section: Particle-derived Free Radicalsmentioning

confidence: 99%

See 1 more Smart Citation

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: Cell-derived Free Radicalsmentioning

confidence: 89%

Section: Particle-derived Free Radicalsmentioning

confidence: 99%

Silica binding and toxicity in alveolar macrophages

Hamilton

Thakur

Holian

2008

Free Radical Biology and Medicine

341

242

View full text Add to dashboard Cite

show abstract

“…At least part of this activation is associated with silica-induced enhancement of°2 and H202 production ( Figure 4). Freshly ground silica is a more potent stimulant of alveolar macrophages than aged silica (18). Indeed, freshly fractured silica causes approximately three times more H202 production and approximately 14 times more chemiluminescence from alveolar macrophages than ground silica, which was aged for 14 days prior to use ( Figure 5).…”

Section: Resultsmentioning

confidence: 99%

“…Such radical production can be monitored by ESR using DMPO (5,5-dimethyl-l-pyroline-l-oxide) as a spin trap (16). As shown in Figure 2A, an ESR spectrum centered around g = 2.0059 and exhibiting a 1:2 Grinding of crystalline silica is not only associated with the generation of radicals but also results in an increase in the direct toxicity of silica in vitro (17,18). As shown in Table 1, freshly ground silica is approximately 19 times more lytic to red blood cells than ground dust tested after a 2-day aging period, is approximately four times more potent in causing loss of membrane integrity in alveolar macrophages than silica aged for 14 days, and induces five times more lipid peroxidation than quartz aged for 4 days.…”

Section: Resultsmentioning

confidence: 99%

Generation of oxygen radicals and mechanisms of injury prevention.

Castranova

1994

Environ Health Perspect

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Exposure to crystalline silica can result in damage to the lung parenchyma and scarring that can lead to fibrosis. Pulmonary damage may be the direct consequence of toxic interaction between quartz particles and cell membranes, or it may be due to silica-induced production of oxidant species by pulmonary phagocytes, that in turn overwhelms pulmonary antioxidant systems and causes lung injury. Data indicate that grinding or fracturing quartz particles breaks Si-O bonds and generates Si and Si-0 radicals on the surface of the cleavage planes. Upon contact with water, these silica-based radicals can generate hydroxyl radicals (OH). These surface radicals decay as fractured silica dust is aged. Freshly fractured quartz is significantly more potent than aged silica in directly causing lipid peroxidation, membrane damage, and cell death. Furthermore, freshly ground silica is a more potent stimulant of alveolar macrophages than aged silica. This silica-induced activation results in the production of superoxide (O°), hydrogen peroxide (H202), nitric oxide (NO), and other oxidant species that can damage lung cells. Tetrandrine, an herbal medicine that exhibits antifibrotic activity in rat models of silicosis, effectively blocks the ability of quartz to stimulate oxidant release from pulmonary phagocytes.-Environ Health Perspect 102(Suppl 10): 65-68 (1994)

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“…A variety of substances such as phospholipid, organosilane, aluminum lactate, and polyvinylpyridine-N-oxide, have been used in a number of in vitro studies in an attempt to coat the silica and reduce its cytotoxicity (21)(22)(23)(24)(25). Based on these in vitro studies, our hypothesis was that the increase in phospholipid levels within the lungs after the induction of phospholipidosis will protect them from damage caused by the exposure to cytotoxic particles.…”

mentioning

confidence: 99%

Acute silica toxicity: attenuation by amiodarone-induced pulmonary phospholipidosis.

Antonini

McCloud²,

Reasor³

1994

Environ Health Perspect

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Exposure to the toxic mineral dust silica has been shown to produce an acute inflammatory response in the lungs of both humans and laboratory animals. Coating silica with phospholipids reduces its toxicity when studied with in vitro systems. The drug amiodarone increases phospholipid within the cells, airways, and alveoli of the lungs. This increase in phospholipid is due to amiodarone's ability to inhibit phospholipase activity within alveolar macrophages (AMs) and whole lung. The purpose of this study was to determine whether the amiodarone-induced increase in pulmonary phospholipid would protect the lungs from acute damage caused by the intratracheal instillation of silica. Treatment of male Fischer 344 rats with amiodarone for 14 days caused an increase in phospholipid content in bronchoalveolar lavage fluid and AMs compared to vehicle-treated controls. The rats were then instilled with silica or saline vehicle. At both 1 and 14 days after silica exposure, pulmonary phospholipidosis was associated with a marked reduction in acute silica-induced pulmonary damage as assessed by biochemical parameters in bronchoalveolar lavage fluid, however, the influx of neutrophils into the airspaces was not reduced. Four times more phospholipid was bound to the silica recovered from amiodarone-treated rats compared to controls. The results of these in vivo experiments indicate that pulmonary phospholipidosis attenuates the acute damage associated with the intratracheal instillation of silica in rats. By using an in vitro cell culture system, we demonstrated that, in contrast to control AMs, phospholipidotic AMs were significantly more resistant to the cytotoxicity of surfactant-coated silica.(ABSTRACT TRUNCATED AT 250 WORDS) Images p372-a Figure 1. Figure 2. Figure 3. Figure 4. Figure 5. Figure 6. Figure 7. Figure 8.

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Response of alveolar macrophages to in vitro exposure to freshly fractured versus aged silica dust: The ability of prosil 28, an organosilane material, to coat silica and reduce its biological reactivity

Cited by 65 publications

References 18 publications

Silica binding and toxicity in alveolar macrophages

Silica binding and toxicity in alveolar macrophages

Generation of oxygen radicals and mechanisms of injury prevention.

Acute silica toxicity: attenuation by amiodarone-induced pulmonary phospholipidosis.

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