Effects of Phospholipid Surfactant on Apoptosis Induction by Respirable Quartz and Kaolin in NR8383 Rat Pulmonary Macrophages

Gao, Ning; Keane, Michael; Ong, T.; Ye, J.; Miller, William E.; Wallace, W.E.

doi:10.1006/taap.2001.9249

Cited by 38 publications

(25 citation statements)

References 26 publications

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“…Where NHBE cells were exposed to particles suspended in specialized medium supplemented with a variety of growth factors and other additives, A549 cells were exposed to particles suspended in protein-free RPMI medium without the use of any supplements besides Lglutamine. The supplements present in NHBE medium might attenuate particle reactivity by coating their reactive surface area leading to decreased oxidative potential [Davoren et al, 2007;Gao et al, 2001]. The fact that ROS levels of A549 cells also returned to control levels as soon as particles were suspended in RPMI medium supplemented with FCS ( Figure 4) also points to this conclusion.…”

Section: Discussionmentioning

confidence: 87%

Dispersion medium modulates oxidative stress response of human lung epithelial cells upon exposure to carbon nanomaterial samples

Herzog¹,

Byrne²,

Davoren³

et al. 2009

Toxicology and Applied Pharmacology

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Section: Discussionmentioning

confidence: 87%

Dispersion medium modulates oxidative stress response of human lung epithelial cells upon exposure to carbon nanomaterial samples

Herzog¹,

Byrne²,

Davoren³

et al. 2009

Toxicology and Applied Pharmacology

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“…Research with DPPC as the protective component indicates that the protection lasts for only 3 days in vitro because the particle coating is destroyed by enzymatic digestion (either by phospolipase A 2 activity or by AM lysosomal enzymes) [31][32][33]. One problem with surfactant overproduction is that sustained and uncontrolled over a period of time, it can become a pathological feature of silica exposure.…”

Section: Modification Of Silica Toxicity By Lung Surfactantmentioning

confidence: 99%

Silica binding and toxicity in alveolar macrophages

Hamilton

Thakur

Holian

2008

Free Radical Biology and Medicine

342

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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“…DPPC dispersion resulted in greater oxidative potential of particles as compared to particles suspended in physiological saline. On the other hand, coating with lung surfactant might mask their oxidative potential leading to decreased reactivity and attenuated toxicity [Gao et al, 2001]. Therefore, the next step of this study was to investigate the effects of SWCNT exposure on the inflammatory response of lung epithelial cells upon SWCNT exposure and examine if DPPC dispersion may modulate cell responses.…”

Section: Dispersion Of Hipco Swcnt and Asbestos Fibresmentioning

confidence: 99%

SWCNT suppress inflammatory mediator responses in human lung epithelium in vitro

Herzog¹,

Byrne²,

Casey³

et al. 2009

Toxicology and Applied Pharmacology

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Effects of Phospholipid Surfactant on Apoptosis Induction by Respirable Quartz and Kaolin in NR8383 Rat Pulmonary Macrophages

Cited by 38 publications

References 26 publications

Dispersion medium modulates oxidative stress response of human lung epithelial cells upon exposure to carbon nanomaterial samples

Dispersion medium modulates oxidative stress response of human lung epithelial cells upon exposure to carbon nanomaterial samples

Silica binding and toxicity in alveolar macrophages

SWCNT suppress inflammatory mediator responses in human lung epithelium in vitro

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