Loss of Cathepsin B activity in alveolar macrophages after in vitro quartz phagocytosis

Pätzold, S.; Schmidt, Angela; Seidel, A.

doi:10.1080/15287399309531818

Cited by 4 publications

(5 citation statements)

References 15 publications

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“…These alterations were less pronounced at 72h of exposure. A more prominent decrease in enzyme activity at short incubation times than upon longer exposures is consistent with reported decreases in cathepsin B upon short exposure of macrophages to quartz D12 and to polystyrene microparticles [58,59]. Decreases in lysosomal sulfatase activities in this study were always greater than those in cathepsin B activity.…”

Section: Discussionsupporting

confidence: 90%

Action of polystyrene nanoparticles of different sizes on lysosomal function and integrity

et al. 2012

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BackgroundData from environmental exposure to nanoparticles (NPs) suggest that chronic exposure may increase the incidence of lung, cardiovascular and neurodegenerative diseases. Impairment of cell function by intracellular accumulation of NPs is also suspected. Many types of NPs have been detected in the endosomal-lysosomal system and, upon repeated exposure, alterations of the endosomal-lysosomal system may occur. To identify such effects we compared the effect of carboxyl polystyrene particles (CPS) of different sizes (20-500 nm) on lysosomes of the endothelial cell line EAhy926 after short (24h) and long (72h-96h) exposure times. Lysosomal localization of CPS, as well as lysosomal pH, lysosomal membrane integrity, morphology of the endosomal-lysosomal system and activities of the lysosomal enzymes,cathepsin B and sulfatases, upon exposure to CPS were recorded.ResultsCPS in sizes ≤100 nm showed high co-localization with lysosomes already after 4h, larger CPS after 24h. None of the particles at non-cytotoxic concentrations caused marked changes in lysosomal pH or destroyed lysosomal membrane integrity. At 24h of exposure, 20 nm CPS induced significant dilatation of the endosomal-lysosomal system and reduced activity of lysosomal sulfatases. After 72h, these alterations were less pronounced.ConclusionsDespite accumulation in lysosomes CPS induced only small changes in lysosomes. Upon longer contact, these changes are even less pronounced. The presented panel of assays may serve to identify effects on lysosomes also for other NPs.

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Section: Discussionsupporting

confidence: 90%

Action of polystyrene nanoparticles of different sizes on lysosomal function and integrity

et al. 2012

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“…The untreated silica caused a significant reduction of lysosomal enzyme (cathepsin B) activity that was inhibited by silica pretreatment with dipalmitoyl lecithin or the presence ammonium chloride [28]. Another study showed that serum-coated silica caused lysosmal rupture in a murine macrophage cell line (J774).…”

Section: The Lysosomal Permeability Hypothesis Of Silica Toxicitymentioning

confidence: 96%

“…The same research group used amiodarone to inhibit phospholipase activity and generate phospholipidosis artificially, which proved to be protective with silica exposure, again having no effect on PMN influx [27]. The surfactant PL component dipalmitoyl phosphatidylcholine (DPPC, also referred to as dipalmitoyl lecithin) has been used as a protective pre-coating agent against silica toxicity [28][29][30], but was ineffective at inhibiting chysotile asbestos toxicity [29]. In addition, SPA and D have been used to attenuate silica toxicity in vitro [19,20].…”

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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“…Studies on pulmonary alveolar macrophages showed the DPPC fully suppressed silica NPs prompt cytotoxic, apoptotic, necrotic and genotoxic activity for 3 days. 15,16,33,52 The interaction between DPPC and different types of silica dust has been suggested to modulate the toxicity of the particles through the molecular orientation of the adsorbed DPPC molecules. This may account for differences in pulmonary disease abnormalities.…”

Section: Effect Of Dppc Coating On Cytotoxicity Of Npsmentioning

confidence: 99%

“…Wallace and et al15 showed that the DPPC treated quartz and kaolin particles incubated for 1 hour with erythrocytes suppressed the hemolytic strength of particles to background levels. Studies on pulmonary alveolar macrophages showed the DPPC fully suppressed silica NPs prompt cytotoxic, apoptotic, necrotic and genotoxic activity for 3 days 15,16,33,52. The interaction between DPPC and different types of silica dust has been suggested to modulate the toxicity of the particles through the molecular orientation of the adsorbed DPPC molecules.…”

mentioning

confidence: 99%