Influence of surfactant components and exposure geometry on the effects of quartz and asbestos on alveolar macrophages.

Abstract

Bovine (BAM) and rat (RAM) alveolar macrophages were incubated in vitro with DQ12 quartz or UICC chrysotile asbestos either alone or in the presence ofdipalmitoyl lecithin (DPL). The reaction of the cells of both species to the untreated dust particles w similar quaHtatively and quantitatively, withalos ofviabibt and releaseof lacate and N-acetyl-3l-glucosaminidase after 20 hr ofincubation. In the presence ofDPL, the toxicity ofquartz to BAM disappeared completely, whereas the protective influence of the phospholipid was distinctly diminished in the case of RAM.The presence oflavage fluid waslss effective tban that of pure DPL. There was no e of DPL with asbestos either for BAM or for RAM. The effects of phagocytizable, suspended quartz particles were compared with the effects ofthe same type of particles fixed on a glass surface to exclude the possibility ofphagocytosis. The effect ofthe suspended particles on the viability and release of enzymes was more pronounced than that of the fixed particles On the other hand, superoxide anion production was stimulated to a much higher degree by the frmed quartz particles. This could be explabned by the continuingcontactofthe outer cell membrne with the silica surfes, whereas free partidles were rapidly phagocytized. The release oflysosomal enzymes induced by fixed quartz particles was a secondary phenomenon following cell death.

In vitro toxicity evaluation of single walled carbon nanotubes on human A549 lung cells

“…Gülden and Seibert (2005) have recently reported that the bioavailability of chemicals in vitro can be reduced due to partitioning into lipids and binding to serum proteins. The 'protective' eVect of serum in silica toxicity has also been well documented (Emerson and Davis, 1983;Schimmelpfeng et al, 1992). demonstrated that coating of silica with a commercially available bovine pulmonary surfactant aVorded short-term protection against its toxicity when tested both in vitro on rat alveolar macrophages and in vivo following intratracheal instillation.…”

Silica binding and toxicity in alveolar macrophages

“…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].…”

Effects of serum on cytotoxicity of nano- and micro-sized ZnO particles

“…In view of the potential discrepancies, a few groups have begun to evaluate the effects of serum on particle toxicity from the aspect of particle agglomeration and surface chemistry (Davoren et al 2007; Murdock et al 2008; Zhu et al 2009). For example, the presence of protein-containing serum in a medium has a protective effect on the toxicity of both silica and single-walled carbon nanotubes (Schimmelpfeng et al 1992; Davoren et al 2007). Recently, studies have found that the protective effect on NP toxicity was derived from the binding of multiple layers of serum proteins (e.g., bovine fibrinogenon, gamma globulin, etc.)…”