Contrasting respirable quartz and kaolin retention of lecithin surfactant and expression of membranolytic activity following phospholipase A₂digestion

Abstract

Respirable-sized quartz, a well-established fibrogenic mineral dust, is compared with kaolin in erythrocyte hemolysis assays after treatment with saline dispersion of dipalmitoyl phosphatidylcholine, a primary phospholipid component of pulmonary surfactant. Both dusts are rendered inactive after treatment, but the membranolytic activity is partly to fully restored after treatment with phospholipase A2, an enzyme normally associated with cellular plasma membranes and lysosomes. Phospholipid-coated dusts were incubated for periods of 2-72 h at a series of applied enzyme concentrations, and the adsorbed lipid species and hemolytic activity were quantitated at each time for both dusts. Surfactant was lost more readily from quartz than from kaolin, with consequent more rapid restoration of mineral surface hemolytic activity for quartz. Interactions of surfactant and mineral surface functional groups responsible for the mineral-specific rate differences, and implications for determining the mineral surface bioavailability of silica and silicate dusts, are discussed.

Biomembrane Phospholipid–Oxide Surface Interactions: Crystal Chemical and Thermodynamic Basis

“…The relation between hemolysis and fibrogenesis is not accepted by all authors and has been debated in the literature (48)(49)(50). However, if the extent of hemolysis per unit surface area of the oxide particles is considered instead of per unit mass of oxide, then it appears that hemolysis is a direct indicator of the oxide surface's affinity for some components of the cell membrane (51).…”

“…On balance, a comprehensive examination of the proxy methods used to estimate cytotoxicity and fibrogenicity indicates that membranolysis and cytotoxicity can explain macrophage activation and inflammation. However, these are probably only the early steps in a complex process that includes radical oxidation reactions, which may or may not lead to fibrogenicity and silicosis (45,49,51,53,61). …”

“…Alternative mechanisms that do not rely on surface interactions have been proposed. The most important alternative theory involves the toxic action of free radicals and is discussed in Appendix B (48)(49)(50)(51)(52)(53)(54)(55)(56)(57)(58)(59)(60)(61).…”

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

“…DPPC, the major component of lung surfactant, dispersed in physiological saline, has been used as simple model of lung surfactant in particle toxicity studies [Foucaud et al, 2007;Porter et al, 2008;Sager et al, 2007;Wallace et al, 1992;Wallace et al, 2007b]. In the case of silica toxicity, DPPC has been used as protective agent, inhibiting toxicity by particle coating [Hamilton et al, 2008;Patzold et al, 1993;Schimmelpfeng et al, 1992;Wallace et al, 1992]. However, it did not have a protective effect on chrysotile asbestos toxicity [Schimmelpfeng et al, 1992].…”

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].…”