Evidence of an oxidative mechanism for the hemolytic activity of silica particles.

Abstract

The formation of reactive oxygen species resulting from the interaction of silica dust particles with red blood cell membranes was investigated; particularly, the effect of surface hydroxyl (silanol) group concentration on the rate of formation of such reactive oxygen species was investigated. The rate of formation was measured indirectly through the effect of catalase, a hemoprotein peroxidase, on silica-induced hemolysis. It was found that the addition of exogenous catalase to erythrocytes markedly reduces the hemolysis caused by silica particles. Furthermore, the amount of catalase required for deactivation of silica per unit area of particle surface is lower for fumed silica particles and calcined crystalline particles than for uncalcined, crystalline silica, suggesting a correlation between the concentration of OH groups at the silica particle surface and its potential for generation of H2O2. The addition of albumin, a copper chelator, also decreases hemolysis. These results suggest that the hemolysis caused by silica particles is at least partly related to the formation of H2O2 at the particle surface and its subsequent reaction with Cu+ ions. The relationship between the concentration of surface silanol groups on the silica surface and the amount of catalase required to decrease hemolysis may also provide a method for testing potential fibrogenicity of respirable dusts.

Pulmonary surfactant augments cytotoxicity of silica nanoparticles: Studies on an in vitro air–blood barrier model

“…Already 24 years ago researchers considered a direct interaction of the reactive silanol groups with the cellular plasma membrane [ 33 ]. A bonding of these silanol groups to polar phospholipid headgroups of the plasma membrane, leads to membranolysis [ 34 – 35 ].…”

“…With respect to possible mechanisms, the interaction of the silanol groups of aSNP–plain with lung surfactant might initiate extracellular ROS production or could trigger a cellular ROS production following internalization of the aSNPs. Extracellular ROS production likewise causes membranolysis [ 33 , 37 , 39 – 40 ]. To verify this hypothesis aSNP-stimulated A549 with and without Alveofact ® was checked for ROS over a period of 20 min to 24 h. However, no ROS could be detected after aSNP-stimulation regardless of the presence or absence of Alveofact ® .…”

Efficacy of Simple Short-Term in Vitro Assays for Predicting the Potential of Metal Oxide Nanoparticles to Cause Pulmonary Inflammation

“…We further investigated the nature of particle/membrane interactions with a hemolysis assay, which detects direct damaging interactions between particle surfaces and membranes, which can be driven by oxidative stress for some particles ( Razzaboni and Bolsaitis 1990 ) but can also occur when there is no direct evidence of a mechanism for free radical activity ( Clouter et al 2001 ). The hemolysis assay was positive for NiO, as expected, probably by an oxidative action.…”

In Vitro and In Vivo Short-Term Pulmonary Toxicity of Differently Sized Colloidal Amorphous SiO2

“…By selecting four differently sized but otherwise identical test materials, the present study allowed for assessment of how the PPS of colloidal SiO 2 affects its intrinsic material properties, system-dependent properties (dispersibility, dissolution rate, and surface reactivity, with a focus on behavior under cell culture conditions), and in vitro and in vivo pulmonary toxicity. Previous studies have attempted to correlate nanoparticle size or specific nanomaterial surface properties with toxic effects [ 40 , 42 , 43 , 44 , 45 , 46 , 47 , 48 , 49 , 50 , 51 ]. Specific correlations could not be shown consistently for different types of test materials with particle sizes of 1–100 nm, the range used in regulatory nanomaterial definitions [ 52 , 53 , 54 ].…”