2 research outputs found
In Search of the Chemical Basis of the Hemolytic Potential of Silicas
The
membranolytic activity of silica particles toward red blood
cells (RBCs) has been known for a long time and is sometimes associated
with silica pathogenicity. However, the molecular mechanism and the
reasons why hemolysis differs according to the silica form are still
obscure. A panel of 15 crystalline (pure and commercial) and amorphous
(pyrogenic, precipitated from aqueous solutions, vitreous) silica
samples differing in size, origin, morphology, and surface chemical
composition were selected and specifically prepared. Silica particles
were grouped into six groups to compare their potential in disrupting
RBC membranes so that one single property differed in each group,
while other features were constant. Free radical production and crystallinity
were not strict determinants of hemolytic activity. Particle curvature
and morphology modulated the hemolytic effect, but silanols and siloxane
bridges at the surface were the main actors. Hemolysis was unrelated
to the overall concentration of silanols as fully rehydrated surfaces
(such as those obtained from aqueous solution) were inert, and one
pyrogenic silica also lost its membranolytic potential upon progressive
dehydration. Overall results are consistent with a model whereby hemolysis
is determined by a defined surface distribution of dissociated/undissociated
silanols and siloxane groups strongly interacting with specific epitopes
on the RBC membrane
Hematite Nanoparticles Larger than 90 nm Show No Sign of Toxicity in Terms of Lactate Dehydrogenase Release, Nitric Oxide Generation, Apoptosis, and Comet Assay in Murine Alveolar Macrophages and Human Lung Epithelial Cells
Three hematite samples were synthesized by precipitation
from a
FeCl<sub>3</sub> solution under controlled pH and temperature conditions
in different morphology and dimensions: (i) microsized (average diameter
1.2 μm); (ii) submicrosized (250 nm); and (iii) nanosized (90
nm). To gain insight into reactions potentially occurring <i>in vivo</i> at the particle–lung interface following
dust inhalation, several physicochemical features relevant to pathogenicity
were measured (free radical generation in cell-free tests, metal release,
and antioxidant depletion), and cellular toxicity assays on human
lung epithelial cells (A549) and murine alveolar macrophages (MH-S)
were carried out (LDH release, apoptosis detection, DNA damage, and
nitric oxide synthesis). The decrease in particles size, from 1.2
μm to 90 nm, only caused a slight increase in structural defects
(disorder of the hematite phase and the presence of surface ferrous
ions) without enhancing surface reactivity or cellular responses in
the concentration range between 20 and 100 μg cm<sup>–2</sup>