Interaction of Layered Silicates with Biomembranes: Ion Exchangers and Non‐Exchangers

Abstract

Layered silicates (LS, clays) are a composite group of minerals whose industrial interest and technological applications are progressively expanding, spanning from catalysis to biomedicine. However, the compatibility of LS with biological systems is not clear, and mechanistic data about biophysicochemical interactions at the interface of LS and biomembranes are scarce. Here, cell membrane damage, assessed using red blood cells as model membranes, is revealed for kaolin (> 75 wt.% kaolinite, 1:1 layer structure) and bentonite (> 90 wt.% montmorillonite, 1:2 layer structure) particles. The high membranolytic capacity of bentonite (i.e., high ion‐exchanger LS) is the result of the combined contribution of both mineral surface features and sample‐specific cation exchange capacity (CEC). For kaolin (i.e., non‐ion‐exchanger LS), the capacity to damage membranes is primarily due to surface hydroxyl species, that is, silanols and aluminols, exposed at the crystal lattice boundaries. When kaolin is thermally disorganized into amorphous metakaolin, membrane damage is driven by a specific sub‐population of surface hydroxyl species, namely the “nearly free silanols”, previously evidenced on quartz. This study establishes the rationale underlying the interactions between LS particles and membranes and can set the basis for the understanding of interfacial phenomena of LS.

Physico-Chemical Approaches to Investigate Surface Hydroxyls as Determinants of Molecular Initiating Events in Oxide Particle Toxicity

“…For these clays, the capacity to damage membranes was related to surface OH terminations, namely silanols and aluminols, that were exposed at the crystal lattice boundaries. The membrane damage observed for amorphous metakaolin was driven by a specific OH family with a surface OH profile that could be assigned to the NFS previously evidenced in quartz [27].…”

“…The NFS have also been identified on the dehydrated kaolinite (i.e., metakaolin) surface. NFS occurrence paralleled the variation of the metakaolin haemolytic activity well following heating at several temperatures (Figure 13C,D) [27]. Moreover, strong chemical treatments, such as etching with hydrofluoric acid (HF), caused a strong decrease of quartz haemolytic activity which was associated with a deletion of NFS (Figure 13E,F) [111].…”

“…A recent study [113] employed shape-engineered TiO 2 particles [114] and proposed a correlation between the extension of the {001} facets of TiO 2 nanocrystals and the haemolytic activity (Figure 14) and invoked the easier release of hydroxyl radicals from the {001} facet as the main mechanism of membrane damage. [1,27,111].…”

“…Emerging evidence was recently advanced about the key role of the topochemistry of surface OH moieties of OxPs as a relevant contributor to the detrimental interactions established with biomolecules and biomembranes [26][27][28][29][30]. Many oxides (e.g., SiO 2 , TiO 2 , Al 2 O 3 ,) and innovative nanomaterials (e.g., graphene oxide and nanoclays) expose hydroxyl groups at their surface, which can arrange in different orientations and relative distances depending on the structural constrain of each material.…”

The hemostatic performance and mechanism of palygorskite with structural regulate by oxalic acid gradient leaching

“…The biocompatibility is also critical criterion in determining the applicability of biomaterials. As reported, the direct contact of clay minerals with the erythrocyte membrane and the imbalance local ion concentration due to cation exchange are the predominant mechanisms leading to hemolysis [38,39]. Therefore, it could be hypothesized that the attenuation of the destructive effect of Pal on erythrocytes was partly assigned to the reduction of metal cations in the skeleton of Pal crystal.…”