From the current state-of-the-art, it is clear that nanotechnology applications are expected to bring a range of benefits to the food sector aiming at providing better quality and conservation. In the meantime, a growing number of studies indicate that the exposure to certain engineered nanomaterials (ENMs) has a potential to lead to health complications and that there is a need for further investigations in order to unravel the biological outcomes of nanofood consumption. In the current review, we summarize the existing data on the (potential) use of ENMs in the food industry, information on the toxicity profiles of the commonly applied ENMs, such as metal (oxide) nanoparticles (NPs), address the potential food safety implications and health hazards connected with the consumption of nanofood. A number of health complications connected with the human exposure to ENMs are discussed, demonstrating that there is a real basis for the arisen concern not only connected with the gut health, but also with the potency to lead to systemic toxicity. The toxicological nature of hazard, exposure levels and risk to consumers from nanotechnology-derived food are on the earliest stage of investigation and this review also highlights the major gaps that need further research and regulation.
The increasing commercial use of silver nanoparticles (Ag-NPs) will inevitably lead to elevated silver exposure and thus to potential human health complications. In this study the acute toxicity of Ag-NPs <20 nm alone and upon co-administration with food matrix component phenolic compounds (PCs) on the cell-based models of the gastrointestinal tract was investigated. An improved co-culture model of Caco-2 and RajiB cells was applied for more precise in vitro simulation of the gastrointestinal tract. The involvement of two major factors contributing to the toxicity of Ag-NPs, i.e. the release of Ag(+) and the induction of oxidative stress, was investigated. Ag-NPs were cytotoxic for Caco-2 cells with an EC50 of ca. 40 µg/ml. Ag-NPs led to oxidative stress starting from ca. 45 µg/ml. The epithelial barrier integrity disruption by Ag-NPs on Caco-2 cell mono- and co-cultures was established by decreased transepithelial electrical resistances and increased passages of Lucifer Yellow, a paracellular marker. Immunofluorescence staining demonstrated that Ag-NPs affect occludin and zonula occludens 1 distributions, suggesting the opening of tight junctions. Ag(+), corresponding to the release from Ag-NPs, demonstrated a partial contribution in the toxic parameters, induced by Ag-NPs. Two PCs, quercetin and kaempferol, partially protected the Caco-2 cells from Ag-NP-induced toxicity and maintained the epithelial barrier integrity, disrupted by NPs. No protective effect was observed for resveratrol. The protective effect could be beneficial and decrease the potential toxicity of ingested Ag-NPs. However, the precise mechanisms of barrier-integrity-destabilising action of Ag-NPs/Ag(+) and protective effect of PCs still require further elucidation.
This work demonstrates gastric mucin-triggered nanocarrier disassembly for release of antisense oligonucleotides and consequent unassisted cellular entry as a novel oral delivery strategy. A fluorescence activation-based reporter system was used to investigate the interaction and mucin-mediated disassembly of chitosan-based nanocarriers containing a 13-mer DNA oligonucleotide with a flanked locked RNA nucleic acid gapmer design. Gastric mucins were shown to trigger gapmer release from nanocarriers that was dependent on the interaction time, mucin concentration and N : P ratio with a maximal release at N : P 10. In contrast to siRNA, naked gapmers exhibited uptake into mucus producing HT-MTX mono-cultures and HT-MTX co-cultured with the carcinoma epithelial cell line Caco-2. Importantly, in vivo gapmer uptake was observed in epithelial tissue 30 min post-injection in murine intestinal loops. The findings present a mucosal design-based system tailored for local delivery of oligonucleotides that may maximize the effectiveness of gene silencing therapeutics within tumours at mucosal sites.
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