Silicon dioxide nanoparticle exposure affects small intestine function in anin vitromodel

Abstract

The use of nanomaterials to enhance properties of food and improve delivery of orally administered drugs has become common, but the potential health effects of these ingested nanomaterials remain unknown. The goal of this study is to characterize the properties of silicon dioxide (SiO) nanoparticles (NP) that are commonly used in food and food packaging, and to investigate the effects of physiologically realistic doses of SiO NP on gastrointestinal (GI) health and function. In this work, an in vitro model composed of Caco-2 and HT29-MTX co-cultures, which represent absorptive and goblet cells, was used. The model was exposed to well-characterized SiO NP for acute (4 h) and chronic (5 d) time periods. SiO NP exposure significantly affected iron (Fe), zinc (Zn), glucose, and lipid nutrient absorption. Brush border membrane intestinal alkaline phosphatase (IAP) activity was increased in response to nano-SiO. The barrier function of the intestinal epithelium, as measured by transepithelial electrical resistance, was significantly decreased in response to chronic exposure. Gene expression and oxidative stress formation analysis showed NP altered the expression levels of nutrient transport proteins, generated reactive oxygen species, and initiated pro-inflammatory signaling. SiO NP exposure damaged the brush border membrane by decreasing the number of intestinal microvilli, which decreased the surface area available for nutrient absorption. SiO NP exposure at physiologically relevant doses ultimately caused adverse outcomes in an in vitro model.

The Nano–Intestine Interaction: Understanding the Location‐Oriented Effects of Engineered Nanomaterials in the Intestine

“…At cellular level, SiO 2 NMs destroyed the brush border by interacting with intestinal micro villi in coculture model of Caco2/HT29MTX, which inhibited the absorption of nutrients, such as iron, zinc, glucose, and lipid. [49] As important metal nanomaterials, pristine Ag NMs can also induce cytotoxicity and DNA damage through oxida tive stress in intestinal epithelial cells or coculture of epithe lial and immune cells; [50][51][52][53][54] even worse, these nanomaterials could disrupt the structure of intestinal villi at animal level. [48] In addition, some studies have shown that the intestinal micro environment, such as intestinal fluid and food matrix, is likely to alter NMs' effects on IECs.…”

“…[93] Copyright 2016, Elsevier Ltd. in vivo. [30,49,54,60,88] These nanomaterials can induce oxidative stress, nitrifying stress (NO), lipid peroxidation, organelles damage (mitochondria and lysosomes), and DNA damage, thus triggering inflammatory responses. [4,54] Along with the effects of NMs per se, a variety of compounds, including phe nolic compounds, quercetin, kaenol, free fatty acid (FFA), and reduced the toxicity of Ag and ZnO NMs on intestinal epithelial cells through maintaining the integrity of epithelial barrier and decreasing the level of oxidative stress, protected the epithelial cells from the damage of inflammatory response.…”

Effect of dietary additives on intestinal permeability in both Drosophila and a human cell co-culture

“…HT29-MTX cells represent goblet cells and form a protective mucus layer on top of the Caco-2 cell layer (Lesuffleur et al, 1995). The Caco-2/HT29-MTX co-culture system has been used previously to model the small intestine and to study the role of NP ingestion on intestinal function (Guo et al, 2017, 2018; Mahler et al, 2012; Richter et al, 2018).…”

Copper Oxide Nanoparticles Cause a Dose-Dependent Toxicity via Inducing Reactive Oxygen Species in Drosophila

“…Oxidative stress is considered to be one of the primary causes of cytotoxicity, genotoxicity, inflammation, cell death and altered nutrient absorption induced by NP exposure in the gut [ 41 , 42 , 43 ]. We have also previously shown that AgNP ingestion causes excessive intracellular ROS induction in the Drosophila testis, leading to oxidative stress responsible for defects in germline stem cell homeostasis and a significant decrease in male fecundity [ 44 ].…”