The Role of Metal Oxide Nanoparticles, Escherichia coli, and Lactobacillus rhamnosus on Small Intestinal Enzyme Activity.

Engineered nanomaterials (ENMs) have become common in the food industry, which motivates the need to evaluate ENM effects on human health. Gastrointestinal (GI) in vitro models (e.g. Caco-2, Caco-2/HT29-MTX) have been used in nanotoxicology research. However, the human gut environment is composed of both human cells and the gut microbiota. The goal of this study is to increase the complexity of the Caco-2/HT29-MTX in vitro model by co-culturing human cells with the Gram-positive, commensal Lactobacillus rhamnosus or the Gram-negative, opportunistic Escherichia coli; with the hypothesis that the presence of bacteria would ameliorate the effects of exposure to metal oxide nanoparticles (NPs) such as iron oxide (Fe2O3), silicone dioxide (SiO2), titanium dioxide (TiO2), or zinc oxide (ZnO). To understand this relationship, Caco-2/HT29-MTX cell barriers were acutely co-exposed (4 hours) to bacteria and/or NPs (pristine or in vitro digested). The activity of the brush border membrane (BBM) enzymes intestinal alkaline phosphatase (IAP), aminopeptidase-N (APN), sucrase isomaltase (SI) and the basolateral membrane enzyme (BLM) Na+/K+ ATPase were assessed. Findings show that (i) the human digestion process alters the physicochemical properties of NPs, (ii) large agglomerates of NPs remain entrapped on the apical side of the intestinal barrier, which (iii) affects the activity of BBM enzymes. Interestingly, some NPs effects were attenuated in the presence of either bacterial strains. Confocal microscopy detected bacteria-NPs interactions, which may impede the NP-intestinal cell contact. These results highlight the importance of improving in vitro models to closely mimic the complexities of the human body.

Can abiotic stresses in plants be alleviated by manganese nanoparticles or compounds?

Abiotic stress has become one of the most challenging problems for agriculture as the world population keeps increasing dramatically. Crop stress management using manganese (Mn) compounds has been recently employed to reduce the negative effects caused by drought, harsh temperature, and salinity. In response to abiotic stress, an adequate supply of Mn has shown to remediate plant manganese deficiency, induce Mn superoxide dismutase at the transcriptional level to face reactive oxygen species production, and stimulate manganese-dependent proteins to maintain cell integrity. Lately, nanoparticles (NPs) have been explored in agriculture applications. Recent studies have implied that Mn NPs may help plants to overcome abiotic stresses at higher efficiency and lower toxicity, compared to their bulk or ionic counterparts. Although studies have shown that Mn compounds promote crop growth and alleviate abiotic stress, many questions related to Mn-plant networking, their mode of signaling, and the Mn-dependent regulation processes need to be answered.

ZnO nanoparticles affect nutrient transport in an in vitro model of the small intestine.

Nano-sized zinc oxide (ZnO) is present in food packaging, putting consumers at risk of ingestion. There is little information on the amount of ZnO nanoparticles (NP) present in food packaging and the effects of ZnO NP ingestion on intestinal function. To estimate physiologically relevant ZnO NP exposures from food that are commonly packaged with ZnO NP, food samples were analyzed with inductively coupled plasma mass spectrometry (ICP-MS). An in vitro model of the small intestine was used to investigate the effects of ZnO NP exposure. Cells were exposed to pristine NP in culture medium and to NP subjected to an in vitro digestion process to better reflect the transformation that the NP undergo in the human gastrointestinal (GI) tract. The findings show that a physiologically relevant dose of ZnO NP can cause a significant decrease in glucose transport, which is consistent with gene expression changes for the basolateral glucose transporter GLUT2. There is also evidence that the ZnO NP affect the microvilli of the intestinal cells, therefore reducing the amount of surface area available to absorb nutrients. These results suggest that the ingestion of ZnO NP can alter nutrient absorption in an in vitro model of the human small intestine.

Retraction: ZnO nanoparticles affect intestinal function in an in vitro model.

Retraction of 'ZnO nanoparticles affect intestinal function in an in vitro model' by Fabiola Moreno-Olivas et al., Food Funct., 2018, 9, 1475-1491.

ZnO nanoparticles affect intestinal function in an in vitro model.

Zinc oxide nanoparticles (ZnO NP) may be present in food packaging, which would put consumers at risk of NP ingestion. There is little information on the amount of ZnO NP that are present in food packaging and the effects of ZnO exposure on intestinal function. To estimate physiologically relevant ZnO exposures, foods that are naturally low in zinc (Zn), but are commonly packaged with ZnO NP, such as tuna, corn, and asparagus, were analyzed with inductively coupled plasma mass spectrometry (ICP-MS). It was found that the Zn present in a serving of these foods is approximately one hundred times higher than the recommended dietary allowance. An in vitro model of the small intestine composed of Caco-2 and HT29-MTX cells was used to investigate the effects of ZnO NP exposure. Cells were exposed to physiologically realistic doses of pristine NP in culture medium and to NP subjected to an in vitro digestion to better reflect the transformation that the NP may undergo once they enter the human GI tract. Uptake and/or transport of iron (Fe), Zn, glucose, and fatty acids were assessed and intestinal alkaline phosphatase (IAP) levels were measured before and after NP exposure. The findings show that there is a 75% decrease in Fe transport and a 30% decrease in glucose transport following ZnO NP exposure. These decreases were consistent with gene expression changes for their transporters. There is also evidence that the ZnO NP affect the microvilli of the intestinal cells, therefore reducing the amount of surface area available to absorb nutrients. These results suggest that the ingestion of physiologically relevant doses of ZnO NP can alter intestinal function in an in vitro model of the human small intestine.

Titanium Dioxide Nanoparticle Ingestion Alters Nutrient Absorption in an In Vitro Model of the Small Intestine.

Ingestion of titanium dioxide (TiO2) nanoparticles from products such as agricultural chemicals, processed food, and nutritional supplements is nearly unavoidable. The gastrointestinal tract serves as a critical interface between the body and the external environment, and is the site of essential nutrient absorption. The goal of this study was to examine the effects of ingesting the 30 nm TiO2 nanoparticles with an in vitro cell culture model of the small intestinal epithelium, and to determine how acute or chronic exposure to nano-TiO2 influences intestinal barrier function, reactive oxygen species generation, proinflammatory signaling, nutrient absorption (iron, zinc, fatty acids), and brush border membrane enzyme function (intestinal alkaline phosphatase). A Caco-2/HT29-MTX cell culture model was exposed to physiologically relevant doses of TiO2 nanoparticles for acute (four hours) or chronic (five days) time periods. Exposure to TiO2 nanoparticles significantly decreased intestinal barrier function following chronic exposure. Reactive oxygen species (ROS) generation, proinflammatory signaling, and intestinal alkaline phosphatase activity all showed increases in response to nano-TiO2. Iron, zinc, and fatty acid transport were significantly decreased following exposure to TiO2 nanoparticles. This is because nanoparticle exposure induced a decrease in absorptive microvilli in the intestinal epithelial cells. Nutrient transporter protein gene expression was also altered, suggesting that cells are working to regulate the transport mechanisms disturbed by nanoparticle ingestion. Overall, these results show that intestinal epithelial cells are affected at a functional level by physiologically relevant exposure to nanoparticles commonly ingested from food.