Arsenic bioaccessibility upon gastrointestinal digestion is highly determined by its speciation and lipid-bile salt interactions.

The release of arsenic (As) from a contaminated food matrix during gastrointestinal digestion, i.e., its bioaccessibility, is an important estimator of its bioavailability, and therefore also its health risk.

An investigation of the effect of gastrointestinal microbial activity on oral arsenic bioavailability.

In vitro gastrointestinal (GI) microbial activity in the colon compartment facilitates the arsenic release from soils into simulated GI fluids. Consequentially, it is possible that in vitro models that neglect to include microbial activity underestimate arsenic bioaccessibility when calculating oral exposure. However, the toxicological relevance of increased arsenic release due to microbial activity is contingent upon the subsequent absorption of arsenic solubilized in the GI lumen.

Biovolatilization of metal(loid)s by intestinal microorganisms in the simulator of the human intestinal microbial ecosystem.

Methylation and hydrogenation of metal(loid)s by microorganisms are widespread and well-known processes in the environment by which mobility and in most cases toxicity are significantly enhanced in comparison to inorganic species. The human gut contains highly diverse and active microbiocenosis, yet little is known about the occurrence and importance of microbial metal(loid) methylation and hydrogenation. In this study, an in vitro gastrointestinal model, the Simulator of the Human Intestinal Microbial Ecosystem (SHIME),was used for investigating volatilization of metal(loid)s by intestinal microbiota.

Gastrointestinal microbes increase arsenic bioaccessibility of ingested mine tailings using the simulator of the human intestinal microbial ecosystem.

It is widely accepted that the use of total metal concentrations in soil overestimates metal risk from human ingestion of contaminated soils. In vitro simulators have been used to estimate the fraction of arsenic present in soil that is bioaccessible in the human digestive track. These approaches assume that the bioaccessible fraction remains constant across soil total metal concentrations and that intestinal microbiota do not contribute to arsenic release.

Comparison of five in vitro digestion models to in vivo experimental results: lead bioaccessibility in the human gastrointestinal tract.

This paper presents a multi-laboratory comparison study of in vitro models assessing bioaccessibility of soil-bound lead in the human gastrointestinal tract under simulated fasted and fed conditions. Oral bioavailability data from a previous human in vivo study on the same soil served as a reference point. In general, the bioaccessible lead fraction was significantly (P<0.

Polycyclic aromatic hydrocarbon release from a soil matrix in the in vitro gastrointestinal tract.

Soil ingestion is an important exposure route by which immobile soil contaminants enter the human body. We assessed polycyclic aromatic hydrocarbon (PAH) release from a contaminated soil, containing 49 mg PAH kg(-1), using a SHIME (Simulator of the Human Intestinal Microbial Ecosystem) reactor comprising the stomach, duodenal, and colon compartments. Polycyclic aromatic hydrocarbon release was defined as that fraction remaining in the digest supernatant after centrifugation for 5 min at 1500 x g.

Liquid chromatography-mass spectrometry analysis of hydroxylated polycyclic aromatic hydrocarbons, formed in a simulator of the human gastrointestinal tract.

Described is a liquid chromatography-mass spectrometry (LC-MS) procedure for the determination of hydroxylated biotransformation products of polycyclic aromatic hydrocarbons (PAH) in the human gastrointestinal tract. The formation of hydroxylated PAHs was monitored upon incubation of PAHs with colon microbiota from the Simulator of the Human Intestinal Microbial Ecosystem (SHIME). The analytical method consisted of a biomass removal step followed by a solid phase extraction (SPE) step using C18 packed columns to remove non-digested food compounds and microbial metabolites that interfere with the detection of the target compounds.