Reduced dietary Ca, Cu, Zn, Mn, and Mg bioavailability but increased Fe bioavailability with polyethylene microplastic ingestion in a mouse model: Changes in intestinal permeability and gut metabolites

Abstract

Microplastics emerge as a new environmental and human health crisis. Minimal research exists on effects of microplastic ingestion on the oral bioavailability of minerals (Fe, Ca, Cu, Zn, Mn, and Mg) in the gastrointestinal tract via impacting intestinal permeability, mineral transcellular transporters, and gut metabolites. Here, mice were exposed to polyethylene spheres of 30 and 200 μm (PE-30 and PE-200) in diet (2, 20, and 200 μg PE g−1) for 35 d to determine the microplastic effects on mineral oral bioavailability. Results showed that for mice fed diet amended with PE-30 and PE-200 at 2–200 μg g−1, Ca, Cu, Zn, Mn, and Mg concentrations in the small intestine tissue were 43.3–68.8 %, 28.6–52.4 %, 19.3–27.1 %, 12.9–29.9 %, and 10.2–22.4 % lower compared to control mice, suggesting hampered bioavailability of these minerals. In addition, Ca and Mg concentrations in mouse femur were 10.6 % and 11.0 % lower with PE-200 at 200 μg g−1. In contrast, Fe bioavailability was elevated, as suggested by significantly (p < 0.05) higher Fe concentration in the intestine tissue of mice exposed to PE-200 than control mice (157–180 vs. 115 ± 7.58 μg Fe g−1) and significantly (p < 0.05) higher Fe concentrations in liver and kidney with PE-30 and PE-200 at 200 μg g−1. Following PE-200 exposure at 200 μg g−1, genes coding for duodenal expression of tight junction proteins (e.g., claudin 4, occludin, zona occludins 1, and cingulin) were significantly up-regulated, possibility weakening intestinal permeability to Ca, Cu, Zn, Mn, and Mg ions. The elevated Fe bioavailability was possibly related to microplastic-induced greater abundances of small peptides in the intestinal tract, which inhibited Fe precipitation and elevated Fe solubility. Results showed that microplastic ingestion may cause Ca, Cu, Zn, Mn, and Mg deficiency but Fe overload via altering intestinal permeability and gut metabolites, posing a threat to human nutrition health.