The Impact of Zinc on Manganese Bioavailability and Cytotoxicity in HepG2 Cells

Author:

Michaelis Vivien1,Kasper Silja1,Naperkowski Lisa1,Pusse Jan1,Thiel Alicia1,Ebert Franziska2,Aschner Michael3,Schwerdtle Tanja245ORCID,Haase Hajo46,Bornhorst Julia14ORCID

Affiliation:

1. Food Chemistry Faculty of Mathematics and Natural Sciences University of Wuppertal Gaußstraße 20 42119 Wuppertal Germany

2. Department of Food Chemistry Institute of Nutritional Science University of Potsdam Arthur‐Scheunert‐Allee 114‐116 14558 Nuthetal Germany

3. Department of Molecular Pharmacology, Neuroscience, and Pediatrics Albert Einstein College of Medicine 1300 Morris Park Avenue Bronx NY 10461 USA

4. TraceAge‐DFG Research Unit on Interactions of Essential Trace Elements in Healthy and Diseased Elderly (FOR 2558) Berlin‐Potsdam‐Jena‐Wuppertal 14558 Nuthetal Germany

5. German Federal Institute for Risk Assessment (BfR) Max‐Dohrn‐Straße 8‐10 10589 Berlin Germany

6. Department of Food Chemistry and Toxicology Berlin Institute of Technology Gustav‐Meyer‐Allee 25 13355 Berlin Germany

Abstract

ScopeDespite their essentiality, several studies have shown that either manganese (Mn) or zinc (Zn) overexposure may lead to detrimental health effects. Although Mn is transported by some of the SLC family transporters that translocate Zn, the role of Zn in hepatocellular Mn transport and Mn‐induced toxicity have yet to be fully characterized.Methods and ResultsThe human hepatoma cell line, HepG2, is utilized. Total cellular Mn and Zn amounts are determined after cells are treated with Zn 2 or 24 h prior to Mn incubation for additional 24 h with inductively coupled plasma‐based spectrometry and labile Zn is assessed with the fluorescent probe FluoZin‐3. Furthermore, mRNA expression of genes involved in metal homeostasis, and mechanistic endpoints associated with Mn‐induced cytotoxicity are addressed. These results suggest that Zn protects against Mn‐induced cytotoxicity and impacts Mn bioavailability to a great extent when cells are preincubated with higher Zn concentrations for longer duration as characterized by decreased activation of caspase‐3 as well as lactate dehydrogenase (LDH) release.ConclusionsZn protects against Mn‐induced cytotoxicity in HepG2 cells possibly due to decreased Mn bioavailability. Additionally, mRNA expression of metal homeostasis‐related genes indicates possible underlying pathways that should to be addressed in future studies.

Publisher

Wiley

Subject

Food Science,Biotechnology

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