TY  - JOUR
A1  - Baesler, Jessica
A1  - Kopp, Johannes Florian
A1  - Pohl, Gabriele
A1  - Aschner, Michael
A1  - Haase, Hajo
A1  - Schwerdtle, Tanja
A1  - Bornhorst, Julia
T1  - Zn homeostasis in genetic models of Parkinson’s disease in Caenorhabditis elegans
JF  - Journal of Trace Elements in Medicine and Biology
N2  - While the underlying mechanisms of Parkinson’s disease (PD) are still insufficiently studied, a complex interaction between genetic and environmental factors is emphasized. Nevertheless, the role of the essential trace element zinc (Zn) in this regard remains controversial. In this study we altered Zn balance within PD models of the versatile model organism Caenorhabditis elegans (C. elegans) in order to examine whether a genetic predisposition in selected genes with relevance for PD affects Zn homeostasis. Protein-bound and labile Zn species act in various areas, such as enzymatic catalysis, protein stabilization pathways and cell signaling. Therefore, total Zn and labile Zn were quantitatively determined in living nematodes as individual biomarkers of Zn uptake and bioavailability with inductively coupled plasma tandem mass spectrometry (ICP-MS/MS) or a multi-well method using the fluorescent probe ZinPyr-1. Young and middle-aged deletion mutants of catp-6 and pdr-1, which are orthologues of mammalian ATP13A2 (PARK9) and parkin (PARK2), showed altered Zn homeostasis following Zn exposure compared to wildtype worms. Furthermore, age-specific differences in Zn uptake were observed in wildtype worms for total as well as labile Zn species. These data emphasize the importance of differentiation between Zn species as meaningful biomarkers of Zn uptake as well as the need for further studies investigating the role of dysregulated Zn homeostasis in the etiology of PD.
KW  - Caenorhabditis elegans
KW  - Zinc
KW  - Zinc homeostasis
KW  - Parkinson disease
KW  - Labile zinc
Y1  - 2019
U6  - https://doi.org/10.1016/j.jtemb.2019.05.005
VL  - 55
SP  - 44
EP  - 49
PB  - Elsevier
CY  - München
ER  - 
TY  - JOUR
A1  - Baesler, Jessica
A1  - Kopp, Johannes F.
A1  - Pohl, Gabriele
A1  - Aschner, Michael
A1  - Haase, Hajo
A1  - Schwerdtle, Tanja
A1  - Bornhorst, Julia
T1  - Zn homeostasis in genetic models of Parkinson’s disease in Caenorhabditis elegans
JF  - Journal of trace elements in medicine and biology
KW  - Caenorhabditis elegans
KW  - Zinc
KW  - Zinc homeostasis
KW  - Parkinson disease
KW  - Labile zinc
Y1  - 2019
U6  - https://doi.org/10.1016/j.jtemb.2019.05.005
SN  - 0946-672X
VL  - 55
SP  - 44
EP  - 49
PB  - Elsevier GMBH
CY  - München
ER  - 
TY  - JOUR
A1  - Rosenkranz, Eva
A1  - Maywald, Martina
A1  - Hilgers, Ralf-Dieter
A1  - Brieger, Anne
A1  - Clarner, Tim
A1  - Kipp, Markus
A1  - Pluemaekers, Birgit
A1  - Meyer, Sören
A1  - Schwerdtle, Tanja
A1  - Rink, Lothar
T1  - Induction of regulatory T cells in Th1-/Th17-driven experimental autoimmune encephalomyelitis by zinc administration
JF  - The journal of nutritional biochemistry
N2  - The essential trace element zinc is indispensable for proper immune function as zinc deficiency accompanies immune defects and dysregulations like allergies, autoimmunity and an increased presence of transplant rejection. This point to the importance of the physiological and dietary control of zinc levels for a functioning immune system. This study investigates the capacity of zinc to induce immune tolerance. The beneficial impact of physiological zinc supplementation of 6 mu g/day (0.3 mg/kg body weight) or 30 mu g/day (1.5 mg/kg body weight) on murine experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis with a Th1/Th17 (Th, T helper) cell-dominated immunopathogenesis, was analyzed. Zinc administration diminished EAE scores in C57BL/6 mice in vivo (P<.05), reduced Th17 ROR gamma T+ cells (P<.05) and significantly increased inducible iTreg cells (P<.05). While Th17 cells decreased systemically, iTreg cells accumulated in the central nervous system. Cumulatively, zinc supplementation seems to be capable to induce tolerance in unwanted immune reactions by increasing iTreg cells. This makes zinc a promising future tool for treating autoimmune diseases without suppressing the immune system. (C) 2015 Elsevier Inc. All rights reserved.
KW  - Zinc
KW  - Regulatory T cells (Treg)
KW  - Foxp3
KW  - Mixed lymphocyte culture (MLC)
KW  - Experimental autoimmune encephalomyelitis (EAE)
KW  - Th17
Y1  - 2016
U6  - https://doi.org/10.1016/j.jnutbio.2015.11.010
SN  - 0955-2863
SN  - 1873-4847
VL  - 29
SP  - 116
EP  - 123
PB  - Elsevier
CY  - New York
ER  -