N-Acetylcysteine as modulator of the essential trace elements copper and zinc

GND
1222559188
Affiliation
Department of Molecular Nutritional Physiology, Institute of Nutritional Sciences, Friedrich Schiller University Jena, 07743 Jena, Germany, theresa.wolfram@uni-jena.de
Wolfram, Theresa;
GND
1206120428
ORCID
0000-0002-0405-6795
Affiliation
Department of Molecular Nutritional Physiology, Institute of Nutritional Sciences, Friedrich Schiller University Jena, 07743 Jena, Germany, schwarz.maria@uni-jena.de
Schwarz, Maria;
GND
1222560119
Affiliation
Department of Molecular Nutritional Physiology, Institute of Nutritional Sciences, Friedrich Schiller University Jena, 07743 Jena, Germany, michaelareuss@yahoo.de
Reuß, Michaela;
GND
1206122390
ORCID
0000-0002-9978-3871
Affiliation
Department of Molecular Nutritional Physiology, Institute of Nutritional Sciences, Friedrich Schiller University Jena, 07743 Jena, Germany, kristina.lossow@uni-jena.de
Lossow, Kristina;
GND
1064282156
ORCID
0000-0002-1811-2049
Affiliation
German Institute of Human Nutrition, 14558 Nuthetal, Germany, mario.ost@dife.de
Ost, Mario;
Affiliation
German Institute of Human Nutrition, 14558 Nuthetal, Germany, klaus@dife.de
Klaus, Susanne;
GND
128451335
ORCID
0000-0002-4873-7488
Affiliation
TraceAge-DFG Research Unit on Interactions of Essential Trace Elements in Healthy and Diseased Elderly, D-13353 Potsdam-Berlin-Jena-Wuppertal, Germany, tanja.schwerdtle@uni-potsdam.de
Schwerdtle, Tanja;
GND
13840044X
ORCID
0000-0002-3307-1038
Affiliation
Department of Molecular Nutritional Physiology, Institute of Nutritional Sciences, Friedrich Schiller University Jena, 07743 Jena, Germany, anna.kipp@uni-jena.de
Kipp, Anna P.

N-acetylcysteine (NAC) is a frequently prescribed drug and known for its metal chelating capability. However, to date it is not well characterized whether NAC intake affects the homeostasis of essential trace elements. As a precursor of glutathione (GSH), NAC also has the potential to modulate the cellular redox homeostasis. Thus, we aimed to analyze effects of acute and chronic NAC treatment on the homeostasis of copper (Cu) and zinc (Zn) and on the activity of the redox-sensitive transcription factor Nrf2. Cells were exposed to 1 mM NAC and were co-treated with 50 µM Cu or Zn. We showed that NAC treatment reduced the cellular concentration of Zn and Cu. In addition, NAC inhibited the Zn-induced Nrf2 activation and limited the concomitant upregulation of cellular GSH concentrations. In contrast, mice chronically received NAC via drinking water (1 g NAC/100 mL). Cu and Zn concentrations were decreased in liver and spleen. In the duodenum, NQO1, TXNRD, and SOD activities were upregulated by NAC. All of them can be induced by Nrf2, thus indicating a putative Nrf2 activation. Overall, NAC modulates the homeostasis of Cu and Zn both in vitro and in vivo and accordingly affects the cellular redox balance.

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