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Article

N-Acetylcysteine as Modulator of the Essential Trace Elements Copper and Zinc

1
Department of Molecular Nutritional Physiology, Institute of Nutritional Sciences, Friedrich Schiller University Jena, 07743 Jena, Germany
2
TraceAge-DFG Research Unit on Interactions of Essential Trace Elements in Healthy and Diseased Elderly, D-13353 Potsdam-Berlin-Jena-Wuppertal, Germany
3
German Institute of Human Nutrition, 14558 Nuthetal, Germany
4
Department of Food Chemistry, Institute of Nutritional Science, University of Potsdam, 14558 Nuthetal, Germany
5
German Federal Institute for Risk Assessment (BfR), 10589 Berlin, Germany
*
Author to whom correspondence should be addressed.
Authors contributed equally.
Antioxidants 2020, 9(11), 1117; https://doi.org/10.3390/antiox9111117
Received: 5 October 2020 / Revised: 7 November 2020 / Accepted: 11 November 2020 / Published: 12 November 2020
(This article belongs to the Special Issue Cellular Redox Homeostasis)
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. View Full-Text
Keywords: N-acetylcysteine; copper; zinc; glutathione; Nrf2 N-acetylcysteine; copper; zinc; glutathione; Nrf2
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MDPI and ACS Style

Wolfram, T.; Schwarz, M.; Reuß, M.; Lossow, K.; Ost, M.; Klaus, S.; Schwerdtle, T.; Kipp, A.P. N-Acetylcysteine as Modulator of the Essential Trace Elements Copper and Zinc. Antioxidants 2020, 9, 1117. https://doi.org/10.3390/antiox9111117

AMA Style

Wolfram T, Schwarz M, Reuß M, Lossow K, Ost M, Klaus S, Schwerdtle T, Kipp AP. N-Acetylcysteine as Modulator of the Essential Trace Elements Copper and Zinc. Antioxidants. 2020; 9(11):1117. https://doi.org/10.3390/antiox9111117

Chicago/Turabian Style

Wolfram, Theresa, Maria Schwarz, Michaela Reuß, Kristina Lossow, Mario Ost, Susanne Klaus, Tanja Schwerdtle, and Anna P. Kipp. 2020. "N-Acetylcysteine as Modulator of the Essential Trace Elements Copper and Zinc" Antioxidants 9, no. 11: 1117. https://doi.org/10.3390/antiox9111117

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