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. 2020 Feb 10;10:2287. doi: 10.1038/s41598-020-58871-1

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Proposed mechanism of the differential action of nandrolone on normal/cancer stem and differentiated cells. The hypothesis is put forward that by inhibiting the mitochondrial respiratory chain CxIII, nandrolone induces a pro-oxidative setting (red arrowed lines) that depending on the cellular antioxidant supply (green arrowed lines) establishes a differential redox signalling. A low increase of reactive oxidant species would favour self-renewal/quiescence of normal or cancer stem cells and possibly retro-differentiation of early progenitors, all equipped with a robust antioxidant armoury. Conversely, a higher pro-oxidative state, such that caused by nandrolone in late progenitor or differentiated cells will induce cell cycle arrest and possibly cell death. See Discussion for further details.