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Redox Biology two (2014) 739Contents lists obtainable at ScienceDirectRedox Biologyjournal homepage: elsevier.com/locate/redoxResearch PaperDifferent style of enzyme-triggered CO-releasing molecules (ET-CORMs) reveals quantitative differences in biological activities with regards to toxicity and inflammationE. Stamellou a,b,1,n, D. Storz b,1, S. Botov c, E. Ntasis b, J. Wedel b, S. Sollazzo c, B.K. Kr er b, W. van Son d, M. Seelen d, H.G. Schmalz c, A. Schmidt c, M. Hafner a, B.A. Yard baInstitute for Molecular and Cellular Biology, Mannheim University of Applied Sciences, Mannheim, Germany Vth. Health-related Department, Healthcare Faculty Mannheim, Ruprecht Karls University, Heidelberg Mannheim, Germany Department of Chemistry, University of Cologne, Cologne, Germany d Division of Nephrology, Academic Health-related Center, Groningen, The Netherlandsb cart ic l e i nf oArticle history: Received 7 May 2014 Received in revised type 29 May well 2014 Accepted 2 June 2014 Out there online 5 June 2014 Key phrases: Endothelial cells Carbon monoxide Adhesion molecules Enzyme-triggered CORMsa b s t r a c tAcyloxydiene e(CO)three complexes can act as enzyme-triggered CO-releasing molecules (ET-CORMs). Their biological activity strongly will depend on the mother compound from which they’re derived, i.e. cyclohexenone or cyclohexanedione, and on the position of the ester functionality they harbour. The present study addresses if the latter characteristic affects CO release, if cytotoxicity of ET-CORMs is mediated by means of iron release or inhibition of cell respiration and to what extent cyclohexenone and cyclohexanedione derived ET-CORMs differ in their capability to counteract TNF- mediated inflammation. Irrespective of your formulation (DMSO or cyclodextrin), toxicity in HUVEC was PAK6 Purity & Documentation drastically larger for ET-CORMs bearing the ester functionality at the outer (rac-4), as in comparison to the inner (rac-1) position on the cyclohexenone moiety. This was paralleled by an increased CO release from the former ET-CORM. Toxicity was not mediated by way of iron as EC50 values for rac-4 have been drastically decrease than for FeCl2 or FeCl3 and have been not influenced by iron chelation. ATP depletion preceded toxicity suggesting impaired cell respiration as putative trigger for cell death. In long-term HUVEC cultures inhibition of VCAM-1 expression by rac-1 waned in time, although for the cyclohexanedione derived rac-8 inhibition seems to increase. NFB was inhibited by each rac-1 and rac-8 independent of IB degradation. Each ET-CORMs activated Nrf-2 and consequently induced the expression of HO-1. This study further supplies a rational framework for designing acyloxydiene e(CO)three complexes as ET-CORMs with differential CO release and biological activities. We also provide a improved understanding of how these complexes have an effect on cell-biology in mechanistic terms. 2014 The Authors. Published by Elsevier B.V. That is an open access post below the CC BY-NC-ND licens.