Virtual issue by COST Action BM1203 (EU-ROS) “Emerging concepts in redox biology and oxidative stress”

The article by Bacic et al. [1] (link to http://dx.doi.org/10.1016/j. redox.2015.10.007) provides an overview on the application of magnetic resonance imaging (MRI) and electron paramagnetic resonance (EPR) spectroscopy of stable nitroxide radicals to monitor metabolically induced changes in the redox status of organs. These techniques will not only contribute to the mechanistic understanding of oxidative stress-associated pathological states but also provide a basis for studying the effectiveness of interventions aimed to modulate oxidative stress (redox medicine approaches). The authors introduce the different MRI and EPR methods that are currently available and describe a broad spectrum of nitroxide-based spin traps and spin probes with emphasis on pharmacokinetic properties. In the second part of the review, the authors provide examples for the application of these techniques to study changes in the redox status in different tissues (e.g. skin, brain, tumors) upon induction of disease states (e.g. sepsis, ischemia/reperfusion, iron overload). With their conclusions, the authors provide an outlook on future technical needs and development of new probes with increased stability towards reduction, enhanced sensitivity to oxidative stress, or increased delivery into cells and through the blood–brain barrier as well as specificity towards certain ROS species or specificity towards certain pathologies such as tumors. The review by Dunn et al. [2] (link to http://dx.doi.org/10.1016/ j.redox.2015.09.005) discusses different pathways of bacteriallyinduced mtROS formation and its role for activation of the NLRP3 inflammasome via direct redox modifications of the NLRP3 components as well as redox-sensitive indirect pathways such as Nrf2/ HO-1, NFκB/iNOS and TXNIP/mtDAMP interaction with the NLRP3 inflammasome leading to the formation of the pro-inflammatory cytokine IL-1β. Mitochondrial damage-associated molecular patterns (mtDAMPs) include the participation of mtDNA and/or cardiolipin that are released or surfaced by dysfunctional mitochondria. This also results in decreased activity of NADþ-dependent deacetylases Sirt1 and Sirt2 that normally inhibit NFκB and NLRP3 activation. ROS in general also contribute to extracellular trap formation originating from nuclear or mitochondrial DNA. The review by Espinosa-Diez et al. [3] (link to http://dx.doi.org/ 10.1016/j.redox.2015.07.008) highlights the adaptive cellular antioxidant responses to oxidative stress. In the first part, the role and function of classical thiol-based antioxidant proteins such as GCL, Grx, GPx, Prx, Trx, GST, GR and TrxR are discussed. In addition, the antioxidant gene response is discussed with the classical examples