Online ISSN:
3042-1772
Volume 1 , Issue 1, (2024)
Published:
29.08.2024.
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Issue 1 - 2024
Published: 29.08.2024.
Authors in this issue:
Abdelhameed Mohamed, Abhipsita De, Adam Sikora, Adrianna Skoneczna, Agnes Tessier, Albrecht Stroh, Aleksandra Andreyeva, Aleksandra Drašković, Aleksandra Korać, Aleksandra Yu Andreyeva, Aleksandra Cvoro, Aleksandra Jankovic, Aleksandra Korac, Aleksandra Ristić Fira, Aleksandra Stanković, Alena Pecinová, Alessandra Pecorelli, Alex Lyakhovich, Ana Popović Bijelić, Ana Ružanović, Ana Vesković, Ana Djordjevic, Ana Kijanović, Ana Ledo, Ana Ninić, Ana Penezic, Ana Teofilovic, Anastasia A Tkachuk, Anastasia Ioanna Papantonaki, Anastasiya Volkova, Andrea Vallese, Andrea Pozzer, Andreas Daiber, Andreas Vitsos, Aneta Wiesyk, Anna Giorak, Anna Guiotto, Anna V Goropashnaya, Anne-Françoise Rousseau, Anthony L. Moore, Arijan Valar, Arvand Haschemi, Azra Guzonjić, Barbara Ostanek, Bárbara S. Rocha, Barry Halliwell, Bato Korac, Bengu Cetinkaya, Biljana Srdić Galić, Biljana Srdic-Galic, Blanca Romero-Llopis, Blandine Poulet, Bojan Labachevski, Branislav Milovanović, Branka R Gavrilović, Bruna Rafaela Pereira Resende, Can Tunçay, Cândida Dias, Carlo Cervellati, Carlo Viscomi, Caroline Le Goff, Cátia F. Lourenço, Cátia Lourenço, Cemile Uslu, Chiranjit Panja, Christina Barda, Christopher Kremslehner, Dalila Laoudj-Chevinesse, Daniel C Moreira, Daniela Ardalic, Daniela Caporossi, Danijela Vojnovic Milutinovic, Danilo Cetic, Darko Davitkov, David Nußbaum, Dejan Stevanovic, Diana Mikhailova, Dimitra Ieronymaki, Dimitrios Katsiris, Dimitrios Vlachodimitropoulos, Dirk Cleppien, Dominika Mihalikova, Dragana Jovanović, Dragana Robajac, Dragica Zendelovska, Eda Kapan, Ekaterina S. Kladchenko, Elina S Chelebieva, Elisabeth Ponweiser, Elizabeth Hood, Emilija Atanasovska, Ena Šimunić, Erdi Sozen, Erika Fernandez-Vizarra, Etienne Cavalier, Etna Abad, Evica Dincić, Federico V Pallardó, Filip Janjić, Florian Gruber, Francesca Marcato, Francesco Galli, Fulvio Ursini, Gaelle Gendronneau, Georgios Gkikas, Georgios Parthymos, Giada Petringa, Giuseppe Valacchi, Giuseppe Poli, Goran Miljus, Guilherme Horta, Guillermo Puertas-Frias, Hagar Fadda, Hamada Elwan, Hansjörg Habisch, Hemdan Mahmoud, Henning Ubbens, Homer Black, Igor Mindukshev, Igor Golic, Iñigo Yoldi Bergua, Ioannis Sfiniadakis, Ionela Mariana Nagelreiter, Irina Iskortseva, Isidora Protic, Iva I. Podgorski, Iva Perović-Blagojević, Ivan Spasojević, Ivan Petrović, Ivana Simić, Ivana Kuntić, Jacek Zielonka, Janja Marc, Jaroslaw Ciesla, Jean-Olivier Defraigne, Jean-Paul Cheramy-Bien, Jelena Kotur Stevuljević, Jelena Kotur-Stevuljević, Jelena Francuski Andrić, Jelena Jevtic, Jelena P Gavrić, Jiayin Zheng, Jiří Neužil, João Gonçalves, João Laranjinha, Joël Pincemai, Johanne Anastassopoulou, Jonathan Maury, Jos Lelieveld, Joussef Hayek, Jovana Stevanovic, Jovana Kuveljić, Juan Sastre, Kelly L Drew, Kristina Spariosu, Kristýna Čunátová, Ksenija Vujacic-Mirski, Larin Deeb, Lazar Karić, Lea Strohm, Leonardo Nardi, Ljupka Gligorovska, Lorena Baquero, Lucija Dončević, Lukáš Alán, Maja Ajduković, Maja Bosković, Maja Vukobratovic, Maja Živković, Marek Vrbacký, María José Saucedo-Rodríguez, Maria Giakoumaki, Maria Kyriazi, Maria S Podolskaya, Maria Teresa Bayo Jimenez, Marie Vanišová, Marie Sophie Narzt, Marija Vasić, Marija Aleksic, Marija D. Milošević, Marija Petrushevska, Marija Popova-Labachevska, Marija Takić, Marijana Popović Hadžija, Marin Kuntić, Marko D Prokić, Marko Mirč, Marta Kaloper, Marta Roldán-Lázaro, Marta Sipko, Martina Marchetti-Deschmann, Masanta Suchismita, Matea Juric, Matthias Kohl, Matthias Oelze, Micael Hardy, Michael Schmeißer, Michaela Sochorová, Michail Christou Rallis, Michelangelo Mancuso, Milena Dimitrijević, Milena Cvijanović, Milena Radaković, Milica Mandic, Milica Kovačević Filipović, Milica Mamić, Milos Sunderic, Miloš Đorđević, Miloš Mitrović, Milos Vrataric, Minja Derikonjić, Mirjana Udicki, Miron Sopić, Mladen Paradžik, Mohamed Mohany, Natalija Samardzić, Nataša Tomašević Kolarov, Natasa Velickovic, Natasa Z Djordjevic, Natzi Sakalihasan, Nejla H Zupic, Nesrin Kartal Ozer, Nevena Đukić, Niki Chondrogianni, Ninoslav Mitic, Ognjen Radojicic, Olga L Gostyukhina, Olgica Nedic, Omar Hahad, Ondrej Kuda, Otilija Keta, Pablo Cirrone, Panagoula Pavlou, Petr Pecina, Phaedra Winstanley-Zarach, Pilar González-Cabo, Radmila Ristić, Raffaele Cerutti, Raheema Hassan Khan, Ratko Tomašević, Rita Noverques, Robert Belužić, Roman Maslanka, Ron Kohen, Roza Kucharczyk, Salim S. Al-Rejaie, Samuele Zoratto, Sandra Sobočanec, Sanja Erceg, Sanja Kovacevic, Sanja Milenkovic, Sanja Stojanovic, Sara Stojanovic, Sebastian Steven, Shaaban S. Elnesr, Slavica Ranković, Snežana Kovačević, Sophie Christelbach, Steffen Daub, Stephan Sudowe, Stevo Najman, Strahinja Đurić, Strahinja Djuric, Sven Danckwardt, Svetlana G Despotović, Sylwia Pilch, Tamara G Petrović, Tamara Lapeña, Tamara Zakic, Tanja Vukov, Tarun Pant, Tatiana B Sigacheva, Tatjana Ivković Kapicl, Tawfeeq Shekh-Ahmad, Thomas Berkemeier, Thomas Münzel, Tihomir Balog, Tijana B Radovanović, Tijana Vučić, Tobias Madl, Tomáš Mráček, Tomáš Čajka, Tristan Junglas, Tugce Demirel-Yalciner, Tuguldur Enkhbaatar, Ufuk Ersoy, Vadim B Fedorov, Valeria Cordone, Valeria Balmaceda, Vanja Pekovic-Vaughan, Vesna Ćeriman Krstić, Vesna Mandic Markovic, Vladana Petković, Vsevolod Belousov, Willem H Koppenol, Yara Shqair, Zana C Dolicanin, Zeljko Mikovic, Zeynep Ülker, Zorana Dobrijevic, Zorana Milosavljević, Zorka Drvendžija,
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Volume 1, Issue 1, 2024
- All Sections
- Opening lecture
- Plenary lectures
- Keynote lectures
- Selected oral presentations
- Short oral presentations
29.08.2024.
Professional paper
NITRIC OXIDE, SUPEROXIDE AND PEROXYNITRITE – REDOX REGULATION OF THE CARDIOVASCULAR SYSTEM BY NITRO-OXIDATIVE STRESS AND S-NITROS(YL)ATION
Oxidative stress is characterized by an excessive and prolonged formation of oxidants, causing an accumulating load of irreversible oxidative modifications of proteins, lipids, and nucleic acids that compromise cell integrity. This competes with the concept of redox regulation, combining the regulatory influence of nitric oxide (•NO), superoxide (O2•―), and their derivatives on redox-sensitive signaling pathways in the cell. The transition from redox regulation to oxidative stress is not only determined by the absolute amount of oxidants formed, but also by the respective intracellular site of formation, by the capacity of the defense machinery of the respective cell type, and by the ratio between •NO and O2•― that determines the nature of secondary radical species formed. Equimolar and concomitant fluxes of •NO and O2•―, for instance, favor the formation of the oxidant peroxynitrite making O2•― an antagonist of •NO as well as an inhibitor of prostacyclin synthesis, while an excess of •NO over O2•― supports the formation of nitrosating species. Secondary •NO-derived species hence not only define cellular targets affected but also the nature of posttranslational modifications. A profound knowledge of redox regulation and the conditions supporting its fluent transition into oxidative stress is hence of outermost importance in molecular cardiovascular medicine. The present overview therefore aims to determine the spectrum of •NO-derived reactive species and the cellular conditions characteristic for reversible modifications and their modulation of cellular targets in redox regulation. The second objective is to define preconditions in cardiovascular cells culminating in an expenditure of the cellular antioxidant system and an accumulation of irreversible modifications that compromise cellular functions to a point of no return.
Andreas Daiber
29.08.2024.
Professional paper
OXYGEN, SULFUR, SELENIUM AND LIPID PEROXIDATION: HOW GPx4 CONTROLS LIFE AND DEATH
The selenoperoxidase GPx4, discovered in 1982, plays a pivotal role in preventing ferroptosis. In a moonlighting function, GPx4, in its mitochondrial and nuclear forms, also contributes to spermatogenesis. The critical advantage of Selenium vs. Sulfur catalysis is the stability of the oxidized form of the chalcogen in the catalytic cycle. While the mechanisms of catalytic cycle are understood, its regulation remains largely unknown. Existing evidence supports the notion that ferroptosis is activated when GPx4 is inhibited, glutathione (GSH) concentration is lowered, or the labile iron pool is expanded. The outcome is framed in the context of oxygen toxicity playing the physiological function of controlling cell death. GPx4 stands out as the sole peroxidase indispensable to aerobic life. Moreover, a recent study exploring the role of the residue Arg152 in GPx4, linked to a fatal although not embryonically lethal disease, revealed that the wild-type enzyme exhibits surface-sensing and positive cooperativity in the presence of cardiolipin. This adds complexity to the mechanism of physiological function encompassing the interaction with acidic phospholipids in mitochondrial membranes. Ferroptosis is implicated in both physio-pathological conditions, including embryogenesis, cancer suppression, neurodegenerations, inflammatory disorders, metabolic syndrome, heart and kidney diseases. No antioxidant enzymatic system can substitute for GPx4 in inhibiting ferroptosis, emphasizing the vital role of selenium. Phenolic antioxidants, which reduce lipid hydroperoxyl radicals, can only inhibit lipid peroxidation under physiological conditions, and thus ferroptosis, when the lipid hydroperoxides formed are immediately reduced by GPx4. In contrast, the ferroptosis inhibitor Ferrostatin-1 (Fer-1) proves to be significantly more efficient than phenolic antioxidants. Analytical and computational evidence supports the notion of a pseudo-catalytic cycle where the ferrostatin-iron complex, both produces and reduces lipid alkoxyl radicals from lipid hydroperoxides. This discloses the roadmap for the identification of innovative antioxidants competent for preventing ferroptosis.
Fulvio Ursini
29.08.2024.
Professional paper
OXYSTEROLS: FROM MOLECULAR BIOLOGY TO MEDICINE AND INDUSTRY
Oxysterols are oxidized derivatives of cholesterol initially considered as simple metabolic byproducts, nowadays recognized to play significant roles in various biological and pathological processes. In physiology, they are involved in the regulation of cellular processes beyond cholesterol metabolism, influencing cell proliferation, differentiation, apoptosis, and inflammation through various signaling pathways. In medicine, the study of oxysterols holds promise for understanding and treating various diseases, particularly those associated with dysregulated cholesterol metabolism and inflammation. Indeed, some oxysterols have been associated with adverse health effects, including cytotoxicity, pro-inflammatory effects, and potential contributions to the development of chronic diseases. Dysfunctions in oxysterol metabolism have been implicated in the pathogenesis of cardiovascular diseases, neurodegenerative disorders, and certain cancers. Targeting oxysterol pathways could therefore offer novel therapeutic strategies for these conditions. Oxysterols have potential applications in the pharmaceutical and biotechnology industries. Those generated by cholesterol autoxidation can be used as biomarkers for assessing oxidative stress conditions. Additionally, defined oxysterols of enzymatic origin and/or synthetic oxysterol analogs might be developed as antiviral agents. Oxysterols generated through autoxidation processes can serve as markers of lipid oxidation in cholesterol-containing foods and their quantification can help assess the quality and shelf life of food products, and also for ensuring food safety and consumer health. Finally, with regard to skin health and cosmetics industry, prolonged or excessive exposure to and/or formation of certain toxic oxysterols could potentially damage skin cells and disrupt skin barrier function. Therefore, careful formulation and dosage control are essential to ensure the safety of skincare products. Overall, the study of oxysterols spans molecular biology, medicine, and industry, with implications for understanding fundamental biological processes, developing new medical, industrial, and advancing biotechnological applications.
Giuseppe Poli
29.08.2024.
Professional paper
CO3•−, THE RADICAL THAT CONNECTS PEROXYNITRITE AND FENTON CHEMISTRY
Oxidative biochemistry centered about 35 years ago on the one-electron reduction of H2O2 by Fe2+, the Fenton reaction, to yield HO· and a Fe(III)-complex. The discovery that NO· is formed in vivo and that it reacts with O2·− at a diffusion-controlled rate led to ONOO− as an additional oxidant. The rate constant of the Fenton reaction is 53 M−1s−1 up to about pH 4, but above it the rate constant increases linearly with pH. This acceleration of the Fenton reaction led to the hypothesis that above pH 5 formation of FeO2+ predominates. Thermodynamically, this species is comparable to HO· as an oxidant. HCO3− accelerates the reaction even more, and convincing evidence has been presented that the complex of Fe2+ with CO32− reacts with H2O2 to form CO3·− and a Fe(III)-complex, conceivably via FeO2+ as an intermediate. The rapid reaction of ONOO− with CO2 (k > 107 M−1s−1) leads to ONOOCO2− that, depending on the CO2 concentration, yields varying amounts of NO2· and CO3·−. These two oxidizing radicals together nitrate aromatic residues. Compared to 35 years ago, oxidative biochemistry is no longer concerned with the indiscriminate oxidations and additions of HO·, but with the more selective reactions of CO3·− and NO2·.
Willem H Koppenol
