Formanowicz Dorota, Radom Marcin, Rybarczyk Agnieszka, Formanowicz Piotr
Department of Clinical Biochemistry and Laboratory Medicine, Poznan University of Medical Sciences, Poznań, Poland.
Institute of Computing Science, Poznan University of Technology, Poznań, Poland; Institute of Bioorganic Chemistry, Polish Academy of Sciences, Poznań, Poland.
Biosystems. 2018 Mar;165:71-87. doi: 10.1016/j.biosystems.2018.01.002. Epub 2018 Jan 6.
The superoxide-driven Fenton reaction plays an important role in the transformation of poorly reactive radicals into highly reactive ones. These highly reactive species (ROS), especially hydroxyl radicals can lead to many disturbances contributing to the endothelial dysfunction being a starting point for atherosclerosis. Although, iron has been identified as a possible culprit influencing formation of ROS, its significance in this process is still debatable. To better understand this phenomenon, the influence of blockade of Fenton reaction in a proposed Petri net-based model of the selected aspects of the iron ROS-induced toxicity in atherosclerosis has been evaluated. As a result of the blockade of iron ions formation in the model, even up to 70% of the paths leading to the progression of atherosclerosis in this model has been blocked. In addition, after adding to the model, the blockade of the lipids peroxidation paths, progression of atherosclerotic plaque has been not observed. This allowed to conclude that the superoxide-driven Fenton reaction plays a significant role in the atherosclerosis.
超氧化物驱动的芬顿反应在将低反应性自由基转化为高反应性自由基的过程中起着重要作用。这些高反应性物种（ROS），尤其是羟基自由基，可导致许多紊乱，促成内皮功能障碍，而内皮功能障碍是动脉粥样硬化的起始点。尽管铁已被确定为影响ROS形成的可能罪魁祸首，但其在这一过程中的重要性仍存在争议。为了更好地理解这一现象，在基于培养皿网络的动脉粥样硬化中铁ROS诱导毒性的选定方面模型中，评估了芬顿反应阻断的影响。由于模型中铁离子形成的阻断，该模型中甚至高达70%的导致动脉粥样硬化进展的路径被阻断。此外，在向模型中添加脂质过氧化路径的阻断后，未观察到动脉粥样硬化斑块的进展。由此可以得出结论，超氧化物驱动的芬顿反应在动脉粥样硬化中起重要作用。
