Moreno Mari-Luz, Escobar Javier, Finamor Isabela, Martinez-Ruiz Antonio, Sastre Juan
Department of Physiology, School of Pharmacy, University of Valencia, Avda. Vicente Andres Estelles s/n, 46100 Burjasot (Valencia), Spain.
Inflamm Allergy Drug Targets. 2014;13(5):312-22. doi: 10.2174/1871528114666141216155759.
Under physiological conditions, the balance between ROS production and removal properly maintains the intracellular redox-sensitive signaling as well as the appropriate status of protein thiols and disulfides. However, inflammation among other factors can modify this balance causing a rapid increase in intracellular ROS levels and hence thiol oxidation, eventually leading to oxidative stress. In the case of acute pancreatitis, both redox signaling and oxidative stress seem to contribute to the progression of the severe form of the disease. In this review we will focus on the reversible oxidation of protein cysteines during the course of acute pancreatitis. We describe disulfide stress in an acute inflammatory process, which is characterized by thiol oxidation in proteins, particularly protein cysteinylation, without significant changes in the glutathione redox status.
在生理条件下，活性氧（ROS）产生与清除之间的平衡可恰当地维持细胞内氧化还原敏感信号以及蛋白质硫醇和二硫键的适当状态。然而，炎症等因素可改变这种平衡，导致细胞内ROS水平迅速升高，进而引起硫醇氧化，最终导致氧化应激。在急性胰腺炎的情况下，氧化还原信号和氧化应激似乎都促成了该疾病严重形式的进展。在本综述中，我们将聚焦于急性胰腺炎病程中蛋白质半胱氨酸的可逆氧化。我们描述了急性炎症过程中的二硫键应激，其特征是蛋白质中的硫醇氧化，特别是蛋白质半胱氨酸化，而谷胱甘肽氧化还原状态无显著变化。
