1.1.Trauma and Oxidative stress
Trauma leads to oxidative stress by increasing the production of SORs and SARs due to the activation of polymorphonuclear cells and neutrophils stemming mainly from tissue damage, ischemia-reperfusion injury and consequently inflammatory response. It is known that oxidative stress is increased as a result of the activation of neutrophils and macrophages and over-production of SOR in inflammatory events [16,17,18]. In inflammation, SORs produced by polymorphonuclear leukocytes lead to lipid peroxidation in cell membranes. These changes in the cell membrane cause an increase in microvascular permeability, intestinal edema, infiltration of inflammatory cells, activation of neutrophils and cell death [17]. In literature, it has been shown in studies conducted by adult patients and animals that the head injury [19-22], burn [23], bone fractures [24], liver damage [25], kidney damage [26], lung injury [27] and similar traumas lead to distortion in oxidative balance resulting in oxidative stress. However, there are very few studies in children [28]. In traumatized children, the development of a test that could show the affected system and organ from trauma more quickly and easily and assist in deciding on surgical intervention would help both early diagnosis and early surgical intervention. In this study, we aimed to investigate the use of thiol-disulfide and ischemia-modified albumin levels as a diagnostic laboratory parameter in trauma children.