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.