Role of melatonin on oxidative stress in traumatic brain injury

Abstract

Oxidative stress occurs in the several  physiological processes such as phagocytic activity and  mitochondrial membrane functions. Oxidative stress is  controlled by several enzymatic and non-enzymatic  antioxidants. Traumatic brain injury is one of the most  common causes of the mortalities. Secondary events  occur after primary events like shearing of nerve cells  and blood vessels, cause posttraumatic  neurodegenerations with an increase in ROS and ROSmediated  lipid peroxidation. Melatonin is a member of  non-enzymatic antioxidant group. The protective effects  of melatonin on traumatic brain injury have been shown  in vivo and in vitro studies (Barlow et al. 2018). Also  melatonin has been shown to counteract oxidative  stress-induced pathophysiologic conditions like  ischemia/reperfusion injury, neuronal excitotoxicity and  chronic inflammation. Recently, it was reported that  TBI-induced oxidative stress in experimental TBI was  inhibited by the melatonin treatment (Senol and  Naziroglu, 2014). In the oral presentation, I will review  recent studies on traumatic brain injury in human and  rodents.  I concluded that the oxidative stress causes  changes through activation of second messengers,  which may lead to the pathology of TBI, although melatonin has protective effects on the pathology. It  seems to that the exact relationship between melatonin  and TBI still remain to be determined.