Özet:

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 Nazıroğlu, 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, althoughmelatonin has protective effects on the pathology. It seems to that the exact relationship between melatonin and TBI still remain to be determined.

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