Abstract:

Oxidative stress induces excessive production of reactive oxygen species (ROS). ROS are including several free oxygen radicals such as singlet oxygen and superoxide radical. Excessive ROS production induces injuries of lipids, nucleic acids and proteins in several cells. Brain and neurons have a high amount of polyunsaturated fatty acids (PUFAs) and consumption of oxygen, but they have low level of antioxidant. Oxidative stress is controlled by several enzymatic and non-enzymatic antioxidants. One of the main nonenzymatic antioxidant is melatonin. Melatonin is secreted from the pineal gland by physiological circadian cycles. It has several physiological functions such as mediator of circannual reproductive rhythms (Tamtaji et al. 2019). However, it has also a regulatory role in the pathophysiological pathways of traumatic brain injury (TBI) in human and rodents (Barlow et al. 2019). TBI 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 ROS-mediated lipid peroxidation. It was reported that TBI-induced oxidative stress in experimental TBI was inhibited by the melatonin treatment (Senol and Nazıroğlu, 2014). Results of a recent study indicated protective role of melatonin through inhibition of Nrf2 signaling pathway, inflammation and oxidative stress in TBI-induced mice (Wang et al. 2019). In human studies, behavioral outcomes of TBI were modulated by the melatonin treatment (Barlow et al. 2019). In the oral presentation, I will review recent studies on TBI in human and experimental animals.   In conclusion, there are pre-clinical and clinical evidences that melatonin treatment after TBI significantly improves both behavior-cognition outcomes and pathophysiological outcomes such as oxidative stress and inflammation. It seems that the certain interaction between melatonin and TBI still remain to be determined.

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