@article{ref1,
title="Oxidative stress: major threat in traumatic brain injury",
journal="CNS and neurological disorders drug targets",
year="2018",
author="Khatri, Nidhi and Thankur, Manisha and Pareek, Vikas and Kumar, Sandeep and Sharma, Sunil and Datusalia, Ashok Kumar",
volume="17",
number="9",
pages="689-695",
abstract="Traumatic Brain Injury, representing mild, moderate and severe effects of physical impact on the brain is the leading cause of mortality and morbidity worldwide. Traumatic injury causes sequential, primary and secondary injuries of brain where primary injury is due to the first physical impact, the blow or jolt to the brain compartment. Secondary injury follows primary injury temporally, involving the biochemical, cellular, and physiological responses like blood brain barrier disruption, inflammation, excitotoxicity, necrosis, apoptosis, mitochondrial dysfunction and oxidative stress. Glutamate induced excitotoxicity is the major factor causing neuronal cell death in its vicinity, explained by higher levels of calcium levels intracellularly in neurons. Excessive glutamate at synaptic junction which in turn activates its NMDA and AMPA receptors that facilitates excessive calcium influx into the neuronal cells and promote oxidative stress and further leads to mitochondrial dysfunction, oxidation of lipids, proteins and DNA leads to the neuronal cell death. Present literature review is intended to give extensive view summarizing effects of reactive oxygen species (ROS) induced oxidative stress and its fatal effects on brain after traumatic brain injury.<br><br>Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.<p /> <p>Language: en</p>",
language="en",
issn="1871-5273",
doi="10.2174/1871527317666180627120501",
url="http://dx.doi.org/10.2174/1871527317666180627120501"
}