Background & Objective:
Traumatic Brain Injury (TBI) is one of the major causes of mortality
and morbidity worldwide. It represents mild, moderate and severe effects of physical assault to
brain which may cause sequential, primary or secondary ramifications. Primary injury can be due to
the first physical hit, blow or jolt to one of the brain compartments. The primary injury is then followed
by secondary injury which leads to biochemical, cellular, and physiological changes like blood
brain barrier disruption, inflammation, excitotoxicity, necrosis, apoptosis, mitochondrial dysfunction
and generation of oxidative stress. Apart from this, there is also an immediate increase in glutamate at
the synapses following severe TBI. Excessive glutamate at synapses in turn activates corresponding
NMDA and AMPA receptors that facilitate excessive calcium influx into the neuronal cells. This leads
to the generation of oxidative stress which further leads to mitochondrial dysfunction, lipid peroxidation
and oxidation of proteins and DNA. As a consequence, neuronal cell death takes place and ultimately
people start facing some serious disabilies.
Conclusion:
In the present review we provide extensive overview of the role of reactive oxygen species
(ROS)-induced oxidative stress and its fatal effects on brain after TBI.
Neuroprotective effect of hydrogen sulfide against glutamate-induced oxidative stress is mediated via the p53/glutaminase 2 pathway after traumatic brain injury
