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Nanocapsulated Antioxidants in Combating Mitochondrial Generated Oxidative Stress in Cerebral Ischemia-Reperfusion Injury

Sibani Sarkar

Toxic reactive oxidative species (ROS) evoked by the induction of oxidative stress in the episode of cerebral ischemia reperfusion (CIR) play the key role in neurodegeneration. As it is the prime source point of ROS, neuronal mitochondria, the cellular energy metabolic centre suffer severe damage in response to cerebral ischemic oxidative thrust. In aging, CIR accelerates the process of mitochondrial dysfunction. Increasing evidence suggests that oxidative stress mediated defects in mitochondrial energy production may be involved in numerous age related neurodegenerative disorders. Impairment of mitochondrial function causes generation of free radicals e.g., O2-, •OH. Normally free radicals are generated as by-products of oxidative metabolism. An increase in super oxide radical generation can have direct as well as indirect damaging consequences on the metabolism of neuron. From therapeutic point, the application of chemical antioxidants is almost ineffective as the blood-brain barrier (BBB) limits the passage of molecules from the circulation into the cerebral region. Nanoencapsulation technology has proven benefits for the ability to cross the BBB as well as their nature to increase cellular drug concentration. Particle size and size distribution play the determining role in drug delivery systems. The NP size less than 100 nm particles experiences reduced hepatic filtration and takes less time to reach the brain, the target organ in my present communication