Oxidative Stress And NAD+ In Ischemic Brain Injury: Current Advances

Stress Replacement Article

Oxidative stress is caused by an imbalance between the production of reactive oxygen and a biological system's ability to readily detoxify the reactive intermediates or easily repair the resulting damage. Nicotinamide Adenine Dinucleotide (NAD+) is a coenzyme which occurs in most living cells and utilized alternately with NADH as an oxidizing or reducing agent in various metabolic processes. Ischemic brain injury is caused when one of the arteries that bring blood to a part of the brain becomes blocked by a blood clot or a cholesterol plaque. The resulting lack of oxygen and nutrients in these areas causes neurons to stop functioning. Typically, an ischemic brain injury is known a stroke. “Ischemic stroke is the major form of stroke. Extensive studies on the disease have discovered many important mechanisms underlying ischemic brain injury, and suggested some potential therapeutic strategies”. Studies have confirmed that oxidative stress is a key element during the cause of ischemic brain injury. There have been suggestions that NAD+ depletion will mediate PARP-1(Poly [ADP-ribose] polymerase 1) cytotoxicity, and NAD+ administration can decrease ischemic brain injury. PARP-1 has the role of being a DNA repair mechanism. Within the article, researches have indicated that there are also other main pathological factors that initiate ischemic brain injury, other than oxidative stress. These components include: impaired calcium homeostasis, mitochondrial dysfunction, and inflammation. Evidence has shown that not only does oxidative stress play a factor in the causation of ischemic brain injury, but also other neurological diseases; such as Parkinson’s Disease and Alzheimer’s Disease.



 Ying, W. W., & Xiong, Z. G. (2010). Oxidative Stress and NAD⁺ in Ischemic Brain Injury: Current Advances and Future Perspectives. Current Medicinal Chemistry, 17(20), 2152-2158. Retrieved from EBSCOhost.