ABSTRACT
Several basic facts have been established that are important to understanding the protective role of nitrone radical traps (NRTs) in brain oxidative damage. The concept that aerobic biological systems experience an oxidative stress at all times simply because they are utilizing oxygen is becoming widely accepted. The notion that very small levels of reactive oxygen species exists continuously in aerobic biological systems is valid but due to technical problems difficult to prove. Oxidative stress can be viewed as the dynamic balance between the oxidative damage potential as opposed to the antioxidant defense capacity. The use of NRTs to characterize trapped free radicals ideally is based on the electron paramagnetic spectrum of the product formed, which is then compared to synthesized authentic trapped products. The chapter examines the action of NRTs on hydroxyl free radicals produced in isolated mitochondria experiencing an anoxia/reoxygenation challenge. It shows that α-phenyl-butyl nitrone prevented brain ischemia/reperfusion insult-mediated lethality in gerbils.
