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It is well established that elevated extracellular adenosine reduces seizure activity in several seizure models, and the anticonvulsant action is mediated through A 1 R adenosine receptors (104, 105)

Although aldosterone-induced oxidative or nitrative stress quickly stimulated antioxidant or detoxifying enzymes such SOD, thioredoxin (TRX), HO-1, or GCSc, this adaptive survival response appeared to be fleeting and overpowered by a chronic increased generation of ROS/RNS

(2004) showed that abnormal neuronal and mitochondrial proteins induce swelling, vacuolization, and increased ROS levels intracellularly, and manifests as learning and memory deficits (Shin et al., 2004, p