Hypoxia-ischemia antioxidants

Free radical formation is an important contributor to cell death and brain injury in many neurological diseases. Shortly after brain damage by hypoxia-ischemia, hemorrhage, or trauma, excessive reactive oxygen species (ROS) production occurs, and at the same time, there is an impairment of antioxidant protective mechanisms, which leads to oxidative stress (Heo et al 2005). 

Liu CL, Siesjo BK, Hu BR (2004) Pathogenesis of hippocampal neuronal death after hypoxia-ischemia changes during brain development. Neuroscience 127 113-123 Lodi R, Tonon C, Calabrese V, Schapira AH (2006) Friedreich s ataxia from disease mechanisms to therapeutic interventions. Antioxid Redox Signal 8 438-443... 

From earlier times when it has first been established that ischemia and hypoxia are the potential causes of coronary heart disease and myocardial infraction [50,51], antioxidants... 

Heat shock proteins is a family of proteins which were identified in relation to heat stress response and they are categorized on the basis of their approximate molecular weights. Heat shock protein induction is a rapid response to altered redox state and closely corresponds to the activity of antioxidant enzymes such as catalase. Heat shock proteins are induced in response to a number of stresses, including sublethal heal, hypoxia, reoxygenation and ischemia and reperfusion. 

Delivery of gene transfer systems of heat shock proteins (Hsp70),250 antioxidant enzymes (catalase)251 or survival genes (Akt)252 has been associated with myocardial protection against ischemia and reperfusion. A vector gene therapy system has also been developed with a hypoxia response element-incorporated promoter to turn on the gene expression in response to hypoxic signal.253... 

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