Oxidative stress hypoxia-ischemia

Hypoxia-ischemia may initiate apoptosis in parallel with excitotoxicity 565 Triggers of ischemic apoptosis may include decreased supply or sensitivity to neurotrophins, oxidative stress, exposure to inflammatory cytokines or damage to mitochondria 566... 

Sheldon, R. A., Christen, S., and Ferriero, D. M. (2008). Genetic and pharmacologic manipulation of oxidative stress after neonatal hypoxia-ischemia. Int.J. Dev. Neurosci. 26, 87-92. 

Das, D.K., Maulik, N., and Moraru, 1.1. 1995. Gene expression in acute myocardial stress. Induction by hypoxia, ischemia, hyperthermia and oxidative stress. J. Mol. Cell. Cardiol. 27 181-193,... 

The authors cited a combination of ischemia and exci-totoxicity due to cocaine exposure as the possible cause of the brain injury. Oxidative stress and free radicals associated with cerebral hypoxia contribute to cell damage and death. 

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). 

JNKs can be activated by a large range of different stimuli, including kainic acid [47], microtubule-disrupting agents [48], double-stranded ribonucleic acid (RNA) [49], viral infections [49], tumor necrosis factors, interleukins [50], osmotic stress [51], and trophic factor withdrawal [30]. JNKs have also been reported to be activated by oxidative stress, particularly that induced by ultraviolet radiation [47], hypoxia [52], ischemia [53], hydrogen peroxide [30,54], peroxynitrite [55], malondialdehyde [56], and 4-hydroxynonenal [57]. 

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