Free radicals in central nervous system ischemia.

Post-traumatic inflammation following spinal cord injury

“…Further, during post-traumatic reperfusion, reactive oxygen radicals may also be formed as byproducts of the biochemical reactions, which produce prostaglandins and leucotrienes from arachidonic acid. 8,45,52 Liberation of catalytic metal ions, that are present in high concentration during the degradation of haemoglobin, is essential to the formation of free radicals.…”

Alpha-ketoglutarate dehydrogenase: a target and generator of oxidative stress

“…Oxidative stress involves an increased production and/or a decreased elimination of ROS in cells and has been shown to contribute to the cell damage caused by ischaemia/reperfusion, trauma, ageing and several neurodegenerative diseases (Halliwell & Gutteridge 1984Cao et al 1988;Schmidley 1990;Halliwell 1992;Hall et al 1993;Olanow 1993;Siesjo et al 1995). The effect of ROS (superoxide, hydrogen peroxide and hydroxyl radical) could be damaging on virtually all cellular components but membrane lipids are particularly sensitive to free radicals due to the presence of polyunsaturated fatty acids, which preferentially undergo lipid peroxidation (Halliwell & Gutteridge 1984.…”

Inhibition of Nonselective Cation Channels Reduces Focal Ischemic Injury of Rat Brain

“…Ischemic injury of the brain is the cumulative result of several pathologies: The primary metabolic impact pro voked by the reduction of blood flow is aggravated by secondary complicating disturbances, involving such dif ferent mechanisms as free radical-mediated membrane injury (Siesjo et aI" 1989;Schmidley, 1990), uncoupling of oxidative respiration (Katsura et aI" 1994;Abe et aI" 1995), inflammatory reactions (Shiga et aI" 1991), peri focal depolarizations (Iijima et aI" 1992;Nedergaard and water declined to below 80% of controll steadily increased by -50% during the initial 6 h of vascular occlusion relative to the first set of data 10 min postocclusion, In the treated animals, in contrast, the ADC lesion volume declined by -20% during the same intervaL Treatment also led to a significant reduction in the number of periinfarct depolarizations, After 6 h of vascular occlusion, blood flow was significantly higher in the treated animals, and the volume of ATP-depleted and morphologically injured tissue representing the infarct core was 60-70% smaller. The volume of severely acidic tissue, in contrast, did not differ, indicating that LOE 908 MS does not reduce the size of ischemic penumbra, These findings demonstrate that post occlusion treatment of permanent focal ischemia with LOE 908 MS delays the expansion of the infarct core into the penumbra for a duration of at least 6 h and therefore substantially pro longs the window of opportunity for the reversal of the isch emic impact in the peripheral parts of the evolving infarct.…”