Stroke, Vol 9, 445-447, Copyright © 1978 by American Heart Association
ES Flamm, HB Demopoulos, ML Seligman, RG Poser and J Ransohoff
The possibility that cerebral ischemia may initiate a series of
pathological free radical reactions within the membrane components of the
CNS was investigated in the cat. The normally occurring electron transport
radicals require adequate molecular oxygen for orderly transport of
electrons and protons. A decrease in tissue oxygen removes the controls
over the electron transport radicals, and allows them to initiate
pathologic radical reactions among cell membranes such as mitochondria.
Pathologic radical reactions result in multiple products, each of which may
be present in too small a concentration to permit their detection at early
time periods. It is possible to follow the time course, however, by the
decrease of a major antioxidant as it is consumed by the pathologic radical
reactions. For this reason, ascorbic acid was measured in ischemic and
control brain following middle cerebral artery occlusion. There was a
progressive decrease in the amount of detectable ascorbic acid ranging from
25% at 1 hour to 65% at 24 hours after occlusion. The reduction of this
normally occurring antioxidant and free radical scavenger may indicate
consumption of ascorbic acid in an attempt to quench pathologic free
radical reactions occurring within the components of cytomembranes.
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