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Activation of Ethanolamine Phospholipase A 2 in Brain During Ischemia
Author(s) -
Edgar Alan D.,
Strosznajder Joanna,
Horrocks Lloyd A.
Publication year - 1982
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1982.tb11503.x
Subject(s) - gerbil , phospholipase a2 , phospholipase , ligation , chemistry , ischemia , ethanolamine , phospholipase a , phospholipase c , biochemistry , medicine , anesthesia , endocrinology , enzyme
Extracts of acetone‐dried powders from ischemic gerbil brain were examined for phospholipase A 1 and A 2 activities with phosphatidylethanolamine at pH 7.2. Ischemia was induced by bilateral ligation, and the animals were killed by immersion into liquid nitrogen. Bilateral ligation with ketamine as general anesthetic resulted in a rapid, transient increase in phospholipase A 2 activity. The activity increased from 0.46 nmolihimg protein at 0 time to 0.82 nmol/h/mg protein at 1 min of ligation. Phospholipase A 1 activity also increased from 0.7 to 1.3 nmol/h/mg protein within the 1st min. When Nembutal was used as anesthetic, the phospholipase activation was earlier, within the first 30 s. Similar results were found for ischemia induced by decapitation of Wistar rats without anesthesia. Bilateral ligation of the carotid arteries of the gerbil is known to increase the concentration of free fatty acids, particularly arachidonate. This increase is, at least in part, due to phospholipase A activation. As ethanolamine phospholipase A 2 in brain does not require Ca 2+ for activity, these results suggest that phospholipase A 2 activation in ischemic brain results from a covalent modification of the enzyme.