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Arachidonic acid metabolism in polymorphonuclear cells in headaches. A methodologic study.
Y D Fragoso1, A Seim, L J Stovner
1Department of Neurology, University Hospital of Trondheim, Norway.
Cephalalgia : an International Journal of Headache
|September 1, 1988
Summary
Headache patients show altered arachidonic acid metabolism in specific cell phospholipids. This finding may link membrane signaling pathways to headache pathogenesis.
Area of Science:
- Biochemistry
- Neuroscience
- Cell Biology
Background:
- Prostaglandins and leukotrienes are implicated in headache pathogenesis.
- The effectiveness of cyclo-oxygenase inhibitors suggests a role for arachidonic acid metabolism.
- Pathological changes in arachidonic acid turnover in headache patients remain under investigation.
Purpose of the Study:
- To investigate pathological changes in arachidonic acid (AA)-containing phospholipid turnover in patients with chronic paroxysmal hemicrania (CPH) and cluster headache.
- To compare AA incorporation into phospholipids in polymorphonuclear cells (PMNs) from headache patients and healthy controls.
Main Methods:
- Isolated polymorphonuclear cells (PMNs) from healthy controls and patients with CPH and cluster headache were used.
- The incorporation of radiolabeled (1-14C)arachidonic acid (AA) into phospholipids was measured.
- Radioactivity in specific phospholipid fractions, particularly phosphatidylserine (PS), was quantified.
Main Results:
- PMNs from healthy controls incorporated 55% of added (1-14C)AA into total lipids, with 0.5% +/- 0.14% in the phosphatidylserine (PS) fraction.
- PMNs from a cluster headache patient showed a 300% increase in PS labeling from AA.
- PMNs from a CPH patient exhibited a 900% increase in PS labeling from AA compared to controls.
- No significant differences in other phospholipid fractions were observed between patients and controls.
Conclusions:
- Patients with cluster headache and CPH demonstrate significantly elevated phosphatidylserine (PS) labeling from arachidonic acid (AA) in their polymorphonuclear cells (PMNs).
- These findings suggest a specific alteration in AA turnover within the PS fraction in these headache types.
- The results may indicate a role for altered membrane signal transduction, potentially involving PS-dependent protein kinase C, in the pathogenesis of CPH and cluster headache.