Pyrularia thionin increases arachidonate liberation and prolactin and growth hormone release from anterior pituitary cells.
Pyrularia thionin is a 47 amino acid peptide isolated from the nuts of Pyrularia pubera. This peptide does not have intrinsic phospholipase A2 activity, but it increases the liberation of arachidonate from several tissues. Exposure of anterior pituitary cells to this toxin increases the liberation of arachidonate, increases the cellular levels of lysophospholipids, and decreases cellular phospholipids. Thus, phospholipase A2 is involved in the liberation of arachidonate stimulated by this peptide. Because this toxin also increases stearate liberation from the pituitary cells, either diacylglycerol lipase, phospholipase A1 or lysophospholipase may be directly or indirectly activated by this toxin. In addition to increasing fatty acid liberation, Pyrularia thionin increases the release of prolactin and growth hormone from anterior pituitary cells over the identical concentration ranges that this toxin liberates the fatty acids. Pyrularia thionin increased arachidonate liberation and prolactin release from perifused pituitary cells within 2 min, and following withdrawal of the toxin, arachidonate liberation and prolactin release returned to near basal levels within 6 min. Dopamine, a physiological inhibitor of prolactin release that closes calcium channels, decreased prolactin release stimulated by Pyrularia thionin. However, dopamine had no effect on the arachidonate liberation stimulated by this peptide. Similarly, D-600, an organic calcium channel blocker, decreased the prolactin and growth hormone release stimulated by the toxin without affecting the toxin-stimulated arachidonate liberation. Therefore, Pyrularia thionin increases arachidonate liberation through the rapid activation of phospholipase A2 by a mechanism that is not dependent on calcium uptake via D-600-inhibitable calcium channels. In contrast, the prolactin and growth hormone release stimulated by this toxin requires calcium uptake via D-600 inhibitable calcium channels.
Judd
A M
AM
Department of Internal Medicine, University of Virginia Health Sciences Center, Charlottesville 22908.
Vernon
L P
LP
MacLeod
R M
RM
D000818:Animals; D023181:Antimicrobial Cationic Peptides; D016718:Arachidonic Acid / Q000378:metabolism*; D004298:Dopamine / Q000378:metabolism; D005260:Female; D005711:Gallopamil / Q000494:pharmacology; D013006:Growth Hormone / Q000378:metabolism*; D066298:In Vitro Techniques; D010741:Phospholipases A / Q000378:metabolism; D054466:Phospholipases A1; D054467:Phospholipases A2; D010743:Phospholipids / Q000378:metabolism; D010903:Pituitary Gland, Anterior / Q000187:drug effects / Q000378:metabolism*; D010940:Plant Proteins / Q000494:pharmacology*; D011388:Prolactin / Q000378:metabolism*; D011863:Radioimmunoassay; D051381:Rats; D017207:Rats, Sprague-Dawley; D013229:Stearic Acids / Q000378:metabolism
D023181:Antimicrobial Cationic Peptides; D010743:Phospholipids; D010940:Plant Proteins; D013229:Stearic Acids; C044942:THI1 protein, Pyrularia pubera; D016718:Arachidonic Acid; D005711:Gallopamil; D011388:Prolactin; D013006:Growth Hormone; D010741:Phospholipases A; D054466:Phospholipases A1; D054467:Phospholipases A2; D004298:Dopamine