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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
24
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pubmed:dateCreated |
1992-7-24
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pubmed:abstractText |
The formation and role of arachidonic acid (AA) and its metabolites during gonadotropin releasing hormone- (GnRH-) induced gonadotropin secretion were investigated in primary cultures of rat pituitary cells. Prelabeled cells ([3H]AA) responded to GnRH challenge with increased formation (about 2-fold) of the leukotrienes LTC4, LTD4, and LTE4 as well as 5- and 15-eicosatetraenoic acids (5- and 15-HETE) as identified by HPLC. Formation of leukotrienes and 15-HETE was further verified by specific radioimmunoassays. No significant increase in the formation of 12-HETE or of the cyclooxygenase products prostaglandin E (PGE) and thromboxane A2 by GnRH was noticed. Addition of physiological concentrations of LTC4 enhanced basal LH release, while subphysiological concentrations of LTC4 (10(-15)-10(-12) M) inhibited GnRH-induced LH release by about 35% (p less than 0.02). Using specific lipoxygenase inhibitors L-656,224 and MK 886, we found inhibition of GnRH-induced LH release by about 40% at concentrations known to specifically inhibit the 5-lipoxygenase pathway. The peptidoleukotriene receptor antagonist ICI 198,615 inhibited LTC4- and LTE4-induced LH release and surprisingly also the effect of GnRH on LH release by 40%. The data strongly suggest a role for AA and its lipoxygenase metabolites in the on/off reactions of GnRH upon LH release. The data also present a novel amplification cycle in which newly formed leukotrienes become first messengers and establish an autocrine/paracrine loop.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/15-hydroxy-5,8,11,13-eicosatetraenoi...,
http://linkedlifedata.com/resource/pubmed/chemical/5-hydroxy-6,8,11,14-eicosatetraenoic...,
http://linkedlifedata.com/resource/pubmed/chemical/Arachidonic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Eicosanoids,
http://linkedlifedata.com/resource/pubmed/chemical/Gonadotropin-Releasing Hormone,
http://linkedlifedata.com/resource/pubmed/chemical/Hydroxyeicosatetraenoic Acids,
http://linkedlifedata.com/resource/pubmed/chemical/ICI 198615,
http://linkedlifedata.com/resource/pubmed/chemical/Indazoles,
http://linkedlifedata.com/resource/pubmed/chemical/Leukotrienes,
http://linkedlifedata.com/resource/pubmed/chemical/Lipoxygenase,
http://linkedlifedata.com/resource/pubmed/chemical/Lipoxygenase Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Luteinizing Hormone
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0006-2960
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
23
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pubmed:volume |
31
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
5442-8
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:1610790-Animals,
pubmed-meshheading:1610790-Arachidonic Acid,
pubmed-meshheading:1610790-Cells, Cultured,
pubmed-meshheading:1610790-Eicosanoids,
pubmed-meshheading:1610790-Exocytosis,
pubmed-meshheading:1610790-Gonadotropin-Releasing Hormone,
pubmed-meshheading:1610790-Hydroxyeicosatetraenoic Acids,
pubmed-meshheading:1610790-Indazoles,
pubmed-meshheading:1610790-Leukotrienes,
pubmed-meshheading:1610790-Lipoxygenase,
pubmed-meshheading:1610790-Lipoxygenase Inhibitors,
pubmed-meshheading:1610790-Luteinizing Hormone,
pubmed-meshheading:1610790-Pituitary Gland,
pubmed-meshheading:1610790-Rats,
pubmed-meshheading:1610790-Rats, Inbred Strains,
pubmed-meshheading:1610790-Second Messenger Systems,
pubmed-meshheading:1610790-Secretory Rate,
pubmed-meshheading:1610790-Signal Transduction
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pubmed:year |
1992
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pubmed:articleTitle |
Gonadotropin releasing hormone activates the lipoxygenase pathway in cultured pituitary cells: role in gonadotropin secretion and evidence for a novel autocrine/paracrine loop.
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pubmed:affiliation |
Department of Biochemistry, Tel Aviv University, Israel.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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