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KMID : 0854719990190030434
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Korean Journal of Asthma, Allergy and Clinical Immunology
1999 Volume.19 No. 3 p.434 ~ p.439
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Leukotriene and asthma
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Gen Tamura
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Abstract
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Formation of leukotrienes
Formation of leukotrienes is shown in Fig. 1. After stimulations, phospholipase
A2 (PLA2) and 5-lipoxygenase (5-LO) move near perinuclear
membrane. Activated PLA2 cleaves arachidonic acid from phospholipids in
the perinuclear membrane. Then, arachidonic acid enters into a series of reactions at the
membrane. The first of these reactions requires a specific 5-LO activating protein which
allows arachidonate to serve as a substrate for the enzyme, 5-LO. 5-LO sequentially
catalyses the addition of oxygen to arachidonic acid to form 5-hydroxyeicosatetraenoic
acid and leukotriene A4 (LTA4) consecutively.
LTA4 is a major branch-point in the formation of the leukotrienes. Thus,
LTA4 is catalyzed to LTB4 by LTA4 hydrolase
and to LTC4 by LTC4 synthase. LTC4 is
catalyzed to LTD4, and then LTE4 in the extracellular
microenvironment. LTC4, LTD4, and LTE4
make up the material formerly known as slow-reacting substance of anaphylaxis and
collectively known as the cysteinyl leukotrienes now.
Cells having 5-LO are neutrophils, alveolar macrophages, monocytes, mast cells,
eosinophils, and basophils. Those with LTC4 synthase are mast cells,
eosinophils, basophils, endothelial cells, and platelets, while those with
LTA4 hydrolase are neutrophils, alveolar macrophages, and monocytes.
Consequently, there is a cell specificity in producing LTB4 and cysteinyl
leukotrienes. Thus, cells with the capacity of LTB4 are neutrophils,
alveolar macrophages, and monocytes. Mast cells, eosinophils, and basophils can produce
cysteinyl leukotrienes independently. On the other hand, platelets and endothelial cells
can produce cysteinyl leukotrienes only when supplying LTA4, because
they retain LTC4 syntase, but not 5-LO.
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