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EspañolARACHIDONATE 5-LIPOXYGENASE
(Redirected from 5-lipoxygenase)
'Arachidonate 5-lipoxygenase' ('5-lipoxygenase', '5-LO' or 'Alox5'), which transforms EFAs into leukotrienes, is a current target for pharmaceutical intervention in a number of diseases.
EFA substrates and leukotriene products of 5-LO include:
★ Arachidonic acid (AA) yields the 4-series leukotrienes (LTB4, LTC4, LTD4, LTE4 — generally proinflammatory)
★ Eicosapentaenoic acid (EPA) yields the 5-series (LTB5, LTC5, LTD5, LTE5 — antiinflammatory)
★ Gamma-linolenic acid (GLA ''via'' the DGLA intermediary) yields no leukotrienes, but inhibits the conversion of AA.
5-LO catalyzes oxidation of AA at the 5-position to yield 5-hydroperoxyeicosatetraenoic acid (5-HPETE).
Two other lipoxygenases, 12-LO and 15-LO, act at the 12- and 15-positions, yielding 12- and 15-HPETE. These pathways lead to the leukotriene 12-hydroxyeicosatetraenoic acid (12-HETE) and to the lipoxins, respectively.
5-LO is a target for pharmaceutical intervention in CAD. Some people with variant alleles for 5-LO are at elevated risk for CAD. 5-LO is expressed in brain cells and may participate in neuropathologic processes [1]. As leukotrienes are important causes of pathological symptoms in asthma, 5-LO inhibitors were developed as asthma treatments. The only 5-LO inhibitor currently licensed for human use in asthma is Zileuton.
5-LO is activated by 5-lipoxygenase activating protein (FLAP).
# UCLA, ''5-Lipoxygenase, A New Therapeutic And Diagnostic Target For Heart Disease Management'' UCLA Case No. 2001-429 PCT Publication Number: WO 03/035670 A2 [2] URL referenced 10/25/05.
# JH Dwyer ''et al'' ''Arachidonate 5-lipoxygenase promoter genotype, dietary arachidonic acid, and atherosclerosis. '' N Engl J Med. 2004 Jan 1;350(1):4-7. [3]
# Dorlands Medical Dictionary, entries at ''arachidonate 5-lipoxygenase'' and following. URL referenced 7 February 2006.
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'Arachidonate 5-lipoxygenase' ('5-lipoxygenase', '5-LO' or 'Alox5'), which transforms EFAs into leukotrienes, is a current target for pharmaceutical intervention in a number of diseases.
| Contents |
| Substrates and products |
| Functions |
| Clinical significance |
| Activation |
| References |
| External links |
Substrates and products
EFA substrates and leukotriene products of 5-LO include:
★ Arachidonic acid (AA) yields the 4-series leukotrienes (LTB4, LTC4, LTD4, LTE4 — generally proinflammatory)
★ Eicosapentaenoic acid (EPA) yields the 5-series (LTB5, LTC5, LTD5, LTE5 — antiinflammatory)
★ Gamma-linolenic acid (GLA ''via'' the DGLA intermediary) yields no leukotrienes, but inhibits the conversion of AA.
Functions
5-LO catalyzes oxidation of AA at the 5-position to yield 5-hydroperoxyeicosatetraenoic acid (5-HPETE).
Eicosanoid synthesis.
Two other lipoxygenases, 12-LO and 15-LO, act at the 12- and 15-positions, yielding 12- and 15-HPETE. These pathways lead to the leukotriene 12-hydroxyeicosatetraenoic acid (12-HETE) and to the lipoxins, respectively.
Clinical significance
5-LO is a target for pharmaceutical intervention in CAD. Some people with variant alleles for 5-LO are at elevated risk for CAD. 5-LO is expressed in brain cells and may participate in neuropathologic processes [1]. As leukotrienes are important causes of pathological symptoms in asthma, 5-LO inhibitors were developed as asthma treatments. The only 5-LO inhibitor currently licensed for human use in asthma is Zileuton.
Activation
5-LO is activated by 5-lipoxygenase activating protein (FLAP).
References
# UCLA, ''5-Lipoxygenase, A New Therapeutic And Diagnostic Target For Heart Disease Management'' UCLA Case No. 2001-429 PCT Publication Number: WO 03/035670 A2 [2] URL referenced 10/25/05.
# JH Dwyer ''et al'' ''Arachidonate 5-lipoxygenase promoter genotype, dietary arachidonic acid, and atherosclerosis. '' N Engl J Med. 2004 Jan 1;350(1):4-7. [3]
# Dorlands Medical Dictionary, entries at ''arachidonate 5-lipoxygenase'' and following. URL referenced 7 February 2006.
External links
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