Peptide (cysteinyl) leukotrienes: molecular mechanisms & dependencies

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

Human evidence only

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What acts on it

After nasal instillation of 12 milligrams of acetylsalicylic acid, significant levels of peptide leukotrienes were detected in sensitive asthmatic patients at 60 minutes in association with a significant increase in symptoms, with no increase in either insensitive patients or healthy subjects, while inhibition of prostaglandin E2 and F2-alpha release was detected in all three groups; aspirin also inhibited prostaglandin D2 release in insensitive asthmatic patients but not in sensitive patients or healthy subjects.
Aspirin / acetylsalicylic acid → Peptide (cysteinyl) leukotrienes source_derived_draftungraded
Experimental context and source evidence
evidence_span
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experimental_model
Double-blind nasal lavage challenge in ten aspirin-sensitive asthmatics, ten insensitive asthmatics and seven healthy subjects
exposure
12 milligrams of acetylsalicylic acid instilled nasally against saline
limitations
Three groups including two control groups, with mediators measured directly in the target tissue. Radioimmunoassay of nasal lavage fluid, and a small number per group.
nutrient_topic
Aspirin research collection; topical membership is not evidence of a direct clinical effect, and aspirin is recorded separately from salicylate, the metabolite it becomes. · Aspirin / acetylsalicylic acid
organism
Human
plain_language
The drug blocks prostaglandins in everyone, but only in the sensitive patients does a flood of leukotrienes follow.
primary_references
[asa-p1309968] Release of peptide leukotriene into nasal secretions after local instillation of aspirin in aspirin-sensitive asthmatic patients. (1992). https://pubmed.ncbi.nlm.nih.gov/1309968/ DOI: 10.1164/ajrccm/145.1.65
tissue_or_cell_type
Nasal mucosa
Aspirin: the serine it acetylates, the enzyme that acetylation creates, the dose that separates platelet from vessel wall, and the metabolite that is a different drug (2026-09-22) · lines 572–583
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind nasal lavage challenge in ten aspirin-sensitive asthmatics, ten insensitive asthmatics and seven healthy subjects · source_derived_draft · unverified_draft
### asa-only-sensitive-patients-release After nasal instillation of 12 milligrams of acetylsalicylic acid, significant levels of peptide leukotrienes were detected in sensitive asthmatic patients at 60 minutes in association with a significant increase in symptoms, with no increase in either insensitive patients or healthy subjects, while inhibition of prostaglandin E2 and F2-alpha release was detected in all three groups; aspirin also inhibited prostaglandin D2 release in insensitive asthmatic patients but not in sensitive patients or healthy subjects. Condition category: normal nutrient_topic: Aspirin research collection; topical membership is not evidence of a direct clinical effect, and aspirin is recorded separately from salicylate, the metabolite it becomes. plain_language: The drug blocks prostaglandins in everyone, but only in the sensitive patients does a flood of leukotrienes follow. organism: Human tissue_or_cell_type: Nasal mucosa experimental_model: Double-blind nasal lavage challenge in ten aspirin-sensitive asthmatics, ten insensitive asthmatics and seven healthy subjects limitations: Three groups including two control groups, with mediators measured directly in the target tissue. Radioimmunoassay of nasal lavage fluid, and a small number per group. exposure: 12 milligrams of acetylsalicylic acid instilled nasally against saline evidence_span: {"source_cache": "artifacts/aspirin-research/1309968.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a81a9ed941df59e6b8aa8c7c730d9a14766e2b8bd358b712ee464ae96c67e4e2", "start_char": 0, "end_char": 1685, "text_sha256": "a81a9ed941df59e6b8aa8c7c730d9a14766e2b8bd358b712ee464ae96c67e4e2"} [asa-p1309968] Release of peptide leukotriene into nasal secretions after local instillation of aspirin in aspirin-sensitive asthmatic patients. (1992). https://pubmed.ncbi.nlm.nih.gov/1309968/ DOI: 10.1164/ajrccm/145.1.65
Complete structured claim and evidence

Where it participates (unsigned role)

The adverse effect of aspirin in asthmatics is often attributed to inhibition of the synthesis and release of defensive modulatory endogenous prostaglandins in the lungs, removing their negative feedback on allergic mediator release, and in addition work suggests diversion of arachidonic acid metabolism via the lipoxygenase pathway after cyclooxygenase inhibition, leading to formation of hydroperoxy acids and leukotrienes whose accumulation in sensitive individuals could explain the mechanism of aspirin-induced asthma.
Aspirin / acetylsalicylic acid → Diversion of unmetabolised arachidonate into the 5-lipoxygenase pathway source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/aspirin-research/6113615.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "184fc232146a3837f396109d951c9755155f181c524a3ffaa330645138d8a616", "start_char": 0, "end_char": 2083, "text_sha256": "184fc232146a3837f396109d951c9755155f181c524a3ffaa330645138d8a616"}
experimental_model
Review of arachidonate metabolism in airway hyperreactivity and aspirin-induced asthma
exposure
Cyclooxygenase inhibition and the proposed diversion of arachidonate into the lipoxygenase pathway
limitations
A review from 1981 setting out the shunting hypothesis. It is recorded as the proposal that later work tested, not as evidence that the proposal is right.
nutrient_topic
Aspirin research collection; topical membership is not evidence of a direct clinical effect, and aspirin is recorded separately from salicylate, the metabolite it becomes. · Aspirin / acetylsalicylic acid
organism
Human
plain_language
The standard explanation: block one pathway and the raw material spills into another that makes bronchoconstrictors.
primary_references
[asa-p6113615] Lipoxygenase pathway and hydroperoxy acids: possible relevance to aspirin-induced asthma and hyperirritability of airways in asthmatics. (1981). https://pubmed.ncbi.nlm.nih.gov/6113615/ DOI: 10.1016/0161-4630(81)90097-5
tissue_or_cell_type
Airway
Aspirin: the serine it acetylates, the enzyme that acetylation creates, the dose that separates platelet from vessel wall, and the metabolite that is a different drug (2026-09-22) · lines 546–557
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Review of arachidonate metabolism in airway hyperreactivity and aspirin-induced asthma · source_derived_draft · unverified_draft
### asa-shunting-proposed The adverse effect of aspirin in asthmatics is often attributed to inhibition of the synthesis and release of defensive modulatory endogenous prostaglandins in the lungs, removing their negative feedback on allergic mediator release, and in addition work suggests diversion of arachidonic acid metabolism via the lipoxygenase pathway after cyclooxygenase inhibition, leading to formation of hydroperoxy acids and leukotrienes whose accumulation in sensitive individuals could explain the mechanism of aspirin-induced asthma. Condition category: normal nutrient_topic: Aspirin research collection; topical membership is not evidence of a direct clinical effect, and aspirin is recorded separately from salicylate, the metabolite it becomes. plain_language: The standard explanation: block one pathway and the raw material spills into another that makes bronchoconstrictors. organism: Human tissue_or_cell_type: Airway experimental_model: Review of arachidonate metabolism in airway hyperreactivity and aspirin-induced asthma limitations: A review from 1981 setting out the shunting hypothesis. It is recorded as the proposal that later work tested, not as evidence that the proposal is right. exposure: Cyclooxygenase inhibition and the proposed diversion of arachidonate into the lipoxygenase pathway evidence_span: {"source_cache": "artifacts/aspirin-research/6113615.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "184fc232146a3837f396109d951c9755155f181c524a3ffaa330645138d8a616", "start_char": 0, "end_char": 2083, "text_sha256": "184fc232146a3837f396109d951c9755155f181c524a3ffaa330645138d8a616"} [asa-p6113615] Lipoxygenase pathway and hydroperoxy acids: possible relevance to aspirin-induced asthma and hyperirritability of airways in asthmatics. (1981). https://pubmed.ncbi.nlm.nih.gov/6113615/ DOI: 10.1016/0161-4630(81)90097-5
Complete structured claim and evidence

The events it takes part in

A mechanism often involves more than two components. These are the full events, with every participant and its role.

Situations it appears in

Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

Open hypotheses

Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.

This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

Peptide (cysteinyl) leukotrienes