Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (715 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
The conjugation product of leukotriene A4 and glutathione. It is the major arachidonic acid metabolite in macrophages and human mast cells as well as in antigen-sensitized lung tissue. It stimulates mucus secretion in the lung, and produces contractions of nonvascular and some vascular smooth muscle. (From Dictionary of Prostaglandins and Related Compounds, 1990)
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Leukotriene C-4; Leukotriene C 4; LTC4; Leukotrienes C; Leukotriene C; Leukotriene C1; Leukotriene C-1; Leukotriene C 1.
Where it fits in the MeSH classification
- Broader topics
- SRS-A
Related concepts
- Leukotrienes
- Vascular Smooth Muscle
Research landscape
PubMed indexes 1,279 records tagged with the MeSH heading “Leukotriene C4” (counts retrieved 2026-10-31). 35 of them (2.7%) were published from 2020 onward, and the busiest period so far is through 1999 with 568 records.
Reviews account for 50 records (3.9%) and meta-analyses for 0. Randomized controlled trials number 17 (1.3%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 568 |
| 2000-2009 | 464 |
| 2010-2019 | 212 |
| 2020 onward | 35 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 50 | 3.9% |
| Meta-analyses | 0 | 0.0% |
| Randomized controlled trials | 17 | 1.3% |
Method: PubMed query "Leukotriene C4"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in drugs and chemicals
Studies of a chemical or drug can answer very different questions: what it is and how it behaves in cells and animals, how the body handles it, and whether it changes outcomes in people. Laboratory and animal findings often do not carry over to patients, and observational studies of exposures are confounded by who uses a substance and why. Nothing on this page is a recommendation to use, avoid, start or stop any substance or medicine; talk to a qualified clinician or pharmacist about your own situation. Check the dose, the species, the comparison group and whether a patient-relevant outcome was measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
Leukotriene C4 is the major trigger of stress-induced oxidative DNA damage [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Endoplasmic reticulum (ER) stress and major chemotherapeutic agents damage DNA by generating reactive oxygen species (ROS).
- Closing excerpt
- LTC4 inhibitors, commonly used for asthma, could find broad clinical use in major human pathologies associated with ER stress-activated NOX4.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (149 words)
Endoplasmic reticulum (ER) stress and major chemotherapeutic agents damage DNA by generating reactive oxygen species (ROS). Here we show that ER stress and chemotherapy induce leukotriene C4 (LTC4) biosynthesis by transcriptionally upregulating and activating the enzyme microsomal glutathione-S-transferase 2 (MGST2) in cells of non-haematopoietic lineage. ER stress and chemotherapy also trigger nuclear translocation of the two LTC4 receptors. Acting in an intracrine manner, LTC4 then elicits nuclear translocation of NADPH oxidase 4 (NOX4), ROS accumulation and oxidative DNA damage. Mgst2 deficiency, RNAi and LTC4 receptor antagonists abolish ER stress- and chemotherapy-induced ROS and oxidative DNA damage in vitro and in mouse kidneys. Cell death and mouse morbidity are also significantly attenuated. Hence, MGST2-generated LTC4 is a major mediator of ER stress- and chemotherapy-triggered oxidative stress and oxidative DNA damage. LTC4 inhibitors, commonly used for asthma, could find broad clinical use in major human pathologies associated with ER stress-activated NOX4.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 26656251 · DOI · PMC4682057
A potential anti-tumor effect of leukotriene C4 through the induction of 15-hydroxyprostaglandin dehydrogenase expression in colon cancer cells [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Colorectal cancer (CRC) is one of the leading causes of cancer-related deaths worldwide.
- Closing excerpt
- In conclusion, the restoration of 15-PGDH expression through CysLT2 signaling promotes the differentiation of colon cancer cells, indicating an anti-tumor effect of CysLT2 signaling.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (213 words)
Colorectal cancer (CRC) is one of the leading causes of cancer-related deaths worldwide. Cyclooxygenase-2, which plays a key role in the biosynthesis of prostaglandin E2 (PGE2), is often up-regulated in CRC and in other types of cancer. PGE2 induces angiogenesis and tumor cell survival, proliferation and migration. The tumor suppressor 15-hydroxyprostaglandin dehydrogenase (15-PGDH) is a key enzyme in PGE2 catabolism, converting it into its inactive metabolite 15-keto-PGE2, and is often down-regulated in cancer. Interestingly, CRC patients expressing high levels of the cysteinyl leukotriene 2 (CysLT2) receptor have a good prognosis; therefore, we investigated a potential link between CysLT2 signaling and the tumor suppressor 15-PGDH in colon cancer cells.We observed a significant up-regulation of 15-PGDH after treatment with LTC4, a CysLT2 ligand, in colon cancer cells at both the mRNA and protein levels, which could be reduced by a CysLT2 antagonist or a JNK inhibitor. LTC4 induced 15-PGDH promoter activity via JNK/AP-1 phosphorylation. Furthermore, we also observed that LTC4, via the CysLT2/JNK signaling pathway, increased the expression of the differentiation markers sucrase-isomaltase and mucin-2 in colon cancer cells and that down-regulation of 15-PGDH totally abolished the observed increase in these markers.In conclusion, the restoration of 15-PGDH expression through CysLT2 signaling promotes the differentiation of colon cancer cells, indicating an anti-tumor effect of CysLT2 signaling.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 28402256 · DOI · PMC5471032
Arachidonic acid metabolism is elevated in Mycoplasma gallisepticum and Escherichia coli co-infection and induces LTC4 in serum as the biomarker for detecting poultry respiratory disease [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Outbreaks of multiple respiratory diseases with high morbidity and mortality have been frequently reported in poultry industry.
- Closing excerpt
- coli: Escherichia coli; AA: Arachidonic acid; LTC4: Leukotriene C4; CRD: chronic respiratory diseases; KEGG: Kyoto Encyclopedia of Genes and Genomes; LTs: leukotrienes; PGs: prostaglandins; NO: nitric oxide; HIS: histamine; PCA: Principal Component Analysis; PLS-DA: Partial Least Squares Discriminant Analysis; CCU: color change unit; UPLC: ultra-performance liquid chromatography; MS: mass spectrometry; DEMs: differentially expressed metabolites; ELISA: enzyme-linked immunosorbent assay; SD: standard deviation; VIP: Variable importance in the projection.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (251 words)
Outbreaks of multiple respiratory diseases with high morbidity and mortality have been frequently reported in poultry industry. Metabolic profiling has showed widespread usage in metabolic and infectious disease for identifying biomarkers and understanding of complex mechanisms. In this study, the non-targeted metabolomics were used on Mycoplasma gallisepticum (MG) and Escherichia coli (E.coli) co-infection model in serum, which showed that Leukotriene C4 (LTC4), Leukotriene D4 (LTD4), Chenodeoxycholate, Linoleate and numerous energy metabolites were varied significantly. KEGG enrichment analysis revealed that the metabolic pathways of linoleic acid, taurine and arachidonic acid (AA) were upregulated. To further characterize the consequences of co-infection, we performed an AA metabolic network pathway with metabolic products and enzyme genes. The results showed that the expression of LTC4 increased extremely significant and accompanied with different degree of infection. Meanwhile, the AA network performed the changes and differences of various metabolites in the pathway when multiple respiratory diseases occurred. Taken together, co-infection induces distinct alterations in the serum metabolome owing to the activation of AA metabolism. Furthermore, LTC4 in serum could be used as the biomarker for detecting poultry respiratory disease.AbbreviationsMG: Mycoplasma gallisepticum; E.coli: Escherichia coli; AA: Arachidonic acid; LTC4: Leukotriene C4; CRD: chronic respiratory diseases; KEGG: Kyoto Encyclopedia of Genes and Genomes; LTs: leukotrienes; PGs: prostaglandins; NO: nitric oxide; HIS: histamine; PCA: Principal Component Analysis; PLS-DA: Partial Least Squares Discriminant Analysis; CCU: color change unit; UPLC: ultra-performance liquid chromatography; MS: mass spectrometry; DEMs: differentially expressed metabolites; ELISA: enzyme-linked immunosorbent assay; SD: standard deviation; VIP: Variable importance in the projection.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32441188 · DOI · PMC7549906
IL-33 Elicits LTC4 Synthesis in Allergic Inflammation via ST2-Mediated Activation of Eosinophils [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Like pieces of a puzzle, IL-33, eosinophils, and cysteinyl leukotrienes seem to come together and orchestrate allergic inflammation.
- Closing excerpt
- Thus, relevant to eosinophil-regulated environments, such IL-33/ST2-driven cellular effect may bear therapeutic potential as a target in cysteinyl leukotrienes-mediated conditions.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (102 words)
Like pieces of a puzzle, IL-33, eosinophils, and cysteinyl leukotrienes seem to come together and orchestrate allergic inflammation. While the IL-33/ST2 receptor axis is known to activate some classical eosinophil functions, its ability to specifically trigger LTC4 synthesis remains elusive. Here, employing a murine model of allergic inflammation, ST2 activation emerged as a key step to LTC4 synthesis, primarily achieved by lipid bodies-enriched eosinophils. Concurring, exogenous IL-33 elicited LTC4 synthesis from activated eosinophils, both in vivo and from human cells in vitro. Thus, relevant to eosinophil-regulated environments, such IL-33/ST2-driven cellular effect may bear therapeutic potential as a target in cysteinyl leukotrienes-mediated conditions.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41761946 · DOI · PMC12949486
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Cysteinyl-leukotrienes and their receptors in asthma and other inflammatory diseases: critical update and emerging trends [5]
- Research article Human basophils: mediator release and cytokine production [6]
- Research article Cysteinyl leukotriene receptors [7]
- Research article Transport of leukotriene C4 and structurally related conjugates [8]
- Research article Roles of cysteinyl leukotrienes and their receptors in immune cell-related functions [9]
- Research article Analysis of the mechanism for the development of allergic skin inflammation and the application for its treatment: aspirin modulation of IgE-dependent mast cell activation: role of aspirin-induced exacerbation of immediate allergy [10]
References
- Dvash E, Har-Tal M, Barak S, Meir O, Rubinstein M. Leukotriene C4 is the major trigger of stress-induced oxidative DNA damage. . 2015. PMID 26656251 · DOI · PMC4682057
- Mehdawi LM, Satapathy SR, Gustafsson A, Lundholm K, Alvarado-Kristensson M, Sjölander A. A potential anti-tumor effect of leukotriene C4 through the induction of 15-hydroxyprostaglandin dehydrogenase expression in colon cancer cells. . 2017. PMID 28402256 · DOI · PMC5471032
- Wu Z, Chen C, Zhang Q, Bao J, Fan Q, Li R, et al.. Arachidonic acid metabolism is elevated in Mycoplasma gallisepticum and Escherichia coli co-infection and induces LTC4 in serum as the biomarker for detecting poultry respiratory disease. . 2020. PMID 32441188 · DOI · PMC7549906
- Rosário-Garcia VF, Guimaraes-Ferreira E, Brito-Leite Y, Oliveira JF, Santos-da-Silva J, Amorim NRT, et al.. IL-33 Elicits LTC4 Synthesis in Allergic Inflammation via ST2-Mediated Activation of Eosinophils. . 2026. PMID 41761946 · DOI · PMC12949486
- Capra V, Thompson MD, Sala A, Cole DE, Folco G, Rovati GE. Cysteinyl-leukotrienes and their receptors in asthma and other inflammatory diseases: critical update and emerging trends. Med Res Rev. 2007. PMID 16894531 · DOI
- Schroeder JT, MacGlashan DW, Lichtenstein LM. Human basophils: mediator release and cytokine production. Adv Immunol. 2001. PMID 11293121 · DOI
- Evans JF. Cysteinyl leukotriene receptors. Prostaglandins Other Lipid Mediat. 2002. PMID 12432945 · DOI
- Jedlitschky G, Keppler D. Transport of leukotriene C4 and structurally related conjugates. Vitam Horm. 2002. PMID 11898391 · DOI
- Kanaoka Y, Austen KF. Roles of cysteinyl leukotrienes and their receptors in immune cell-related functions. Adv Immunol. 2019. PMID 31296303 · DOI
- Suzuki Y, Ra C. Analysis of the mechanism for the development of allergic skin inflammation and the application for its treatment: aspirin modulation of IgE-dependent mast cell activation: role of aspirin-induced exacerbation of immediate allergy. J Pharmacol Sci. 2009. PMID 19609060 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.