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 (782 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
A specific inhibitor of phosphoserine/threonine protein phosphatase 1 and 2a. It is also a potent tumor promoter. It is produced by dinoflagellates and causes diarrhetic shellfish poisoning.
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: Ocadaic Acid.
Where it fits in the MeSH classification
- Broader topics
- Ethers, Cyclic; Polyether Toxins; Marine Toxins
Related concepts
- Dinoflagellates
- Shellfish Poisoning
Research landscape
PubMed indexes 4,000 records tagged with the MeSH heading “Okadaic Acid” (counts retrieved 2026-10-31). 269 of them (6.7%) were published from 2020 onward, and the busiest period so far is through 1999 with 1,881 records.
Reviews account for 93 records (2.3%) and meta-analyses for 0. Randomized controlled trials number 0 (0.0%) 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 | 1,881 |
| 2000-2009 | 1,225 |
| 2010-2019 | 625 |
| 2020 onward | 269 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 93 | 2.3% |
| Meta-analyses | 0 | 0.0% |
| Randomized controlled trials | 0 | 0.0% |
Method: PubMed query "Okadaic Acid"[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.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Okadaic acid: more than a diarrheic toxin | 2013 | Review article Design not recorded in structured metadata | 167 | cc by PMID 24184795 · DOI · PMC3853731 |
| Quercetin Protects against Okadaic Acid-Induced Injury via MAPK and PI3K/Akt/GSK3β Signaling Pathways in HT22 Hippocampal Neurons | 2016 | Research article Design not recorded in structured metadata | 76 | cc by PMID 27050422 · DOI · PMC4822954 |
| Graphene oxide-assisted non-immobilized SELEX of okdaic acid aptamer and the analytical application of aptasensor | 2016 | Research article Design not recorded in structured metadata | 58 | cc by PMID 26898784 · DOI · PMC4761938 |
| Okadaic acid triggers NFκB and STAT3 phosphorylation followed by a release of inflammatory markers in human and mouse endothelial cells | 2026 | Research article Design not recorded in structured metadata | 0 | cc by PMID 41699315 · DOI · PMC13086646 |
Okadaic acid: more than a diarrheic toxin [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Okadaic acid (OA) is one of the most frequent and worldwide distributed marine toxins.
- Closing excerpt
- Despite further investigations are required to elucidate OA mechanisms of action, toxicokinetics, and harmful effects, there are enough evidences illustrating its toxicity, not related to DSP induction, and, consequently, supporting a revision of the current regulation on OA levels in food.
- 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 (221 words)
Okadaic acid (OA) is one of the most frequent and worldwide distributed marine toxins. It is easily accumulated by shellfish, mainly bivalve mollusks and fish, and, subsequently, can be consumed by humans causing alimentary intoxications. OA is the main representative diarrheic shellfish poisoning (DSP) toxin and its ingestion induces gastrointestinal symptoms, although it is not considered lethal. At the molecular level, OA is a specific inhibitor of several types of serine/threonine protein phosphatases and a tumor promoter in animal carcinogenesis experiments. In the last few decades, the potential toxic effects of OA, beyond its role as a DSP toxin, have been investigated in a number of studies. Alterations in DNA and cellular components, as well as effects on immune and nervous system, and even on embryonic development, have been increasingly reported. In this manuscript, results from all these studies are compiled and reviewed to clarify the role of this toxin not only as a DSP inductor but also as cause of alterations at the cellular and molecular levels, and to highlight the relevance of biomonitoring its effects on human health. Despite further investigations are required to elucidate OA mechanisms of action, toxicokinetics, and harmful effects, there are enough evidences illustrating its toxicity, not related to DSP induction, and, consequently, supporting a revision of the current regulation on OA levels in food.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 24184795 · DOI · PMC3853731
Quercetin Protects against Okadaic Acid-Induced Injury via MAPK and PI3K/Akt/GSK3β Signaling Pathways in HT22 Hippocampal Neurons [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Increasing evidence shows that oxidative stress and the hyperphosphorylation of tau protein play essential roles in the progression of Alzheimer's disease (AD).
- Closing excerpt
- Our findings suggest the therapeutic potential of quercetin to treat AD.
- 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 (197 words)
Increasing evidence shows that oxidative stress and the hyperphosphorylation of tau protein play essential roles in the progression of Alzheimer's disease (AD). Quercetin is a major flavonoid that has anti-oxidant, anti-cancer and anti-inflammatory properties. We investigated the neuroprotective effects of quercetin to HT22 cells (a cell line from mouse hippocampal neurons). We found that Okadaic acid (OA) induced the hyperphosphorylation of tau protein at Ser199, Ser396, Thr205, and Thr231 and produced oxidative stress to the HT22 cells. The oxidative stress suppressed the cell viability and decreased the levels of lactate dehydrogenase (LDH), superoxide dismutase (SOD), mitochondria membrane potential (MMP) and Glutathione peroxidase (GSH-Px). It up-regulated malondialdehyde (MDA) production and intracellular reactive oxygen species (ROS). In addition, phosphoinositide 3 kinase/protein kinase B/Glycogen synthase kinase3β (PI3K/Akt/GSK3β) and mitogen activated protein kinase (MAPK) were also involved in this process. We found that pre-treatment with quercetin can inhibited OA-induced the hyperphosphorylation of tau protein and oxidative stress. Moreover, pre-treatment with quercetin not only inhibited OA-induced apoptosis via the reduction of Bax, and up-regulation of cleaved caspase 3, but also via the inhibition of PI3K/Akt/GSK3β, MAPKs and activation of NF-κB p65. Our findings suggest the therapeutic potential of quercetin to treat AD.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 27050422 · DOI · PMC4822954
Graphene oxide-assisted non-immobilized SELEX of okdaic acid aptamer and the analytical application of aptasensor [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Okadaic acid (OA) is a low-molecular-weight marine toxin from shellfish that causes abdominal pain, vomiting and diarrhea, i.
- Closing excerpt
- The proposed method can be used to detect OA in seafood products with high sensitivity and can potentially be adapted for the determination of other small molecular analytes.
- 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 (131 words)
Okadaic acid (OA) is a low-molecular-weight marine toxin from shellfish that causes abdominal pain, vomiting and diarrhea, i.e., diarrheic shellfish poisoning. In this study, a ssDNA aptamer that specifically binds to OA with high affinity was obtained via Systematic Evolution of Ligands by Exponential Enrichment (SELEX) assisted by graphene oxide (GO). This aptamer was then applied to fabricate a novel direct competitive enzyme-linked aptamer assay (ELAA). At the optimized conditions, this ELAA method showed a low detection limit (LOD of 0.01 ng/mL), wide linear range (from 0.025 to 10 ng/mL), good recovery rate (92.86-103.34% in OA-spiked clam samples) and repeatability (RSD of 2.28-4.53%). The proposed method can be used to detect OA in seafood products with high sensitivity and can potentially be adapted for the determination of other small molecular analytes.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 26898784 · DOI · PMC4761938
Okadaic acid triggers NFκB and STAT3 phosphorylation followed by a release of inflammatory markers in human and mouse endothelial cells [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Okadaic acid (OA) is a lipophilic phycotoxin that causes acute diarrhoea when ingested.
- Closing excerpt
- Altogether, these data suggest that the toxic effect of OA in endothelial cells could be related with the activation of the inflammatory cascade.
- 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 (233 words)
Okadaic acid (OA) is a lipophilic phycotoxin that causes acute diarrhoea when ingested. OA is an inhibitor of protein phosphatase 2 A, but the mechanism of toxicity behind the diarrhoea remains unclear. OA modulated inflammatory markers in epithelial cells, however, the effect on endothelial cells, with a key role in the inflammatory cascade, has not been previously addressed. Therefore, the aim of the present work was to test the effect of OA in human (HMEC-1) and mouse (MS1) endothelial cells. After 3, 6 and 24 h of incubation in the presence of OA (10-1000 nM) cell viability was significantly reduced, showing a higher effect on human cells with half inhibitory concentrations (IC50) in HMEC-1 cells five times lower than in mouse cells. Furthermore, when cells were treated with OA, significant amounts of the proinflammatory mediators ROS, CD147, IL-6 and monocyte chemoattractant protein 1 (MCP-1) were detected. Some of these effects were observed only in HMEC-1 cells and around three hours earlier, pointing again to a higher sensitivity in human models. Finally, OA triggered phosphorylation of NFκB at 100 nM after 3 and 6 h of treatment, while the signal transducer and activator of transcription 3 (STAT3) was increased after 3 h but decreased after 6 h in both cell lines. Altogether, these data suggest that the toxic effect of OA in endothelial cells could be related with the activation of the inflammatory cascade.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41699315 · DOI · PMC13086646
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 Microcystin-LR and okadaic acid-induced cellular effects: a dualistic response [5]
- Research article Okadaic acid, useful tool for studying cellular processes [6]
- Research article Okadaic acid: the archetypal serine/threonine protein phosphatase inhibitor [7]
- Research article Molecular and cellular mechanism of okadaic acid (OKA)-induced neurotoxicity: a novel tool for Alzheimer's disease therapeutic application [8]
- Research article Dinoflagellate polyether within the yessotoxin, pectenotoxin and okadaic acid toxin groups: characterization, analysis and human health implications [9]
- Research article Marine toxins and the cytoskeleton: okadaic acid and dinophysistoxins [10]
References
- Valdiglesias V, Prego-Faraldo MV, Pásaro E, Méndez J, Laffon B. Okadaic acid: more than a diarrheic toxin. . 2013. PMID 24184795 · DOI · PMC3853731
- Jiang W, Luo T, Li S, Zhou Y, Shen XY, He F, et al.. Quercetin Protects against Okadaic Acid-Induced Injury via MAPK and PI3K/Akt/GSK3β Signaling Pathways in HT22 Hippocampal Neurons. . 2016. PMID 27050422 · DOI · PMC4822954
- Gu H, Duan N, Wu S, Hao L, Xia Y, Ma X, et al.. Graphene oxide-assisted non-immobilized SELEX of okdaic acid aptamer and the analytical application of aptasensor. . 2016. PMID 26898784 · DOI · PMC4761938
- Nyback K, Alfonso A, Alvariño R, Suzuki T, Watanabe R, Uchida H, et al.. Okadaic acid triggers NFκB and STAT3 phosphorylation followed by a release of inflammatory markers in human and mouse endothelial cells. . 2026. PMID 41699315 · DOI · PMC13086646
- Gehringer MM. Microcystin-LR and okadaic acid-induced cellular effects: a dualistic response. FEBS Lett. 2004. PMID 14741332 · DOI
- Fernández JJ, Candenas ML, Souto ML, Trujillo MM, Norte M. Okadaic acid, useful tool for studying cellular processes. Curr Med Chem. 2002. PMID 11860357 · DOI
- Dounay AB, Forsyth CJ. Okadaic acid: the archetypal serine/threonine protein phosphatase inhibitor. Curr Med Chem. 2002. PMID 12369865 · DOI
- Kamat PK, Rai S, Swarnkar S, Shukla R, Nath C. Molecular and cellular mechanism of okadaic acid (OKA)-induced neurotoxicity: a novel tool for Alzheimer's disease therapeutic application. Mol Neurobiol. 2014. PMID 24710687 · DOI
- Dominguez HJ, Paz B, Daranas AH, Norte M, Franco JM, Fernández JJ. Dinoflagellate polyether within the yessotoxin, pectenotoxin and okadaic acid toxin groups: characterization, analysis and human health implications. Toxicon. 2010. PMID 19925818 · DOI
- Vale C, Botana LM. Marine toxins and the cytoskeleton: okadaic acid and dinophysistoxins. FEBS J. 2008. PMID 19016863 · 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.