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Isoprostanes

Drugs and Chemicals · NLM MeSH · updated 2026-10-31 · version 1

Citations verified against PubMedNot yet clinician-reviewed10 referencesApproximately 4 min read

A series of prostaglandin-like compounds that are produced by the attack of free-radical species on unsaturated fatty acids, especially arachidonic acid, of cellular membranes.

Table of Contents

1. Definition2. Research landscape3. Reading the evidence4. Open-access studies5. Key reviews6. References7. About this article

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 (721 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 series of prostaglandin-like compounds that are produced by the attack of free-radical species on unsaturated fatty acids, especially arachidonic acid, of cellular membranes. Once cleaved from the lipid membrane by the action of phospholipases they can circulate into various bodily fluids and eventually be excreted. Although these compounds resemble enzymatically synthesized prostaglandins their stereoisometric arrangement is usually different than the naturally occurring compounds.

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: Isoprostane.

Where it fits in the MeSH classification

Broader topics
Arachidonic Acids; Fatty Acids, Unsaturated
Narrower topics
F2-Isoprostanes; Neuroprostanes

Related concepts

  • Arachidonic Acid
  • Membranes

Research landscape

PubMed indexes 2,069 records tagged with the MeSH heading “Isoprostanes” (counts retrieved 2026-10-31). 161 of them (7.8%) were published from 2020 onward, and the busiest period so far is 2000-2009 with 1,033 records.

Reviews account for 223 records (10.8%) and meta-analyses for 10. Randomized controlled trials number 253 (12.2%) as a share of all records on the topic. Randomized trials make up a comparatively large share of this literature, which means many treatment questions have been tested directly.

PubMed records by publication periodthrough 1999: 78 records; 2000-2009: 1,033 records; 2010-2019: 797 records; 2020 onward: 161 records78through 19991,0332000-20097972010-20191612020 onward
Records in PubMed indexed with this heading, by publication period. Real counts from NCBI E-utilities; the final period covers only part of the current year. Volume reflects how much has been published, not how strong the evidence is.
Show the data
PeriodRecords
through 199978
2000-20091,033
2010-2019797
2020 onward161
Share of records by publication typeReviews: 10.8 percent; Meta-analyses: 0.5 percent; Randomized controlled trials: 12.2 percentReviews10.8% (223)Meta-analyses0.5% (10)Randomized controlled trials12.2% (253)
Share of all PubMed records on this heading that carry each publication type. Types overlap with other records, so the shares do not sum to 100%.
Publication-type chart data
Publication types among 2,069 PubMed records
TypeRecordsShare
Reviews22310.8%
Meta-analyses100.5%
Randomized controlled trials25312.2%

Method: PubMed query "Isoprostanes"[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 comparison — selected abstracts, not a systematic review
Study / authorsYearSource label / designEurope PMC citationsLicence / source
Isoprostanes and neuroprostanes as biomarkers of oxidative stress in neurodegenerative diseases
Miller E, Morel A, Saso L, Saluk J
2014Review article
Design not recorded in structured metadata
116cc by
PMID 24868314 · DOI · PMC4020162
Effects of 2 years of caloric restriction on oxidative status assessed by urinary F2-isoprostanes: The CALERIE 2 randomized clinical trial
Il'yasova D, Fontana L, Bhapkar M, Pieper CF, Spasojevic I, Redman LM, et al.
2018Randomized controlled trial
Design not recorded in structured metadata
74cc by
PMID 29424490 · DOI · PMC5847862
Platelet function and Isoprostane biology. Should isoprostanes be the newest member of the orphan-ligand family?
Ting HJ, Khasawneh FT
2010Review article
Design not recorded in structured metadata
41cc by
PMID 20370921 · DOI · PMC2854111
Effects of Holder Pasteurization on 15-F2t-Isoprostane and Total Antioxidant Power in Donor Human Milk
Bellisario V, El Sherbiny S, Squillacioti G, Spadavecchia A, Punziano E, Coscia A, et al.
2026Research article
Design not recorded in structured metadata
0cc by
PMID 41897373 · DOI · PMC13023567

Isoprostanes and neuroprostanes as biomarkers of oxidative stress in neurodegenerative diseases [1]

Review article Miller E, Morel A, Saso L, Saluk J · · 2014 · cited 116 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
Accumulating data shows that oxidative stress plays a crucial role in neurodegenerative disorders.
Closing excerpt
We summarize the knowledge of these novel biomarkers of oxidative stress and the advantages of monitoring their formation to better define the involvement of oxidative stress in neurological diseases.
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 (171 words)

Accumulating data shows that oxidative stress plays a crucial role in neurodegenerative disorders. The literature data indicate that in vivo or postmortem cerebrospinal fluid and brain tissue levels of F2-isoprostanes (F2-IsoPs) especially F4-neuroprotanes (F4-NPs) are significantly increased in some neurodegenerative diseases: multiple sclerosis, Alzheimer's disease, Huntington's disease, and Creutzfeldt-Jakob disease. Central nervous system is the most metabolically active organ of the body characterized by high requirement for oxygen and relatively low antioxidative activity, what makes neurons and glia highly susceptible to destruction by reactive oxygen/nitrogen species and neurodegeneration. The discovery of F2-IsoPs and F4-NPs as markers of lipid peroxidation caused by the free radicals has opened up new areas of investigation regarding the role of oxidative stress in the pathogenesis of human neurodegenerative diseases. This review focuses on the relationship between F2-IsoPs and F4-NPs as biomarkers of oxidative stress and neurodegenerative diseases. We summarize the knowledge of these novel biomarkers of oxidative stress and the advantages of monitoring their formation to better define the involvement of oxidative stress in neurological diseases.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 24868314 · DOI · PMC4020162

Effects of 2 years of caloric restriction on oxidative status assessed by urinary F2-isoprostanes: The CALERIE 2 randomized clinical trial [2]

Randomized controlled trial Il'yasova D, Fontana L, Bhapkar M, Pieper CF, Spasojevic I, Redman LM, et al. · · 2018 · cited 74 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
Calorie restriction (CR) without malnutrition slows aging in animal models.
Closing excerpt
We conclude that two-year CR intervention in healthy, nonobese men and women reduced whole body oxidative stress as assessed by urinary concentrations of F2-isoprostanes.
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 (263 words)

Calorie restriction (CR) without malnutrition slows aging in animal models. Oxidative stress reduction was proposed to mediate CR effects. CR effect on urinary F2-isoprostanes, validated oxidative stress markers, was assessed in CALERIE, a two-year randomized controlled trial. Healthy volunteers (n = 218) were randomized to prescribed 25% CR (n = 143) or ad libitum control (AL, n = 75) stratifying the randomization schedule by site, sex, and BMI. F2-isoprostanes were quantified using LC-MS/MS in morning, fasted urine specimens at baseline, at 12 and 24 months. The primary measure of oxidative status was creatinine-adjusted 2,3-dinor-iPF(2α)-III concentration, additional measured included iPF(2α)-III, iPF2a-VI, and 8,12-iso-iPF2a-VI. Intention-to-treat analyses assessed change in 2,3-dinor-iPF(2α)-III using mixed models assessing treatment, time, and treatment-by-time interaction effects, adjusted for blocking variables and baseline F2-isoprostane value. Exploratory analyses examined changes in iPF(2α)-III, iPF(2α)-VI, and 8,12-iso-iPF(2α)-VI. A factor analysis used aggregate information on F2-isoprostane values. In CR group, 2,3-dinor-iPF(2α)-III concentrations were reduced from baseline by 17% and 13% at 12 and 24 months, respectively; these changes were significantly different from AL group (p < .01). CR reduced iPF(2α)-III concentrations by 20% and 27% at 12 and 24 months, respectively (p < .05). The effects were weaker on the VI-species. CR caused statistically significant reduction in isoprostane factor at both time points, and mean (se) changes were -0.36 (0.06) and -0.31 (0.06). No significant changes in isoprostane factor were at either time point in AL group (p < .01 between-group difference). We conclude that two-year CR intervention in healthy, nonobese men and women reduced whole body oxidative stress as assessed by urinary concentrations of F2-isoprostanes.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 29424490 · DOI · PMC5847862

Platelet function and Isoprostane biology. Should isoprostanes be the newest member of the orphan-ligand family? [3]

Review article Ting HJ, Khasawneh FT · · 2010 · cited 41 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
While there have been many reports investigating the biological activity and signaling mechanisms of isoprostanes, their role in biology, particularly in platelets, appears to still be underestimated.
Closing excerpt
This paper provides a review of the important literature of isoprostanes and provides reasoning that isoprostanes should be classified as orphan ligands until their receptor(s) is/are identified.
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 (81 words)

While there have been many reports investigating the biological activity and signaling mechanisms of isoprostanes, their role in biology, particularly in platelets, appears to still be underestimated. Moreover, whether these lipids have their own receptors is still debated, despite multiple reports that discrete receptors for isoprostane do exist on platelets, vascular tissues, amongst others. This paper provides a review of the important literature of isoprostanes and provides reasoning that isoprostanes should be classified as orphan ligands until their receptor(s) is/are identified.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 20370921 · DOI · PMC2854111

Effects of Holder Pasteurization on 15-F2t-Isoprostane and Total Antioxidant Power in Donor Human Milk [4]

Research article Bellisario V, El Sherbiny S, Squillacioti G, Spadavecchia A, Punziano E, Coscia A, et al. · · 2026

Abstract reading summary — source excerpts
Opening excerpt
Human milk is the optimal standard for neonatal nutrition, particularly for preterm infants.
Closing excerpt
Although this effect could offer protective benefits for vulnerable preterm infants, further studies are needed to clarify the clinical implications of HoP on redox status and neonatal outcomes.
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 (206 words)

Human milk is the optimal standard for neonatal nutrition, particularly for preterm infants. Several conditions associated with oxidative stress (OS) may be transmitted from mother to infant through milk, making the preservation of milk quality essential. When maternal milk is unavailable, donor human milk (DM) is commonly used and treated with Holder pasteurization (HoP) to ensure microbiological safety, although this process may affect bioactive components. This study aimed to evaluate the impact of HoP on OS biomarkers, specifically total antioxidant power (TAP) and 15-F2t-isoprostane, using colorimetric and ELISA methods as cost-effective alternatives to analytical gold standards. Twenty paired DM and HoP samples from the Human Milk Bank of Sant'Anna Hospital (Turin, Italy) were analyzed. No significant differences were observed in TAP levels between DM and HoP samples. In contrast, 15-F2t-isoprostane concentrations were significantly lower in DM compared to pasteurized milk (3.16 (1.59-5.27) vs. 0.76 (0.62-1.54), p-value < 0.001). This reduction remained consistent after stratification by sampling day. These findings suggest that HoP may reduce oxidative stress markers in donor milk, potentially limiting neonatal exposure to maternal oxidative imbalance. Although this effect could offer protective benefits for vulnerable preterm infants, further studies are needed to clarify the clinical implications of HoP on redox status and neonatal outcomes.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41897373 · DOI · PMC13023567

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 Is depression associated with increased oxidative stress? A systematic review and meta-analysis [5]
    Black CN, Bot M, Scheffer PG, Cuijpers P, Penninx BW · Psychoneuroendocrinology · 2015 · cited 547 times (Europe PMC)
  • Research article Isoprostanes: markers and mediators of oxidative stress [6]
    Montuschi P, Barnes PJ, Roberts LJ · FASEB J · 2004 · cited 528 times (Europe PMC)
  • Research article The neuroprotective actions of oestradiol and oestrogen receptors [7]
    Arevalo MA, Azcoitia I, Garcia-Segura LM · Nat Rev Neurosci · 2015 · cited 377 times (Europe PMC)
  • Research article Quantification of isoprostanes as indices of oxidant stress and the risk of atherosclerosis in humans [8]
    Morrow JD · Arterioscler Thromb Vasc Biol · 2005 · cited 324 times (Europe PMC)
  • Research article Disease Modification in Parkinson's Disease: Current Approaches, Challenges, and Future Considerations [9]
    Lang AE, Espay AJ · Mov Disord · 2018 · cited 271 times (Europe PMC)
  • Research article Carbon tetrachloride-induced lipid peroxidation: eicosanoid formation and their regulation by antioxidant nutrients [10]
    Basu S · Toxicology · 2003 · cited 259 times (Europe PMC)

References

  1. Miller E, Morel A, Saso L, Saluk J. Isoprostanes and neuroprostanes as biomarkers of oxidative stress in neurodegenerative diseases. . 2014. PMID 24868314 · DOI · PMC4020162
  2. Il'yasova D, Fontana L, Bhapkar M, Pieper CF, Spasojevic I, Redman LM, et al.. Effects of 2 years of caloric restriction on oxidative status assessed by urinary F2-isoprostanes: The CALERIE 2 randomized clinical trial. . 2018. PMID 29424490 · DOI · PMC5847862
  3. Ting HJ, Khasawneh FT. Platelet function and Isoprostane biology. Should isoprostanes be the newest member of the orphan-ligand family?. . 2010. PMID 20370921 · DOI · PMC2854111
  4. Bellisario V, El Sherbiny S, Squillacioti G, Spadavecchia A, Punziano E, Coscia A, et al.. Effects of Holder Pasteurization on 15-F2t-Isoprostane and Total Antioxidant Power in Donor Human Milk. . 2026. PMID 41897373 · DOI · PMC13023567
  5. Black CN, Bot M, Scheffer PG, Cuijpers P, Penninx BW. Is depression associated with increased oxidative stress? A systematic review and meta-analysis. Psychoneuroendocrinology. 2015. PMID 25462890 · DOI
  6. Montuschi P, Barnes PJ, Roberts LJ. Isoprostanes: markers and mediators of oxidative stress. FASEB J. 2004. PMID 15576482 · DOI
  7. Arevalo MA, Azcoitia I, Garcia-Segura LM. The neuroprotective actions of oestradiol and oestrogen receptors. Nat Rev Neurosci. 2015. PMID 25423896 · DOI
  8. Morrow JD. Quantification of isoprostanes as indices of oxidant stress and the risk of atherosclerosis in humans. Arterioscler Thromb Vasc Biol. 2005. PMID 15591226 · DOI
  9. Lang AE, Espay AJ. Disease Modification in Parkinson's Disease: Current Approaches, Challenges, and Future Considerations. Mov Disord. 2018. PMID 29644751 · DOI
  10. Basu S. Carbon tetrachloride-induced lipid peroxidation: eicosanoid formation and their regulation by antioxidant nutrients. Toxicology. 2003. PMID 12821287 · 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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At a glance

2,069
PubMed records on this heading
8%
published since 2020
223
review articles
253
randomized trials
10
verified references below

Counts come from PubMed on 2026-10-31; they show how much has been written, not how strong the evidence is.

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