MétaCan
Menu
Back to cohort
Record W4416534860 · doi:10.1016/j.rbc.2025.100066

Proteomic identification of protein radicals from myeloperoxidase-mediated mefenamic acid oxidation reveals a mechanism of NSAID-induced oxidative injury

2025· article· en· W4416534860 on OpenAlexafffund
Newton H. Tran, Steven Lockhart, Othman Eldalal, Phuc Tran, J. R. Cooper, Lusine Tonoyan, Richard P. Fahlman, Arno G. Siraki

Bibliographic record

VenueRedox Biochemistry and Chemistry · 2025
Typearticle
Languageen
FieldImmunology and Microbiology
TopicNeutrophil, Myeloperoxidase and Oxidative Mechanisms
Canadian institutionsUniversity of Alberta
FundersNatural Sciences and Engineering Research Council of CanadaCanada Foundation for InnovationUniversity of Alberta
KeywordsOxidative stressMefenamic acidMyeloperoxidaseOxidative phosphorylationReactive oxygen speciesMitochondrionAntioxidantCytosol

Abstract

fetched live from OpenAlex

Mefenamic acid (MFA; Ponstel®, USA) is a nonsteroidal anti-inflammatory drug (NSAID) used to treat inflammatory pain. Despite its effectiveness, it carries an FDA black box warning for serious adverse effects, including hepatotoxicity, agranulocytosis, and gastrointestinal injury. While these toxicities are often linked to oxidative stress, the molecular mechanisms remain poorly understood. A key interaction occurs between MFA and myeloperoxidase (MPO), a heme enzyme released from activated neutrophils during inflammation. MPO catalyzes MFA’s one-electron oxidation, forming reactive metabolites that modify cellular macromolecules and potentially induce oxidative stress and immune-mediated cytotoxicity. This study examined whether MPO-mediated metabolism of MFA contributes to oxidative damage and cell death in HL-60 promyelocytic leukemia cells. Using compartment-specific spin probes and EPR spectroscopy, MFA was found to increase oxidant production in both cytosolic and mitochondrial compartments. MFA also caused an 80% loss of mitochondrial membrane potential, activated the Nrf2 antioxidant response, and suppressed phospho-ERK1/2 signaling—changes significantly reversed by PF-1355, a selective MPO inhibitor. Immuno-spin trapping revealed a 133-fold increase in protein-centered radicals following MFA exposure, which was reduced by 97% with MPO inhibition. Proteomic analysis identified MPO and HSPD1 among the most significantly modified proteins. These findings provide mechanistic insight that MPO-mediated oxidation of MFA generates reactive protein-free radicals, which disrupt redox signaling and protein integrity—ultimately contributing to mitochondrial dysfunction, oxidative stress, and cytotoxicity under inflammatory conditions. This mechanism provides insight into NSAID-induced oxidative injury and supports targeting MPO to improve drug safety under inflammatory conditions. • MFA forms protein radicals via MPO-catalyzed bioactivation in HL-60 cells • PF-1355 attenuates MFA-induced oxidative stress and cytotoxicity • Mitochondrial dysfunction and redox signaling disruption observed with MFA • Proteomic profiling reveals Hsp60, MPO, and TRiC complex as radical targets • MPO-mediated protein adduction may underlie MFA-induced immune toxicity

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame machine prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.000
Version: metacan-v3-hybrid-931329e0061cValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Bench or experimental · Consensus signal: Bench or experimental
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.001
Threshold uncertainty score0.002

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0000.000
Insufficient payload (model declined to judge)0.0010.000

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.006
GPT teacher head0.229
Teacher spread0.223 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designBench or experimental
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

Quick stats

Citations1
Published2025
Admission routes2
Has abstractyes

Explore more

Same venueRedox Biochemistry and ChemistrySame topicNeutrophil, Myeloperoxidase and Oxidative MechanismsFrench-language works237,207