Evidence map›Paper›PMID 25654095›Full record

ArticleBioMed research international2015

Tetrahydrocannabinol induces brain mitochondrial respiratory chain dysfunction and increases oxidative stress: a potential mechanism involved in cannabis-related stroke.

Valérie Wolff, Anna-Isabel Schlagowski, Olivier Rouyer, Anne-Laure Charles, François Singh, Cyril Auger, Valérie Schini-Kerth, Christian Marescaux, Jean-Sébastien Raul, Joffrey Zoll and 1 more

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed, 1 pooled it
8.7field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

79 citing papers in PubMed, 1 synthesis or guideline pooled it, 145 citations in OpenAlex.

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  14. The effects of cannabidiol and its main metabolites on human neural stem cells.Experimental biology and medicine (Maywood, N.J.) · 2025
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19 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 4 institutions in 1 country.

Valérie WolffEA 3072, Fédération de Médecine Translationnelle de Strasbourg, Institut de Physiologie, Université de Strasbourg, 67000 Strasbourg, France ; Unité Neuro-Vasculaire, Service de Neurologie, Hôpitaux Universitaires de Strasbourg, 67000 Strasbourg, France ; CNRS, ICube UMR-7357, Fédération de Médecine Translationnelle de Strasbourg, Université de Strasbourg, 67000 Strasbourg, France.
Anna-Isabel SchlagowskiEA 3072, Fédération de Médecine Translationnelle de Strasbourg, Institut de Physiologie, Université de Strasbourg, 67000 Strasbourg, France ; Service de Physiologie et d'Explorations Fonctionnelles, Pôle de Pathologie Thoracique Hôpitaux Universitaires, NHC, CHRU de Strasbourg, 67000 Strasbourg Cedex, France.
Olivier RouyerEA 3072, Fédération de Médecine Translationnelle de Strasbourg, Institut de Physiologie, Université de Strasbourg, 67000 Strasbourg, France ; Service de Physiologie et d'Explorations Fonctionnelles, Pôle de Pathologie Thoracique Hôpitaux Universitaires, NHC, CHRU de Strasbourg, 67000 Strasbourg Cedex, France.
Anne-Laure CharlesEA 3072, Fédération de Médecine Translationnelle de Strasbourg, Institut de Physiologie, Université de Strasbourg, 67000 Strasbourg, France.
François SinghEA 3072, Fédération de Médecine Translationnelle de Strasbourg, Institut de Physiologie, Université de Strasbourg, 67000 Strasbourg, France ; Service de Physiologie et d'Explorations Fonctionnelles, Pôle de Pathologie Thoracique Hôpitaux Universitaires, NHC, CHRU de Strasbourg, 67000 Strasbourg Cedex, France.
Cyril AugerUMR CNRS 7213, Laboratoire de Biophotonique et Pharmacologie, Faculté de Pharmacie, Université de Strasbourg, 67401 Illkirch, France.
Valérie Schini-KerthUMR CNRS 7213, Laboratoire de Biophotonique et Pharmacologie, Faculté de Pharmacie, Université de Strasbourg, 67401 Illkirch, France.
Christian MarescauxUnité Neuro-Vasculaire, Service de Neurologie, Hôpitaux Universitaires de Strasbourg, 67000 Strasbourg, France.
Jean-Sébastien RaulLaboratoire de Toxicologie, Institut de Médecine Légale, Université de Strasbourg, 67000 Strasbourg, France.
Joffrey ZollEA 3072, Fédération de Médecine Translationnelle de Strasbourg, Institut de Physiologie, Université de Strasbourg, 67000 Strasbourg, France ; Service de Physiologie et d'Explorations Fonctionnelles, Pôle de Pathologie Thoracique Hôpitaux Universitaires, NHC, CHRU de Strasbourg, 67000 Strasbourg Cedex, France.
Bernard GenyEA 3072, Fédération de Médecine Translationnelle de Strasbourg, Institut de Physiologie, Université de Strasbourg, 67000 Strasbourg, France ; Service de Physiologie et d'Explorations Fonctionnelles, Pôle de Pathologie Thoracique Hôpitaux Universitaires, NHC, CHRU de Strasbourg, 67000 Strasbourg Cedex, France.
Université de Strasbourg · FRHôpitaux Universitaires de Strasbourg · FRCentre National de la Recherche Scientifique · FRLaboratoire de Biophotonique et Pharmacologie · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cannabis has potential therapeutic use but tetrahydrocannabinol (THC), its main psychoactive component, appears as a risk factor for ischemic stroke in young adults. We therefore evaluate the effects of THC on brain mitochondrial function and oxidative stress, key factors involved in stroke. Maximal oxidative capacities V max (complexes I, III, and IV activities), V succ (complexes II, III, and IV activities), V tmpd (complex IV activity), together with mitochondrial coupling (V max/V 0), were determined in control conditions and after exposure to THC in isolated mitochondria extracted from rat brain, using differential centrifugations. Oxidative stress was also assessed through hydrogen peroxide (H2O2) production, measured with Amplex Red. THC significantly decreased V max (-71%; P < 0.0001), V succ (-65%; P < 0.0001), and V tmpd (-3.5%; P < 0.001). Mitochondrial coupling (V max/V 0) was also significantly decreased after THC exposure (1.8±0.2 versus 6.3±0.7; P < 0.001). Furthermore, THC significantly enhanced H2O2 production by cerebral mitochondria (+171%; P < 0.05) and mitochondrial free radical leak was increased from 0.01±0.01 to 0.10±0.01% (P < 0.001). Thus, THC increases oxidative stress and induces cerebral mitochondrial dysfunction. This mechanism may be involved in young cannabis users who develop ischemic stroke since THC might increase patient's vulnerability to stroke.

Indexed as

AnimalsBrainCannabisDronabinolElectron TransportFree RadicalsHydrogen PeroxideMaleMitochondriaOxidation-ReductionOxidative StressRats, WistarStrokeDronabinolFree RadicalsHydrogen Peroxide

Identifiers

PMID25654095
PMCPMC4310259
OpenAlexW2008841747

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.