Young Age and Concomitant Cannabis (THC) and Ethanol (EtOH) Exposure Enhances Rat Brain Damage Through Decreased Cerebral Mitochondrial Respiration

The reason why young people taking concomitantly cannabis (THC) and ethanol (EtOH) are more prone to stroke is underresearched. To investigate whether an underlying mechanism of increased brain damage could be an impaired mitochondrial function, this experiment determined the acute effects of EtOH,...

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Veröffentlicht in:Molecules (Basel, Switzerland) Jg. 30; H. 4; S. 918
Hauptverfasser: Quenardelle, Véronique, Charles, Anne-Laure, Charloux, Anne, Raul, Jean-Sébastien, Wolff, Valérie, Geny, Bernard
Format: Journal Article
Sprache:Englisch
Veröffentlicht: Switzerland MDPI AG 17.02.2025
MDPI
Schlagworte:
Age
Alcohol
Animals
Brain
Brain - drug effects
Brain - metabolism
Brain - pathology
Brain Injuries - chemically induced
Brain Injuries - metabolism
Brain Injuries - pathology
cannabis
Cannabis - adverse effects
Cannabis - chemistry
Cell Respiration - drug effects
Cognition & reasoning
Dronabinol - adverse effects
Dronabinol - pharmacology
Drug dosages
Ethanol
Ethanol - adverse effects
Ethanol - pharmacology
Ethanol - toxicity
EtOH
Heart attacks
Hydrogen Peroxide - metabolism
Hypothesis testing
Male
Marijuana
Mental disorders
mitochondria
Mitochondria - drug effects
Mitochondria - metabolism
Neuropsychology
Oxidative Stress - drug effects
Protons
Rats
Respiration
Stroke
Tetrahydrocannabinol
THC
Young adults
mitochondria
cannabis
EtOH
hydrogen peroxide (H2O2)
brain
ethanol
stroke
THC
oxidative stress
mitochondrial respiration
ISSN:1420-3049, 1420-3049
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Zusammenfassung:The reason why young people taking concomitantly cannabis (THC) and ethanol (EtOH) are more prone to stroke is underresearched. To investigate whether an underlying mechanism of increased brain damage could be an impaired mitochondrial function, this experiment determined the acute effects of EtOH, both alone and associated with THC, on mitochondrial respiration and oxidative stress (hydrogen peroxide H2O2) on young (11 weeks) and middle-aged (45 weeks) brain in rats, using a high-resolution oxygraph (Oxygraph-2K, Oroboros instruments). In young brains, EtOH decreased mitochondrial respiration by −51.76 ± 2.60% (from 32.76 ± 3.82 to 17.41 ± 1.42 pmol/s/mL, p < 0.0001). In 45-week-old brains, the decrease was lesser, but still significant −36.0 ± 2.80% (from 30.73 ± 7.72 to 20.59 ± 5.48 pmol/s/mL, p < 0.0001). Concomitant THC aggravated brain mitochondrial respiration decreases at 11 weeks (−86.86 ± 1.74%, p < 0.0001) and at 45 weeks (−73.95 ± 3.69%, p < 0.0001). Such additional injury was enhanced in young brains (p < 0.01). H2O2 production was similar in both age groups (1.0 ± 0.2 versus 1.1 ± 0.08 pmol O2/s/mL) and was not modified by THC addition. In conclusion, EtOH alone significantly impairs brain mitochondrial respiration and concomitant THC further aggravates such damage, particularly in young brains. These data support the hypothesis that enhanced mitochondrial dysfunction might participate in the increased occurrence of stroke in the young and urge for better prevention against EtOH and THC addictions in adolescents.
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ISSN:1420-3049
1420-3049
DOI:10.3390/molecules30040918