Cannabis (THC) Aggravates the Deleterious Effects of Alcohol (EtOH) on Skeletal Muscles’ Mitochondrial Respiration: Modulation by Age and Metabolic Phenotypes
The anti-inflammatory and analgesic properties of cannabis might be useful to treat muscle diseases, including those linked or not to alcohol. Nevertheless, delta 9 tetrahydrocannabinol (THC) and ethanol (EtOH), often used concomitantly, can have deleterious effects on cardiac mitochondria. We there...
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| Published in: | Biology (Basel, Switzerland) Vol. 13; no. 12; p. 1080 |
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21.12.2024
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| Abstract | The anti-inflammatory and analgesic properties of cannabis might be useful to treat muscle diseases, including those linked or not to alcohol. Nevertheless, delta 9 tetrahydrocannabinol (THC) and ethanol (EtOH), often used concomitantly, can have deleterious effects on cardiac mitochondria. We therefore determined whether EtOH, alone and associated with THC, impairs skeletal muscle mitochondrial respiration. Further, we investigated potential modulation by metabolic phenotype and age by analyzing predominantly glycolytic gastrocnemius and oxidative soleus muscles in young and middle-aged rats (12 and 49 weeks). Considering the gastrocnemius, EtOH impaired mitochondrial respiration in a similar manner in young- and middle-aged muscles (−34.97 ± 2.97% vs. −37.50 ± 6.03% at 2.1 × 10−5 M; p < 0.05). Interestingly, concomitant THC aggravated EtOH-related mitochondrial impairment in young gastrocnemius (−49.92 ± 1.69%, vs. −34.97 ± 2.97 p < 0.05). Concerning the soleus, EtOH alone mainly decreased young muscle mitochondrial respiration (−42.39 ± 2.42% vs. −17.09 ± 7.61% at 2.1 × 10−5 M, p < 0.001, at 12 and 49 weeks). The soleus was less impaired at 12 weeks by THC and EtOH association than the gastrocnemius (−49.92 ±1.69 vs. −27.22 ± 8.96% in gastrocnemius and soleus, respectively, p < 0.05). In conclusion, EtOH, alone and associated with THC, significantly impairs skeletal muscle mitochondrial respiration and THC aggravates EtOH-induced effects on young glycolytic muscle. Age and metabolic phenotypes modulate these deleterious effects, with the glycolytic muscles of young rats being more prone to impairments than oxidative muscles. |
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| AbstractList | The anti-inflammatory and analgesic properties of cannabis might be useful to treat muscle diseases, including those linked or not to alcohol. Nevertheless, delta 9 tetrahydrocannabinol (THC) and ethanol (EtOH), often used concomitantly, can have deleterious effects on cardiac mitochondria. We therefore determined whether EtOH, alone and associated with THC, impairs skeletal muscle mitochondrial respiration. Further, we investigated potential modulation by metabolic phenotype and age by analyzing predominantly glycolytic gastrocnemius and oxidative soleus muscles in young and middle-aged rats (12 and 49 weeks). Considering the gastrocnemius, EtOH impaired mitochondrial respiration in a similar manner in young- and middle-aged muscles (-34.97 ± 2.97% vs. -37.50 ± 6.03% at 2.1 × 10-5 M; p < 0.05). Interestingly, concomitant THC aggravated EtOH-related mitochondrial impairment in young gastrocnemius (-49.92 ± 1.69%, vs. -34.97 ± 2.97 p < 0.05). Concerning the soleus, EtOH alone mainly decreased young muscle mitochondrial respiration (-42.39 ± 2.42% vs. -17.09 ± 7.61% at 2.1 × 10-5 M, p < 0.001, at 12 and 49 weeks). The soleus was less impaired at 12 weeks by THC and EtOH association than the gastrocnemius (-49.92 ±1.69 vs. -27.22 ± 8.96% in gastrocnemius and soleus, respectively, p < 0.05). In conclusion, EtOH, alone and associated with THC, significantly impairs skeletal muscle mitochondrial respiration and THC aggravates EtOH-induced effects on young glycolytic muscle. Age and metabolic phenotypes modulate these deleterious effects, with the glycolytic muscles of young rats being more prone to impairments than oxidative muscles.The anti-inflammatory and analgesic properties of cannabis might be useful to treat muscle diseases, including those linked or not to alcohol. Nevertheless, delta 9 tetrahydrocannabinol (THC) and ethanol (EtOH), often used concomitantly, can have deleterious effects on cardiac mitochondria. We therefore determined whether EtOH, alone and associated with THC, impairs skeletal muscle mitochondrial respiration. Further, we investigated potential modulation by metabolic phenotype and age by analyzing predominantly glycolytic gastrocnemius and oxidative soleus muscles in young and middle-aged rats (12 and 49 weeks). Considering the gastrocnemius, EtOH impaired mitochondrial respiration in a similar manner in young- and middle-aged muscles (-34.97 ± 2.97% vs. -37.50 ± 6.03% at 2.1 × 10-5 M; p < 0.05). Interestingly, concomitant THC aggravated EtOH-related mitochondrial impairment in young gastrocnemius (-49.92 ± 1.69%, vs. -34.97 ± 2.97 p < 0.05). Concerning the soleus, EtOH alone mainly decreased young muscle mitochondrial respiration (-42.39 ± 2.42% vs. -17.09 ± 7.61% at 2.1 × 10-5 M, p < 0.001, at 12 and 49 weeks). The soleus was less impaired at 12 weeks by THC and EtOH association than the gastrocnemius (-49.92 ±1.69 vs. -27.22 ± 8.96% in gastrocnemius and soleus, respectively, p < 0.05). In conclusion, EtOH, alone and associated with THC, significantly impairs skeletal muscle mitochondrial respiration and THC aggravates EtOH-induced effects on young glycolytic muscle. Age and metabolic phenotypes modulate these deleterious effects, with the glycolytic muscles of young rats being more prone to impairments than oxidative muscles. Simple SummaryCannabis (THC) and ethanol (EtOH) are widely used for their anti-inflammatory and analgesic properties. Whether both drugs have deleterious effects on skeletal muscle needs further investigations, particularly looking at mitochondria, the energy producers of the cells. We determined the effects of EtOH, alone and associated with THC, on skeletal muscle mitochondrial respiration, on predominantly glycolytic gastrocnemius muscles (less mitochondria) and oxidative soleus (many mitochondria) muscles in young and middle-aged rats (12 and 49 weeks). Considering the gastrocnemius, EtOH impaired mitochondrial respiration in a similar manner in young- and middle-aged muscles (−34.97 ± 2.97% vs. −37.50 ± 6.03%). Interestingly, concomitant THC aggravated EtOH-related mitochondrial impairment in young gastrocnemius muscles (−49.92 ± 1.69%, vs. −34.97 ± 2.97). Concerning the soleus, EtOH alone mainly decreased young muscle mitochondrial respiration (−42.39 ± 2.42% vs. −17.09 ± 7.61%, at 12 and 49 weeks). The soleus was less impaired at 12 weeks by THC and EtOH association than the gastrocnemius. In conclusion, EtOH, alone and associated with THC, significantly impairs skeletal muscle mitochondrial respiration and THC aggravates EtOH-induced alterations in young glycolytic muscle. Caution is therefore warranted if using THC or EtOH alone, and even more caution is needed if both drugs are concomitantly used. Cannabis (THC) and ethanol (EtOH) are widely used for their anti-inflammatory and analgesic properties. Whether both drugs have deleterious effects on skeletal muscle needs further investigations, particularly looking at mitochondria, the energy producers of the cells. We determined the effects of EtOH, alone and associated with THC, on skeletal muscle mitochondrial respiration, on predominantly glycolytic gastrocnemius muscles (less mitochondria) and oxidative soleus (many mitochondria) muscles in young and middle-aged rats (12 and 49 weeks). Considering the gastrocnemius, EtOH impaired mitochondrial respiration in a similar manner in young-and middle-aged muscles (-34.97 ± 2.97% vs. -37.50 ± 6.03%). Interestingly, concomitant THC aggravated EtOH-related mitochondrial impairment in young gastrocnemius muscles (-49.92 ± 1.69%, vs.-34.97 ± 2.97). Concerning the soleus, EtOH alone mainly decreased young muscle mitochondrial respiration (-42.39 ± 2.42% vs. -17.09 ± 7.61%, at 12 and 49 weeks). The soleus was less impaired at 12 weeks by THC and EtOH association than the gastrocnemius. In conclusion, EtOH, alone and associated with THC, significantly impairs skeletal muscle mitochondrial respiration and THC aggravates EtOH-induced alterations in young glycolytic muscle. Caution is therefore warranted if using THC or EtOH alone, and even more caution is needed if both drugs are concomitantly used. Cannabis (THC) and ethanol (EtOH) are widely used for their anti-inflammatory and analgesic properties. Whether both drugs have deleterious effects on skeletal muscle needs further investigations, particularly looking at mitochondria, the energy producers of the cells. We determined the effects of EtOH, alone and associated with THC, on skeletal muscle mitochondrial respiration, on predominantly glycolytic gastrocnemius muscles (less mitochondria) and oxidative soleus (many mitochondria) muscles in young and middle-aged rats (12 and 49 weeks). Considering the gastrocnemius, EtOH impaired mitochondrial respiration in a similar manner in young- and middle-aged muscles (−34.97 ± 2.97% vs. −37.50 ± 6.03%). Interestingly, concomitant THC aggravated EtOH-related mitochondrial impairment in young gastrocnemius muscles (−49.92 ± 1.69%, vs. −34.97 ± 2.97). Concerning the soleus, EtOH alone mainly decreased young muscle mitochondrial respiration (−42.39 ± 2.42% vs. −17.09 ± 7.61%, at 12 and 49 weeks). The soleus was less impaired at 12 weeks by THC and EtOH association than the gastrocnemius. In conclusion, EtOH, alone and associated with THC, significantly impairs skeletal muscle mitochondrial respiration and THC aggravates EtOH-induced alterations in young glycolytic muscle. Caution is therefore warranted if using THC or EtOH alone, and even more caution is needed if both drugs are concomitantly used. The anti-inflammatory and analgesic properties of cannabis might be useful to treat muscle diseases, including those linked or not to alcohol. Nevertheless, delta 9 tetrahydrocannabinol (THC) and ethanol (EtOH), often used concomitantly, can have deleterious effects on cardiac mitochondria. We therefore determined whether EtOH, alone and associated with THC, impairs skeletal muscle mitochondrial respiration. Further, we investigated potential modulation by metabolic phenotype and age by analyzing predominantly glycolytic gastrocnemius and oxidative soleus muscles in young and middle-aged rats (12 and 49 weeks). Considering the gastrocnemius, EtOH impaired mitochondrial respiration in a similar manner in young- and middle-aged muscles (−34.97 ± 2.97% vs. −37.50 ± 6.03% at 2.1 × 10−5 M; p < 0.05). Interestingly, concomitant THC aggravated EtOH-related mitochondrial impairment in young gastrocnemius (−49.92 ± 1.69%, vs. −34.97 ± 2.97 p < 0.05). Concerning the soleus, EtOH alone mainly decreased young muscle mitochondrial respiration (−42.39 ± 2.42% vs. −17.09 ± 7.61% at 2.1 × 10−5 M, p < 0.001, at 12 and 49 weeks). The soleus was less impaired at 12 weeks by THC and EtOH association than the gastrocnemius (−49.92 ±1.69 vs. −27.22 ± 8.96% in gastrocnemius and soleus, respectively, p < 0.05). In conclusion, EtOH, alone and associated with THC, significantly impairs skeletal muscle mitochondrial respiration and THC aggravates EtOH-induced effects on young glycolytic muscle. Age and metabolic phenotypes modulate these deleterious effects, with the glycolytic muscles of young rats being more prone to impairments than oxidative muscles. The anti-inflammatory and analgesic properties of cannabis might be useful to treat muscle diseases, including those linked or not to alcohol. Nevertheless, delta 9 tetrahydrocannabinol (THC) and ethanol (EtOH), often used concomitantly, can have deleterious effects on cardiac mitochondria. We therefore determined whether EtOH, alone and associated with THC, impairs skeletal muscle mitochondrial respiration. Further, we investigated potential modulation by metabolic phenotype and age by analyzing predominantly glycolytic gastrocnemius and oxidative soleus muscles in young and middle-aged rats (12 and 49 weeks). Considering the gastrocnemius, EtOH impaired mitochondrial respiration in a similar manner in young- and middle-aged muscles (−34.97 ± 2.97% vs. −37.50 ± 6.03% at 2.1 × 10−5 M; p < 0.05). Interestingly, concomitant THC aggravated EtOH-related mitochondrial impairment in young gastrocnemius (−49.92 ± 1.69%, vs. −34.97 ± 2.97 p < 0.05). Concerning the soleus, EtOH alone mainly decreased young muscle mitochondrial respiration (−42.39 ± 2.42% vs. −17.09 ± 7.61% at 2.1 × 10−5 M, p < 0.001, at 12 and 49 weeks). The soleus was less impaired at 12 weeks by THC and EtOH association than the gastrocnemius (−49.92 ±1.69 vs. −27.22 ± 8.96% in gastrocnemius and soleus, respectively, p < 0.05). In conclusion, EtOH, alone and associated with THC, significantly impairs skeletal muscle mitochondrial respiration and THC aggravates EtOH-induced effects on young glycolytic muscle. Age and metabolic phenotypes modulate these deleterious effects, with the glycolytic muscles of young rats being more prone to impairments than oxidative muscles. The anti-inflammatory and analgesic properties of cannabis might be useful to treat muscle diseases, including those linked or not to alcohol. Nevertheless, delta 9 tetrahydrocannabinol (THC) and ethanol (EtOH), often used concomitantly, can have deleterious effects on cardiac mitochondria. We therefore determined whether EtOH, alone and associated with THC, impairs skeletal muscle mitochondrial respiration. Further, we investigated potential modulation by metabolic phenotype and age by analyzing predominantly glycolytic gastrocnemius and oxidative soleus muscles in young and middle-aged rats (12 and 49 weeks). Considering the gastrocnemius, EtOH impaired mitochondrial respiration in a similar manner in young- and middle-aged muscles (-34.97 ± 2.97% vs. -37.50 ± 6.03% at 2.1 × 10 M; < 0.05). Interestingly, concomitant THC aggravated EtOH-related mitochondrial impairment in young gastrocnemius (-49.92 ± 1.69%, vs. -34.97 ± 2.97 < 0.05). Concerning the soleus, EtOH alone mainly decreased young muscle mitochondrial respiration (-42.39 ± 2.42% vs. -17.09 ± 7.61% at 2.1 × 10 M, < 0.001, at 12 and 49 weeks). The soleus was less impaired at 12 weeks by THC and EtOH association than the gastrocnemius (-49.92 ±1.69 vs. -27.22 ± 8.96% in gastrocnemius and soleus, respectively, < 0.05). In conclusion, EtOH, alone and associated with THC, significantly impairs skeletal muscle mitochondrial respiration and THC aggravates EtOH-induced effects on young glycolytic muscle. Age and metabolic phenotypes modulate these deleterious effects, with the glycolytic muscles of young rats being more prone to impairments than oxidative muscles. |
| Author | Meyer, Alain Giannini, Margherita Talha, Samy Charles, Anne-Laure Charloux, Anne Geny, Bernard Wolff, Valérie Vogel, Thomas Raul, Jean-Sébastien |
| AuthorAffiliation | 5 Neuro-Vascular Department, University Hospital of Strasbourg, 67200 Strasbourg, France 4 Toxicology Laboratory, Institute of Legal Medicine, Faculty of Medicine, University of Strasbourg, 67000 Strasbourg, France; js.raul@unistra.fr 3 Geriatrics Department, University Hospital of Strasbourg, 67200 Strasbourg, France 2 Physiology and Functional Explorations Department, University Hospital of Strasbourg, 67000 Strasbourg, France 1 UR 3072, “Mitochondria, Oxidative Stress and Muscle Plasticity”, Biomedicine Research Center of Strasbourg (CRBS), Faculty of Medicine, University of Strasbourg, 67000 Strasbourg, France; anne.laure.charles@unistra.fr (A.-L.C.); margherita.giannini@chru-strasbourg.fr (M.G.); alain.meyer1@chru-strasbourg.fr (A.M.); anne.charloux@chru-strasbourg.fr (A.C.); samy.talha@chru-strasbourg.fr (S.T.); thomas.vogel@chru-strasbourg.fr (T.V.); valerie.wolff@chru-strasbourg.fr (V.W.) |
| AuthorAffiliation_xml | – name: 1 UR 3072, “Mitochondria, Oxidative Stress and Muscle Plasticity”, Biomedicine Research Center of Strasbourg (CRBS), Faculty of Medicine, University of Strasbourg, 67000 Strasbourg, France; anne.laure.charles@unistra.fr (A.-L.C.); margherita.giannini@chru-strasbourg.fr (M.G.); alain.meyer1@chru-strasbourg.fr (A.M.); anne.charloux@chru-strasbourg.fr (A.C.); samy.talha@chru-strasbourg.fr (S.T.); thomas.vogel@chru-strasbourg.fr (T.V.); valerie.wolff@chru-strasbourg.fr (V.W.) – name: 5 Neuro-Vascular Department, University Hospital of Strasbourg, 67200 Strasbourg, France – name: 3 Geriatrics Department, University Hospital of Strasbourg, 67200 Strasbourg, France – name: 2 Physiology and Functional Explorations Department, University Hospital of Strasbourg, 67000 Strasbourg, France – name: 4 Toxicology Laboratory, Institute of Legal Medicine, Faculty of Medicine, University of Strasbourg, 67000 Strasbourg, France; js.raul@unistra.fr |
| Author_xml | – sequence: 1 givenname: Anne-Laure orcidid: 0000-0003-3557-2642 surname: Charles fullname: Charles, Anne-Laure – sequence: 2 givenname: Margherita surname: Giannini fullname: Giannini, Margherita – sequence: 3 givenname: Alain surname: Meyer fullname: Meyer, Alain – sequence: 4 givenname: Anne surname: Charloux fullname: Charloux, Anne – sequence: 5 givenname: Samy orcidid: 0000-0002-2094-2842 surname: Talha fullname: Talha, Samy – sequence: 6 givenname: Thomas surname: Vogel fullname: Vogel, Thomas – sequence: 7 givenname: Jean-Sébastien surname: Raul fullname: Raul, Jean-Sébastien – sequence: 8 givenname: Valérie surname: Wolff fullname: Wolff, Valérie – sequence: 9 givenname: Bernard orcidid: 0000-0002-5824-6359 surname: Geny fullname: Geny, Bernard |
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| Keywords | alcohol tetrahydrocannabinoid mitochondria cannabis EtOH marijuana ethanol THC glycolytic metabolic phenotype oxidative aging skeletal muscle skeletal muscle metabolic phenotype glycolytic oxidative aging mitochondria tetrahydrocannabinoid cannabis marijuana THC alcohol ethanol EtOH |
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| Title | Cannabis (THC) Aggravates the Deleterious Effects of Alcohol (EtOH) on Skeletal Muscles’ Mitochondrial Respiration: Modulation by Age and Metabolic Phenotypes |
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