Simon 2022 Function (Oxf): Difference between revisions

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|area=Pharmacology;toxicology
|area=Pharmacology;toxicology
|enzymes=Complex II;succinate dehydrogenase
|enzymes=Complex II;succinate dehydrogenase
|instruments=Oxygraph-2k
|additional=EtOH
|additional=EtOH
}}
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[[File:Simon 2022 Function (Oxf) CORRECTION.png|right|800px]]
[[File:Simon 2022 Function (Oxf) CORRECTION.png|right|800px]]
{{Template:Correction FADH2 and S-pathway}}
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Revision as of 12:11, 12 July 2023

Publications in the MiPMap
Simon L, Molina PE (2022) Cellular bioenergetics: experimental evidence for alcohol-induced adaptations. Function (Oxf) 3:zqac039. https://doi.org/10.1093/function/zqac039

Β» PMID: 36120487 Open Access

Simon L, Molina PE (2022) Function (Oxf)

Abstract: At-risk alcohol use is associated with multisystemic effects and end-organ injury, and significantly contributes to global health burden. Several alcohol-mediated mechanisms have been identified, with bioenergetic maladaptation gaining credence as an underlying pathophysiological mechanism contributing to cellular injury. This evidence-based review focuses on the current knowledge of alcohol-induced bioenergetic adaptations in metabolically active tissues: liver, cardiac and skeletal muscle, pancreas, and brain. Alcohol metabolism itself significantly interferes with bioenergetic pathways in tissues, particularly the liver. Alcohol decreases states of respiration in the electron transport chain, and activity and expression of respiratory complexes, with a net effect to decrease ATP content. In addition, alcohol dysregulates major metabolic pathways, including glycolysis, the tricarboxylic acid cycle, and fatty acid oxidation. These bioenergetic alterations are influenced by alcohol-mediated changes in mitochondrial morphology, biogenesis, and dynamics. The review highlights similarities and differences in bioenergetic adaptations according to tissue type, pattern of (acute vs. chronic) alcohol use, and energy substrate availability. The compromised bioenergetics synergizes with other critical pathophysiological mechanisms, including increased oxidative stress and accelerates cellular dysfunction, promoting senescence, programmed cell death, and end-organ injury.

β€’ Bioblast editor: Gnaiger E


Labels: MiParea: Pharmacology;toxicology 



Enzyme: Complex II;succinate dehydrogenase 


HRR: Oxygraph-2k 

EtOH 

Simon 2022 Function (Oxf) CORRECTION.png

Correction: FADH2 and Complex II

Ambiguity alert.png
FADH2 is shown as the substrate feeding electrons into Complex II (CII). This is wrong and requires correction - for details see Gnaiger (2024).
Gnaiger E (2024) Complex II ambiguities ― FADH2 in the electron transfer system. J Biol Chem 300:105470. https://doi.org/10.1016/j.jbc.2023.105470 - Β»Bioblast linkΒ«
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