Differential Investigation of the Capacity of Succinate Oxidation in Human Skeletal Muscle

Overview

Journal Clin Chim Acta

Specialty Biochemistry

Date 1985 Nov 29

PMID 3000647

Citations 159

Authors

J C Fischer

W Ruitenbeek

J A Berden

J M Trijbels

J H Veerkamp

A M STADHOUDERS

R C Sengers

A J Janssen

Affiliations

Soon will be listed here.

Abstract

Procedures are described for the estimation of the succinate:ubiquinone oxidoreductase and succinate:phenazine methosulfate oxidoreductase activities in post-nuclear supernatants of human skeletal muscle homogenates using 2,6-dichlorophenol indophenol as the terminal electron acceptor. The influence of ionic strength and of sucrose upon these assays and upon the succinate:cytochrome c oxidoreductase activity has been investigated. Sucrose markedly interferes with the activation of the succinate dehydrogenase complex. Succinate:cytochrome c oxidoreductase activity and succinate:phenazine methosulfate oxidoreductase activity are inhibited by increasing concentrations of ions and of sucrose. Our results lead us to propose the existence of a single acceptor site for phenazine methosulfate at the succinate dehydrogenase complex, not involved in the physiological electron flux across ubiquinone. Estimation of the enzymatic activities mentioned above allows differential investigation of the functional integrity of a large part of the respiratory chain in patients suspected of suffering from a neuromuscular disorder.

Citing Articles

α-Ketoisocaproic Acid Disrupts Mitochondrial Bioenergetics in the Brain of Neonate Rats: Molecular Modeling Studies of α-ketoglutarate Dehydrogenase Subunits Inhibition.

Zemniacak A, Ribeiro R, das Neves G, Cunha S, Tavares T, Carvalho A Neurochem Res. 2025; 50(1):76.

PMID: 39786600 DOI: 10.1007/s11064-024-04328-0.

Increased ROS levels, antioxidant defense disturbances and bioenergetic disruption induced by thiosulfate administration in the brain of neonatal rats.

Glanzel N, da Rosa-Junior N, Signori M, de Andrade Silveira J, Pinheiro C, Marcuzzo M Metab Brain Dis. 2024; 40(1):73.

PMID: 39704910 DOI: 10.1007/s11011-024-01510-9.

Ayahuasca Pretreatment Prevents Sepsis-Induced Anxiety-Like Behavior, Neuroinflammation, and Oxidative Stress, and Increases Brain-Derived Neurotrophic Factor.

de Camargo R, Joaquim L, Machado R, de Souza Ramos S, da Rosa L, de Novais Junior L Mol Neurobiol. 2024; .

PMID: 39613951 DOI: 10.1007/s12035-024-04597-4.

Targeting glycolysis for neuroprotection in early LPS-induced neuroinflammation.

Vizuete A, Froes F, Seady M, Caurio A, Ramires Junior O, Leite A Brain Behav Immun Health. 2024; 42:100901.

PMID: 39583162 PMC: 11582448. DOI: 10.1016/j.bbih.2024.100901.

Oxidative stress and mitochondrial dysfunction contributes to postoperative cognitive dysfunction in elderly rats dependent on NLRP3 activation.

Bonfante S, Netto M, de Oliveira Junior A, Mathias K, Machado R, Joaquim L Metab Brain Dis. 2024; 40(1):1.

PMID: 39535569 DOI: 10.1007/s11011-024-01425-5.