Effect of succinate on mitochondrial lipid peroxidation. 2. The protective effect of succinate against functional and structural changes induced by lipid peroxidation

Tretter, László; Szabados, Gy.; Ando, Akio; Horváth, István

doi:10.1007/bf00769730

Cited by 27 publications

(2 citation statements)

References 23 publications

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“…Pharmaceutical preparations containing succinic acid have been used for a long time as antioxidants that normalize intracellular metabolism and promote the restoration of organ functions impaired by diseases or natural cell aging. The antihypoxic effects of succinic acid salts are enhanced by their antioxidant properties, their ability to modify phospholipids and facilitate their resynthesis, as well as reduce ion permeability of membranes and the efflux of K+ from mitochondria against the concentration gradient [2,17].…”

Section: Discussionmentioning

confidence: 99%

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Quantitative characteristics of structural changes in the myocardium of white rats during the modeling of adrenaline myocardiodystrophy and its pharmacological correction

Herasymyuk

2023

Rep. of Morph.

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Pathology of the cardiovascular system is one of the leading causes of mortality and disability. In anesthesiology practice, it is the most common comorbid condition that leads to perioperative complications and fatal outcomes. The aim of the study was to substantiate the cardioprotective properties of succinic acid, sodium oxybutyrate, and quercetin based on the study of the myocardial morphological structure in the correction of experimental cardiac pathology. The experiments were conducted on white rats, in which adrenaline-induced myocardial dystrophy was modeled. The correction was performed using succinic acid, sodium oxybutyrate, and quercetin. Morphological studies were conducted at 2 and 24 hours after correction. At 2 hours after adrenaline administration, pronounced venous and arterial congestion was observed in the myocardium. The lumen of vessels appeared dilated, and their walls appeared thinner. In animals that received corrective agents after adrenaline, a positive effect of their application was noted. Vascular congestion was significantly reduced. The arterial walls had normal thickness, and the internal elastic membranes were moderately tortuous. No significant changes were observed in cardiomyocytes. At 24 hours from the start of pathology modeling and its pharmacological correction, the changes in the myocardium of the animals were much more pronounced compared to those with a 2-hour exposure, although in animals treated with corrective agents, the changes were less pronounced than in untreated animals. Rats exposed only to adrenaline showed significant trophic disturbances in cardiomyocytes, which developed against the background of coronary circulation disorders, manifested as wall thickening and narrowing of arterial lumens. The veins were congested, and blood extravasation was observed in the interstitium. Perivascular spaces expanded due to edema. Cardiomyocytes exhibited dystrophic changes, including areas with clarified cytoplasm, often with its homogenization and karyolysis. Histological data were morphometrically confirmed by changes in the Wogenworth index and nuclear-cytoplasmic ratios. The obtained results indicate the positive effect of the used corrective agents. Quercetin demonstrated slightly higher efficacy in this regard.

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Section: Discussionmentioning

confidence: 99%

“…Potentially, all antihypoxants, regardless of their chemical structure, can have secondary antioxidant effects due to their energy-stabilizing and antacid properties, which prevent excessive formation of free radicals and suppress endogenous ones [17].…”

Section: Discussionmentioning

confidence: 99%

Quantitative characteristics of structural changes in the myocardium of white rats during the modeling of adrenaline myocardiodystrophy and its pharmacological correction

Herasymyuk

2023

Rep. of Morph.

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Stimulation of H₂O₂ generation by calcium in brain mitochondria respiring on α‐glycerophosphate

Tretter

Takács

Kövér

et al. 2007

J of Neuroscience Research

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It has been reported recently (Tretter et al., 2007b) that in isolated guinea pig brain mitochondria supported by alpha-glycerophosphate (alpha-GP) reactive oxygen species (ROS) are produced through the reverse electron transport (RET) in the respiratory chain and by alpha-glycerophosphate dehydrogenase (alpha-GPDH). We studied the effect of calcium on the generation of H(2)O(2) as measured by the Amplex Red fluorescent assay in this model. H(2)O(2) production in alpha-GP-supported mitochondria was increased significantly in the presence of 100, 250, and 500 nM Ca(2+), respectively. In addition, Ca(2+) enhanced the membrane potential, the rate of oxygen consumption, and the NAD(P)H autofluorescence in these mitochondria. Direct measurement of alpha-GPDH activity showed that Ca(2+) stimulated the enzyme by decreasing the Km for alpha-GP. In those mitochondria where RET was eliminated by the Complex I inhibitor rotenone (2 microM) or due to depolarization by ADP (1 mM), the rate of H(2)O(2) formation was smaller and the stimulation of H(2)O(2) generation by Ca(2+) was prevented partly, but the stimulatory effect of Ca(2+) was still significant. These data indicate that in alpha-GP-supported mitochondria activation of alpha-GPDH by Ca(2+) leads to an accelerated RET-mediated ROS generation as well as to a stimulated ROS production by alpha-GPDH.

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Ferrous-iron induces lipid peroxidation with little damage to energy transduction in mitochondria

1993

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Addition of ferrous sulfate, but not ferric chloride, in micromolar concentrations to rat liver mitochondria induced high rates of consumption of oxygen. The oxygen consumed was several times in excess of the reducing capacity of ferrous-iron (O:Fe ratios 5-8). This occurred in the absence of NADPH or any exogenous oxidizable substrate. The reaction terminated on oxidation of ferrous ions. Malondialdehyde (MDA), measured as thiobarbituric acid-reacting material, was produced indicating peroxidation of lipids. The ratio of O2:MDA was about 4:1. Pretreatment of mitochondria with ferrous sulfate decreased the rate of oxidation (state 3) with glutamate (+ malate) as the substrate by about 40% but caused little damage to energy transduction process as represented by ratios of ADP:O and respiratory control, as well as calcium-stimulated oxygen uptake and energy-dependent uptake of [45Ca]-calcium. Addition of succinate or ubiquinone decreased ferrous iron-induced lipid peroxidation in intact mitochondria. In frozen-thawed mitochondria, addition of succinate enhanced lipid peroxidation whereas ubiquinone had little effect. These results suggest that ferrous-iron can cause peroxidation of mitochondrial lipids without affecting the energy transduction systems, and that succinate and ubiquinone can offer protection from damage due to such ferrous-iron released from the stores within the cells.

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Effect of succinate on mitochondrial lipid peroxidation. 2. The protective effect of succinate against functional and structural changes induced by lipid peroxidation

Cited by 27 publications

References 23 publications

Quantitative characteristics of structural changes in the myocardium of white rats during the modeling of adrenaline myocardiodystrophy and its pharmacological correction

Quantitative characteristics of structural changes in the myocardium of white rats during the modeling of adrenaline myocardiodystrophy and its pharmacological correction

Stimulation of H₂O₂ generation by calcium in brain mitochondria respiring on α‐glycerophosphate

Ferrous-iron induces lipid peroxidation with little damage to energy transduction in mitochondria

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Effect of succinate on mitochondrial lipid peroxidation. 2. The protective effect of succinate against functional and structural changes induced by lipid peroxidation

Cited by 27 publications

References 23 publications

Quantitative characteristics of structural changes in the myocardium of white rats during the modeling of adrenaline myocardiodystrophy and its pharmacological correction

Quantitative characteristics of structural changes in the myocardium of white rats during the modeling of adrenaline myocardiodystrophy and its pharmacological correction

Stimulation of H2O2 generation by calcium in brain mitochondria respiring on α‐glycerophosphate

Ferrous-iron induces lipid peroxidation with little damage to energy transduction in mitochondria

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Stimulation of H₂O₂ generation by calcium in brain mitochondria respiring on α‐glycerophosphate