[58] Preparation of succinate dehydrogenase and reconstitution of succinate oxidase

SummaryThe effect of administration of thioacetamide on rat liver mitochondrial functions and the protective effect of an aqueous extract of Phyllanthus fraternus against thioacetamide-induced damage were studied. When rats were treated with thioacetamide, the rate of mitochondrial respiration was decreased significantly with both NAD+ linked and FAD linked substrates, and the respiratory control ratio, an index of membrane integrity and the P/O ratio, a measure of phosphorylation efficiency, decreased significantly. Also, there was a significant decrease in the activities of NADH dehydrogenase, succinate cytochrome c reductase, and cytochrome oxidase; whereas succinate dehydrogenase was not affected. A significant decrease was seen in membrane potential and in the level of mitochondrial ATP. There was a significant decrease in the levels of phosphatidylcholine, phosphatidylethanolamine, and cardiolipin by thioacetamide treatment. The lipid peroxide level increased significantly in thioacetamide-treated rats. Administration of P. fraternus prior to thioacetamide treatment relieved the inhibition of all the parameters studied, and brought down the lipid peroxide levels significantly in liver homogenates and mitochondria. This study shows that P, fraternus protects against thioacetamide-induced toxicity by its ability to suppress the elevated lipid peroxide levels in the mitochondrial membrane.

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“…The reduction of DCPIP was followed at 600 nm [14]. The activity of the enzyme was expressed as nmol of DCPIP reduced per min per mg protein.…”

Section: Methodsmentioning

confidence: 99%

Protective Effect of Phyllanthus fraternus against Thioacetamide-Induced Mitochondrial Dysfunction.

Padma

Setty

1997

J. Clin. Biochem. Nutr.

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“…SDH was measured spectrophotometrically by the method reported by King (1967). It involves the oxidation of succinate by an artificial electron acceptor, potassium ferricyanide.…”

Section: Complex-ii [Succinate Dehydrogenase (Sdh) Activity]mentioning

confidence: 99%

Ameliorative effect of naringin against doxorubicin-induced acute cardiac toxicity in rats

Kwatra

Kumar

Jangra

et al. 2015

Pharmaceutical Biology

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Context: Doxorubicin (Dox) is one of the most active chemotherapeutic agents used to treat various types of cancers. Its clinical utility is compromised due to fatal cardiac toxicity characterized by an irreversible cardiomyopathy. Objective: This study evaluates the cardioprotective potential of naringin (NR) against Dox-induced acute cardiac toxicity in rats. Materials and methods: Male Wistar rats were randomly divided into five groups. NR (50 and 100 mg/kg) was administered intraperitoneally (i.p.) daily from 0 to 14 d. Doxorubicin (15 mg/kg, i.p.) was given as a single dose on the 10th day. On the 14th day, all animals were sacrificed and oxidative stress parameters that include malondialdehyde (MDA), glutathione (GSH) level, superoxide dismutase (SOD), catalase (CAT) activities, and all mitochondrial complexes (I-IV) activities were evaluated along with histopathological studies of the heart. Results: Doxorubicin-induced cardiotoxicity was confirmed by increased (p50.05) MDA, decreased (p50.05) GSH levels, SOD, and CAT activities, mitochondrial complexes (I-IV) activities in the heart tissue. NR (100 mg/kg) showed cardioprotection as evident from significant decreased MDA (p50.001) level, raised (p50.001) GSH level, SOD and CAT activities and increased mitochondrial complexes I (p50.01), II (p50.001), III (p50.001), and IV (p50.05) activities. Further, Dox-induced cardiotoxicity was confirmed by histopathological studies. These obtained results indicated the protective role of NR against Dox-induced cardiac toxicity in rats. Conclusion: NR can be used in combination with Dox due to its high cardioprotective effect against Dox-induced cardiomyopathy.

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“…Complex II-Complex II (succinate decylubiquinone 2,6-dichloroindophenol oxidoreductase) activity was determined by measuring the reduction of 2,6-dichloroindophenol at 600 nm as described previously (43,44). The Complex II assay was performed in buffer containing 25 mM potassium phosphate (pH 7.4), 20 mM succinate, 2 mM KCN, 50 M 2,6-dichloroindophe-nol, 2 g/ml rotenone, and 2 g/ml antimycin.…”

Section: Enzymatic Characterization Of Electron Transport Chain and Fmentioning

confidence: 99%

Myocardial Regulation of Lipidomic Flux by Cardiolipin Synthase

Kiebish

Yang

Sims

et al. 2012

Journal of Biological Chemistry

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Background: Maintenance of cardiolipin molecular speciation by remodeling directly regulates mitochondrial bioenergetic efficiency. Results: Transgenic expression of cardiolipin synthase accelerates cardiolipin remodeling, improves mitochondrial function, modulates mitochondrial signaling, and attenuates mitochondrial dysfunction during diabetes. Conclusion: Cardiolipin synthase integrates multiple aspects of mitochondrial bioenergetic and signaling functions. Significance: Cardiolipin synthase expression attenuates mitochondrial dysfunction in diabetic myocardium.

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[58] Preparation of succinate dehydrogenase and reconstitution of succinate oxidase

Cited by 453 publications

References 4 publications

Protective Effect of Phyllanthus fraternus against Thioacetamide-Induced Mitochondrial Dysfunction.

Protective Effect of Phyllanthus fraternus against Thioacetamide-Induced Mitochondrial Dysfunction.

Ameliorative effect of naringin against doxorubicin-induced acute cardiac toxicity in rats

Myocardial Regulation of Lipidomic Flux by Cardiolipin Synthase

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