Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.3.5.1 (succinate dehydrogenase)
 8,177 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of rhein on the oxygen consumption, oxidative phosphorylation, ATPase activity and redox state of electron carriers of rat liver mitochondria has been studied. Rhein inhibits ADP- and uncoupler-stimulated respiration on various NAD-linked substrates and succinate, but stimulates state 4 respiration of mitochondria respiring on succinate. Experiments on specific segments of the respiratory chain showed that rhein does not inhibit electron flow through cytochrome oxidase. Electron flow through site 2, the ubiquinone-cytochrome b-cytochrome c1 complex, was also unaffected by rhein, which failed to inhibit the oxidation of duroquinol. Rhein affects oxidative phosphorylation by inhibiting both electron transfer and ADP-driven H+ uptake. The inhibition of succinate oxidation by rhein was found to take place at a point between succinate and ubiquinone, perhaps at the level of succinic dehydrogenase. Spectroscopic evidence demonstrated that rhein induces a NAD(P)H oxidation in mitochondria respiring either on endogenous substrates or on glutamate + malate, and an inhibition of the cytochrome b reduction by succinate. These observations, together with other evidence, suggest that rhein inhibits electron transport in rat liver mitochondria at the dehydrogenase-coenzyme level, particularly when the electron carriers are in a relatively oxidized state and/or when the inner membrane-matrix compartment is in the condensed state.
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PMID:Sites of inhibition of mitochondrial electron transport by rhein. 252 79

The biochemical consequences of moderate chronic ethanol ingestion has been scarcely investigated in spite of the fact that most of the human population drinks ethanol on a moderate basis. This paper describes some metabolic effects produced by moderate ethanol consumption. The substitution of drinking water in rats for a 10% ethanol solution during 4 weeks resulted in: a) a decrease of blood urea and citrulline synthesis in liver mitochondria; b) a slight inhibition in state 3 and state 4 respiration either with glutamate-malate as substrates or succinate as substrate; c) no change in ADP/O ratio with succinate but slight increase with glutamate-malate; d) a reduction of the cytochrome oxidase activity and cytochromes a+a3 content; e) a 42% increase in the succinate dehydrogenase activity and a small but constant increase in the Vmax (no change in the Km) of the adenine nucleotide translocase activity in liver mitochondria. These results show that even moderate, but continuous ethanol ingestion, produces metabolic responses that must be carefully evaluated to define health risk in larger human groups.
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PMID:Effects of moderate chronic ethanol consumption on rat liver mitochondrial functions. 254 37

The inhibitory effects of pure galloylglucose (1,2,3,4,6-penta-O-galloyl-beta-D-glucose) on the respiratory chain of rat liver mitochondria were investigated. The respiratory control ratio (RCR) decreased by 50% on addition of 20 microM pentagalloylglucose to highly coupled mitochondria, but the adenosine-5'-diphosphate/oxygen (ADP/O) ratio decreased only slightly. The RCR disappeared and the ADP/O ratio could not be measured at concentrations of pentagalloylglucose above 30 microM. On the other hand, the uncoupler-induced oxygen consumption was also inhibited. These findings suggest that pentagalloylglucose at low concentrations inhibits the electron transport system to decrease the RCR, but scarcely impairs the membrane, practically retaining the coupled reaction, while at high concentrations it impairs the structural integrity of the mitochondrial membrane. Pentagalloylglucose competitively inhibited succinate dehydrogenase activity, and noncompetitively inhibited reduced nicotinamide adenine dinucleotide (NADH) dehydrogenase and ubiquinol-1 oxidase activities of submitochondrial particles (SMP). However, it did not show significant inhibition of the cytochrome c oxidase activity of SMP. It is thus concluded that pentagalloylglucose, which is the lowest-molecular-weight component of tannic acid, exerts its effect on mitochondrial respiration and oxidative phosphorylation through action on the membrane and on succinate dehydrogenase, NADH dehydrogenase and cytochrome bc1 complex of mitochondria.
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PMID:The effects of 1,2,3,4,6-penta-O-galloyl-beta-D-glucose on rat liver mitochondrial respiration. 263 Jan

Lipid peroxidation in brain mitochondria was induced by NADH in the presence of ADP and FeCl3. A novel quinone compound, idebenone, inhibited this peroxidation and the inhibition was markedly enhanced by succinate, a substrate of mitochondrial respiration. The concentration of succinate required to exert the maximal effect was 1.5 mM. The concentration of idebenone giving 50% inhibition (IC50) was 0.5 and 84 microM in the presence and absence of succinate, respectively, indicating that succinate enhances the inhibition by 170-fold. Moreover, the inhibitory effect of idebenone in the presence of succinate was abolished by adding thenoyltrifluoroacetate (TTFA), an inhibitor of complex II in the mitochondrial respiratory chain. These results indicate that idebenone is changed through complex II to its reduced form, which protects mitochondria against lipid peroxidation.
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PMID:Inhibition of lipid peroxidation by idebenone in brain mitochondria in the presence of succinate. 276 44

The effects of several natural products extracted from the leaves of Stevia rebaudiana on rat liver mitochondria were investigated. The compounds used were stevioside (a non-caloric sweetener), steviolbioside, isosteviol and steviol. Total aqueous extracts of the leaves were also investigated. S. rebaudiana natural products inhibited oxidative phosphorylation, ATPase activity NADH-oxidase activity, succinate-oxidase activity, succinate dehydrogenase, and L-glutamate dehydrogenase. The ADP/O ratio was decreased. Substrate respiration (state II respiration) was increased at low concentrations (up to 0.5 mM) and inhibited at higher concentrations (1 mM or more). In uncoupled mitochondria, inhibition of substrate respiration was the only effect observed. Net proton ejection induced by succinate and swelling induced by several substrates were inhibited. Of the compounds investigated, the sweet principle stevioside was less active. It was concluded that, in addition to the inhibitory effects, S. rebaudiana natural products may also act as uncouplers of oxidative phosphorylation. The possible physiologic consequences of the ingestion of stevioside and S. rebaudiana aqueous extracts are discussed.
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PMID:Effects of Stevia rebaudiana natural products on rat liver mitochondria. 285 11

It has been proposed that the acquisition of efficient energy-transducing mitochondria after birth is mediated by an ATP-dependent mechanism "that causes the rapid maturation of mitochondria without requiring either transcription or translation" (Pollak, J. K., and Sutton, R. (1980) Trends Biochem. Sci. 5, 23-27). Investigation of developmental changes in rat liver mitochondria during the first 6 postnatal h showed that fetal mitochondria had low State 4, State 3, and uncoupled rates of respiration, inefficient coupling between respiration and phosphorylation, and low membrane potentials and proton electrochemical gradients under State 4 conditions. In contrast, hepatic mitochondria from 1-h-old neonates showed increased respiratory control and ADP/O ratios and adult proton electrochemical gradient and membrane potential values. In parallel with these changes, mitochondria became enriched in adenine nucleotides and underwent a 50% reduction in matrix volume. During the first postnatal hour, an increase in mitochondrial succinic dehydrogenase, cytochrome c oxidase, and F1-ATPase activities takes place in the neonatal liver concurrent with a preferential postnatal increase in the in vivo rates of protein synthesis for mitochondrial proteins. In particular, the amount of F1-ATPase increased from 109 +/- 9 to 206 +/- 5 ng/microgram of mitochondrial protein in the first hour of postnatal life. Inhibitors of cytosolic protein synthesis present during the first 2 h of life blocked the postnatal increase in respiratory control and ADP/O ratios, succinic dehydrogenase activity, and F1-ATPase content; but they had no effect on the increase in adenine nucleotide concentrations and mitochondrial volume contraction. This indicates that the acquisition of an efficient coupling between respiration and phosphorylation is dependent on de novo protein synthesis and cannot be brought about by the postnatal increase in adenine nucleotides. The increase of State 4 and uncoupled rates of respiration during the first 2 postnatal h was resistant to protein synthesis inhibitors. We suggest that the postnatal increase in these parameters is due to the reduction of mitochondrial volume occurring during that time, which, in turn, may be triggered by the concurrent enrichment in adenine nucleotides.
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PMID:Postnatal development of rat liver mitochondrial functions. The roles of protein synthesis and of adenine nucleotides. 289 64

Mitochondrial enzymes and respiration were studied in the hearts of mice exposed to ethanol in utero from gestational Day 8 to parturition. This treatment had previously been shown by electron microscopy to result in myofibril loss and mitochondrial abnormalities. Ethanol was administered to pregnant mice by a liquid diet paradigm and pair-fed dams were used as controls. Ethanol exposure in utero reduced the activities of two mitochondrial inner membrane enzymes, cytochrome c oxidase and succinate dehydrogenase, in the hearts of perinatal mice. Secondly, mitochondrial respiration under both State 3 and 4 conditions with a NAD-linked substrate was depressed in the hearts obtained from the ethanol-exposed fetal mice. However, when a flavin-linked substrate was used, State 3 (ADP-stimulated) but not State 4 respiration was depressed. This study illustrates that in utero exposure to ethanol is deleterious to the functioning of cardiac mitochondria in newborn mice, which in turn could contribute to the development of the heart pathologies present in the Fetal Alcohol Syndrome.
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PMID:Cardiac mitochondrial abnormalities in a mouse model of the fetal alcohol syndrome. 289 3

The effect of Prudhoe Bay crude oil (PBCO) and its different fractions [aliphatic, aromatic, heterocyclic (NOS)] on the bioenergetic functions of isolated rat liver mitochondria were studied. A DMSO extract of PBCO inhibited state 3 respiration (in the presence of ADP) with either succinate or beta-hydroxybutyrate as substrate. The ascorbate-TMPD dependent state 3 respiration was not affected. Succinate dehydrogenase and beta-hydroxybutyrate dehydrogenase activities were also lost in the presence of the PBCO extract suggesting that inhibition of state 3 respiration may be due to blockage of the electron transport chain. Stimulation of state 4 respiration (in the absence of ADP) and of the oligomycin sensitive ATPase activity by the PBCO extract was observed. Fractionation of PBCO indicated that the aromatic fraction was mainly responsible for its inhibitory effects. By comparison, the heterocyclic fraction had weak inhibitory properties while the aliphatic fraction was essentially inactive. It is concluded that the aromatic components of PBCO inhibit mitochondrial respiration and oxidative phosphorylation mainly through impairment of the mitochondrial membrane and inhibition of beta-hydroxybutyrate and succinate dehydrogenase supported electron transfer activities of the respiratory chain.
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PMID:Mechanisms of petroleum hydrocarbon toxicity: studies on the response of rat liver mitochondria to Prudhoe Bay crude oil and its aliphatic, aromatic and heterocyclic fractions. 294 97

The effect of W. somnifera on glycosaminoglycan synthesis in the granulation tissue of carrageenin-induced air pouch granuloma was studied. W. somnifera was shown to exert significant inhibitory effect on incorporation of 35S into the granulation tissue. The uncoupling effect on oxidative phosphorylation (ADP/O ratio reduction) was also observed in the mitochondria of granulation tissue. Further, Mg2+ dependent ATPase activity was found to be influenced by W. somnifera. W. somnifera also reduced the succinate dehydrogenase enzyme activity in the mitochondria of granulation tissue.
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PMID:Effect of Withania somnifera on glycosaminoglycan synthesis in carrageenin-induced air pouch granuloma. 296 52

Proteolytic activities in bovine adrenocortical mitochondria were investigated using [14C-methyl]casein as a substrate. Washed mitochondria showed a low proteolytic activity at pH 7.5 or 8.2. ATP (5 mM) plus MgCl2 (7.5 mM) stimulated the proteolysis 9 times at pH 8.2. It was further demonstrated unequivocally by various approaches that the ATP-dependent proteolytic activity localizes in mitochondrial matrix. The activity of the solubilized protease was sensitive to N-ethylmaleimide, mersalyl acid, phenylmethylsulfonyl fluoride, o-vanadate, m-vanadate, vanadyl sulfate, and quercetin but not by oligomycin and ouabain. The ATP-dependent proteolytic activity was eluted at the position of 650,000 daltons on an Ultrogel AcA 22 column as a single symmetrical peak. The gel-filtered enzyme showed high specificity to ATP. GTP and UTP partially substituted ATP. ADP, AMP, tripolyphosphate, alpha, beta-methylene ATP, and beta, gamma-methylene ATP had little or no stimulating activity. ATP did not stimulate the activity in the absence of MgCl2. We measured ATP-dependent proteolytic activities in mitochondrial fractions from several tissues in rat and bovine. Adrenal cortex was one of the tissues of highest activity. In addition, we investigated the effect of adrenal atrophy on the ATP-dependent protease activity in rat adrenal. The ATP-dependent protease activity/adrenal decreased by dexamethasone treatment. The extent of the decrease was similar to that of cytochrome oxidase and succinate dehydrogenase, but smaller than that of cytochrome P-450.
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PMID:ATP-dependent protease in bovine adrenal cortex. Tissue specificity, subcellular localization, and partial characterization. 298 96


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