Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

An analysis of starvation and starvation followed by refeeding was undertaken to characterize some organismic, organ, and mitochondrial responses to these two circumstances. Body weight, organismic respiration as well as weight protein and succinic dehydrogenase activity for liver, kidney, and heart were determined over the course of 6 days of starvation and 5 days refeeding for adult male rats. Assays of marker enzyme activities for mitochondria (cytochrome oxidase), lysosomes (acid phosphatase), endoplasmic reticulum (glucose-6-phosphatase), and plasma membranes (5'-nucleotidase) were conducted for liver in addition to quantitations of mitochondrial protein. All enzyme determinations were done on whole tissue homogenates and reported as total organ activity. Liver mitochondria were harvested quantitatively directly from whole liver homogenates by zonal centrifugation for determination of mitochondrial protein. Starvation resulted in a major loss of body weight, organ weight, and organ protein; liver greater than kidney greater than heart. These changes were accompanied by a major reduction in organ succinic dehydrogenase activity; liver greater than kidney. In heart, succinic dehydrogenase was doubled in activity at day 2 of starvation and subsequently diminished to values not significantly lower than controls. In liver, mitochondrial mass (protein) was severely diminished. From analysis of marker enzyme activities, it appeared that lysosomes, endoplasmic reticulum, and plasma membrane were also decreased. Refeeding restored the greatest part of these losses within 5 days.
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PMID:Starvation and refeeding in rats: effect on organismic respiration, cytoplasmic constituents of liver, and succinic dehydrogenase activity in liver, kidney, and heart. 70 2

Male rats were subjected to early undernutrition by limiting the mothers' food supply by 50% during pregnancy and lactation. At age 36 weeks, quantitative cytochemical determinations of succinic dehydrogenase activity were made in muscle fibres from the anterior tibialis and soleus muscles. Marked decreases were found in the former muscle but relatively little decrease was seen in the latter. This response of the muscles to early undernutrition was discussed with reference to other studies on pre and post-natal starvation.
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PMID:The effects of pre- and perinatal undernutrition on the succinic dehydrogenase content of muscle fibres from fast and slow rat muscles. 73 May 56

Succinate dehydrogenase activity was determined in the liver and heart of newborn rats after 3 and 48 hours' exposure to anoxic hypoxia (10% O2) and after 48 hours' starvation. Control determinations were made on newborn animals of corresponding ages, full term foetuses (21 days), infantile (1 and 2 weeks) and full grown animals. Hypoxia for 3 h had no influence on succinate dehydrogenase activity at all in either the heart or liver mitochondria of the newborn animals. After 48 h no difference was observed in the liver between the hypoxic animals and the starved controls of the same age, though starvation itself had resulted in a significant increase in activity, as much as 42%. When liver mitochondrial succinate dehydrogenase in normal mitochondria was activated by preincubation mitochondria with the substrate, the activity increase obtained was greater than that resulting from starvation. The increase in activity in the heart of the hypoxic or starved animals was not significant (less than 10%).
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PMID:Liver and heart mitochondrial succinate dehydrogenase activity of newborn rats in anoxic hypoxia and starvation. 96 47

Whole cells, homogenates and mitochondrial obtained from the livers of albino rats which were starved for 6 days or more showed a 50% decrease in oxidative activity. The decrease could be corrected by the addition of cytochrome c in vitro. The phosphorylative activity of mitochondria remained unaffected. The decrease in oxidative rate was not observed when starving animals were given the anti-hypercholesterolaemic drug clofibrate. The total cellular concentration of cytochrome c was not affected by starvation. However, the concentration of the pigment in hepatic mitochondria isolated from starving animals was less than half that in normal mitochondria. Clofibrate-treated animals did not show a decreased concentration of cytochrome c in hepatic mitochondria. Mitochondria isolated from starving animals, though deficient in cytochrome c, did not show any decrease in succinate dehydrogenase activity or in the rate of substrate-dependent reduction of potassium ferricyanide or attendant phosphorylation. In coupled mitochondria, ferricyanide may not accept electrons from the cytochrome c in the respiratory chain. Starvation decreases the concentration of high-affinity binding sites for cytochrome c on the mitochondrial membrane. The dissociation constant increases in magnitude.
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PMID:Influence of starvation and clofibrate administration on oxidative phosphorylation by rat liver mitochondria. 625 42

This study examined the effects of acute dietary restriction on aerobic and anaerobic metabolic capacity of skeletal and cardiac muscles. Male weanling Sprague-Dawley rats were fed a 28% casein diet to a body weight of 100 g. The control group was killed at 100 g and the experimental groups were starved to 70 g body weight by either 4-day total restriction (TR) or 9-day partial restriction (PR). The heart, soleus, extensor digitorum longus (EDL), biceps brachii, psoas and red and white portions of the gastrocnemius (GR and GW) were assayed for oxygen uptake and succinic dehydrogenase (SDH) and pyruvate kinase (PK) activity. Cytochrome c was also measured in the gastrocnemius and psoas. The decrease in muscle weight was similar to the 30% decrease in body weight with the exception of the soleus which decreased by only 10% due to either TR or PR. PK, an estimate of anaerobic capacity, appeared to increase per unit weight in all tissues after both TR and PR; however, total muscle PK remained unchanged. Total cytochrome c and SDH activity, estimate of aerobic capacity, decreased in all muscles after either treatment. The largest decreases in SDH were 38% in the soleus and 51% in the heart after TR and 50% in the GR and 48% in the GW after PR. Oxygen uptake increased in the soleus (20%) and heart (70%) but decreased in all other skeletal muscles with the greatest effect after PR (50%). This study has shown that there is a decrease in aerobic capacity during acute starvation and that total muscle anaerobic metabolic capacity remains near normal.
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PMID:Changes in aerobic and anaerobic metabolism in rat cardiac and skeletal muscles after total or partial dietary restrictions. 626 53

Exposure of rats to higher environmental temperature (36-37 degrees C) decreased the capacity of their kidney mitochondria to oxidize succinate. The decrease was corrected on the addition of exogenous cytochrome c. Kidney mitochondria of heat-exposed animals showed decreased rates of H2O2 generation when alpha-glycerophosphate, but not succinate, was used as electron donor. These mitochondria also showed decreased activity of alpha-glycerophosphate dehydrogenase but not of succinate dehydrogenase. The content of cytochrome c in kidney mitochondria of heat-exposed animals was low even though the concentration of the pigment in the whole tissue did not decrease. Starvation as well as administration of an antithyroid agent like propylthiouracil simulated some of the effects of heat exposure on kidney mitochondria, but the cytochrome c-dependent reversal of inhibition of oxidation was obtained only in heat exposure.
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PMID:Oxidations in kidney mitochondria of heat-exposed rats: regulation by cytochrome c. 653 33

Antibodies specific for the Mr 65,000 (flavoprotein) and the Mr 28,000 subunits of the succinic dehydrogenase (SDH) of Bacillus subtilis were obtained. By using these antibodies it was shown that both subunits accumulated in the cytoplasm during 5-aminolevulinic acid starvation of a 5-aminolevulinic acid auxotroph. In the cytoplasm the subunits were not associated since they precipitated essentially independently of each other with subunit-specific antibody. In sodium dodecyl sulfate-polyacrylamide gel electrophoresis the cytoplasmic subunits migrated identically with the corresponding subunits from the purified membrane-bound SDH complex. Cytoplasmic subunits were pulse-labeled with L-[35S]methionine during 5-aminolevulinic acid starvation. The labeled subunits bound to the membrane when heme synthesis was resumed and also when protein synthesis was blocked by chloramphenicol before readdition of 5-aminolevulinic acid. The experiments thus demonstrated a precursor relationship between cytoplasmic subunits and the subunits of the membrane-bound SDH complex. All SDH-negative mutants isolated so far carry mutations in the citF locus. None of the mutants was found to have either the Mr 65,000 or the Mr 28,000 SDH subunits in the membrane. Four citF mutants, however, contained both subunits in the cytoplasm. Three of these mutants lacked spectrally detectable cytochrome b558. The respective mutations mapped at one end of the citF locus. These results strongly support our previous suggestion that cytochrome b558 is (part of) a membrane binding site for SDH in B. subtilis.
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PMID:Biosynthesis and membrane binding of succinate dehydrogenase in Bacillus subtilis. 677 71

Male inbred Fischer rats were fed a diet containing 5 p.p.m. aflatoxin for 1, 3, 4 1/2 and 6 weeks at which times groups were killed for histological and histochemical study. Aflatoxin produced a scattered individual cell necrosis of parenchymal cells by 1 week. At 3 weeks small basophilic proliferative foci were seen which increased in size and abundance to 6 weeks. These foci showed starvation-resistant glycogen, variable depletion of glucose-6-phosphatase, succinic dehydrogenase, aniline hydrogenase, membrane ATPase and acid phosphatase. At 6 weeks the foci showed the presence of gamma glutamyl transpeptidase and glucose-6-phosphate dehydrogenase. The basophilic foci were not preceded by other focal histological and histochemical change. The basophilic proliferative lesions are observed when an irreversible change has been induced in the liver. The role of such lesions in the histogenesis of hepatocellular carcinoma is discussed.
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PMID:Histochemical studies on the early proliferative lesion induced in the rat liver by aflatoxin. 724 Dec 69

Hepatic metabolism of fatty acids is impaired in experimental animals with long-term bile duct ligation. To characterize the underlying defects, fatty acid metabolism was investigated in isolated hepatocytes and isolated liver mitochondria from rats subjected to long-term bile duct ligation or sham surgery. After starvation for 24 hr, the plasma beta-hydroxybutyrate concentration was decreased in rats with bile duct ligation as compared with control rats. Production of beta-hydroxybutyrate from butyrate, octanoate and palmitate by hepatocytes isolated from rats subjected to bile duct ligation was also decreased. Liver mitochondria from rats subjected to bile duct ligation showed decreased state 3 oxidation rates for L-glutamate, succinate, duroquinone, and fatty acids but not for ascorbate as substrate. State 3u oxidation rates (uncoupling with dinitrophenol) and activities of mitochondrial oxidases were also decreased in mitochondria from rats subjected to bile duct ligation. Direct assessment of the activities of the subunits of the electron transport chain revealed reduced activities of complex I, complex II and complex III in mitochondria from rats subjected to bile duct ligation. Activities of the beta-oxidation enzymes specific for short-chain fatty acids were all reduced in rats subjected to bile duct ligation. Mitochondrial protein content per hepatocyte was increased by 32% in rats subjected to bile duct ligation compared with control rats. Thus the studies directly demonstrate mitochondrial defects in fatty acid oxidation in rats subjected to bile duct ligation, which explain decreased ketosis during starvation.
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PMID:Mechanisms of impaired hepatic fatty acid metabolism in rats with long-term bile duct ligation. 817 52

Using two-dimensional gel electrophoresis and N-terminal amino acid sequencing analysis, we demonstrate that a mutant of the global regulatory protein ArcA fails to decrease the synthesis of the TCA cycle enzymes malate dehydrogenase, isocitrate dehydrogenase, lipoamide dehydrogenase E3 and succinate dehydrogenase in response to stasis, while the increased production of the glycolysis enzymes phosphoglycerate mutase and pyruvate kinase is unaffected. Microcalorimetric and respiratory measurements show that the continued production of TCA cycle enzymes in the (delta)arcA mutant is manifested as an elevated rate of respiration and total metabolic activity during starvation. The (delta)arcA mutant is severely impaired in surviving prolonged periods of exogenous carbon starvation, a phenotype that can be alleviated by overproducing the superoxide dismutase SodA. In addition, flow cytometry demonstrates that starving (delta)arcA mutant cells, in contrast to wild-type cells, fail to perform reductive division, remain large and contain multiple chromosomal copies. We suggest that the ArcA-dependent reduced production of electron donors and the decreased level and activity of the aerobic respiratory apparatus during growth arrest is an integral part of a defense system aimed at avoiding the damaging effects of oxygen radicals and controlling the rate of utilization of endogenous reserves.
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PMID:Bacterial defense against aging: role of the Escherichia coli ArcA regulator in gene expression, readjusted energy flux and survival during stasis. 867 Aug 22


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