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)

Two muscles involved in locomotion the vastus lateralis and the gastrocnemius, were compared on a variety of histochemical an biochemical properties. Ten active males, age 20 - 24 years, served as subjects. Fibre type distributions, type I, type IIA and type IIB, as determined from samples extracted by muscle biopsy were similar in both muscles. In addition, no significant difference (p greater than 0.05) was found between fibre types in each muscle for fibre size, relative area, capillaries per fibre and the ratio of capillaries per fibre area. The activities of a number of enzymes representative of energy supplying pathways - the citric acid cycle (succinate dehydrogenase, SHD; beta-hydroxyacyl CoA dehydrogenase, HADH), glycogenolysis (total phosphorylase, PHOSP), glycolysis (phosphofructokinase, PFK) - were of similar magnitude between the two muscles. The only exception noted was for the activity of a glycolytic enzyme, lactate dehydrogenase, LDH, where a 16% higher value was observed in the vastus lateralis. The close degree of homogeneity displayed between these two muscles may be of significance in providing for a functional synchrony to occur in locomotor activities of varying intensity.
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PMID:Human vastus lateralis and gastrocnemius muscles. A comparative histochemical and biochemical analysis. 617 18

To investigate sex differences in the organization of enzyme activities of energy supplying metabolism in skeletal muscle, samples of the vastus lateralis were extracted from active but untrained males (n = 16) and females (n = 17), ranging in age from 18 to 22 years. Muscle tissue from 2 different biopsy samples from each subject were analyzed for enzymes representative of the citric acid cycle (succinic dehydrogenase, SDH), beta-oxidation of fatty acids (3-hydroxyacyl CoA dehydrogenase, HAD), glycogenolysis (phosphorylase, PHOSPH), glycolysis (pyruvate kinase, PK; phosphofructokinase, PFK and lactate dehydrogenase, LDH) and glucose phosphorylation (hexokinase, HK). The results indicated that the maximal activities of PFK, PK, LDH and PHOSPH, HK and SDH averaged between 15 and 32% higher in the males than in the females. No significant differences between the sexes were found for HAD. When enzyme activity ratios were calculated, sex differences were only evident for the HAD/SDH ratio (mean +/- SD; females = 0.56 +/- 0.20; males = 0.41 +/- 0.11 and for the PFK/HAD ratio (females = 7.40 +/- 1.6; males = 9.58 +/- 1.9). The findings suggest that (1) the females have a significantly lower overall capacity for aerobic oxidation and for anaerobic glycolysis than the males; (2) the females have a greater capacity for beta-oxidation relative to the capacity of the citric acid cycle; and (3) the glycolytic potential relative to the potential for beta-oxidation is lower in the females.
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PMID:Male and female differences in enzyme activities of energy metabolism in vastus lateralis muscle. 623 35

Cefotiam (CGP 14221/E; SCE 963), a semisynthetic cephalosporin, was administered as a single dose by i.v. injection to rats l(up to 1.8 g/kg body-weight) and rabbits (up to 1.7 g/kg body-weight). Cephaloridine served as positive control (1.0 and 0.75 g/kg in rats; 0.3 and 0.28 g/kg in rabbits). The animals were sacrificed 24 h after injection and the kidneys preserved for routine histology and enzyme histochemistry (alkaline phosphatase, aminopeptidase, succinate dehydrogenase, esterase). Serum samples (Na+, K+, Cl-, urea, creatinine, LDH, alkaline phosphatase) and 24-h urine (Na+, K+, Cl-, urea, creatinine, protein, LDH, aminopeptidase) were analysed before and 24 h after injection. Minimal, irregularly scattered, degenerative changes in the proximal tubules which were not dose-dependent in degree were observed in rat kidneys following cefotiam injection. A slight dose-dependent degeneration in up to 50% of proximal tubular cells with loss of brush-border membrane enzyme activity was observed in rabbit kidneys. In both animal species the ability to concentrate urine was retained and urea and creatinine serum levels hardly affected. Following cefotiam injection a dose-dependent 4-fold excretion of urinary protein but not of LDH was observed in rabbits only. By contrast, cephaloridine caused extensive degeneration and necrosis in up to 90% of proximal tubular cells in both rats and rabbits, which was accompanied with formation of enzymically active hyaline casts, loss of urine-concentrating capacity of the kidney, elevated serum levels of urea and creatinine and an increased urinary excretion of LDH (60-fold in rats, 20-fold in rabbits) and protein (3-fold in rats, 10-fold in rabbits). Histochemistry and electron microscopy of rabbit kidneys suggested a loss of microvilli from proximal tubule cells by endocytosis and thus degeneration following injection of large doses of cefotiam, whereas cell disruption and necrosis prevailed after cephaloridine. The action of cefotiam on the proximal tubule cells is, therefore, not only quantitatively but possibly also qualitatively different from that of cephaloridine. Semiquantitative evaluation of tubular injuries in alkaline phosphatase-stained kidney sections and measurements of LDH and protein content in 24-h urine samples were advantageous in determining the quantity and the quality of nephrotoxic effects.
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PMID:Nephrotoxicity of cefotiam (CGP 14221/E) in rats and rabbits. 627 Oct 94

Primary cultures of glial cells prepared from brains of newborn rats were grown for periods of 1-5 weeks. After a proliferative phase of between 2 and 3 weeks, the cultures were maintained in stationary phase, during which a significant increase of oxygen consumption and of the activities of lactate dehydrogenase, succinate dehydrogenase, and mitochondrial glycerolphosphate dehydrogenase could be observed. Furthermore, qualitative changes in the lactate dehydrogenase isoenzyme pattern were found with time, characterized by a shift toward an enhanced synthesis of H subunits. A similar development was found in comparing the LDH isoenzyme pattern in the brain of 15-day-old rat embryo with those of newborn and adult rat brains. It is suggested that some aspects of maturation of glial cells in culture are comparable to those occurring in whole brain in vivo, namely a shift towards an enhanced aerobic metabolism.
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PMID:Development of glial cells in primary cultures: energy metabolism and lactate dehydrogenase isoenzymes. 678 Sep 21

The relative efficiencies of phenazine methosulfate (PMS), 1-methoxy-phenazine methosulfate (MPMS) and Meldola Blue (MB) as electron carriers were determined biochemically (non-enzymic NADH-tetrazolium salt-test) and by quantitative histochemistry (heart and kidney slices; succinate dehydrogenase, SDH; lactate dehydrogenase, LDH). MPMS developed the highest electron transfer velocity in biochemical assays. The reaction was independent of the pH value between 7.0-8.5. PMS and MB always showed a lower transfer ability in biochemical tests which was higher with iodonitrotetrazolium chloride (INT) than with nitro blue tetrazolium chloride (NBT). A distinct pH dependence was demonstrable with MB in this respect, preferentially using INT as tetrazolium salt. Quantitative histochemical results with electron carriers are often at variance with biochemical ones. MPMS leads to somewhat higher demonstrable activities only in the determination of the NAD-dependent LDH, whereas MB results in somewhat higher LDH activity than PMS (reaction medium with agarose). MB and PMS yielded almost equally high activities in the demonstration of the flavoprotein-dependent SDH using a reaction medium with agarose. With an aqueous reaction medium, PMS resulted in higher SDH activities than MB. MPMS always had the lowest efficiency in electron transfer ability using an aqueous or agarose containing reaction medium (SDH). With PVA in the reaction medium (SDH determination) PMS was clearly superior to MPMS. MB showed only a small transfer activity under these conditions because PVA seems to bind MB almost completely. It is concluded that in histochemistry an appropriate electron carrier and electron carrier concentration must be determined for different incubation conditions, tissues, tissue preparations and dehydrogenases studied. General statements about the efficiency or inefficiency of an electron carrier as a result of only one incubation condition does not seem to be justified.
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PMID:Quantitative dehydrogenase histochemistry with exogenous electron carriers (PMS, MPMS, MB). 711 85

The conduction system of bovine heart was studied to clarify the characteristics of its energy metabolism. Results showed that its mitochondrial oxygen uptake was much lower than that of ordinary heart muscle with succinate as substrate but similar to that of ordinary heart muscle with glutamate + malate as substrate. The activity of succinate dehydrogenase was lower than that in ordinary heart muscle. The total activity of isozymes of lactate dehydrogenase was lower in the specialized heart muscle than in ordinary heart muscle. The main isozyme of lactate dehydrogenase in the specialized heart muscle was LDH 1 (H4). The cytoplasmic NAD+/NADH ratio as much higher in the specialized heart muscle than in ordinary heart muscle. These results suggest that in the specialized heart muscle energy is mainly derived from aerobic metabolism.
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PMID:Biochemical studies on energy metabolism in the conduction system of bovine heart. 743 71

It has been proposed that highly biosynthetic cells oxidize fatty acids to generate ATP while maintaining high levels of glucose metabolism through the glycolytic and pentose shunt systems to supply biosynthetic intermediates. We investigated the metabolic strategies and substrate for ATP production in the osteoclast. We used in situ quantitative microcytophotometric techniques to determine the maximal activity of the pentose shunt (glucose-6-phosphate dehydrogenase; G6PD), the glycolytic pathway (glyceraldehyde-3-phosphate dehydrogenase and lactate dehydrogenase; G3PD and LDH), fatty acid oxidation (beta-hydroxyacyl dehydrogenase; HOAD), and the Krebs cycle (succinate dehydrogenase; SDH) in human osteoclasts in situ, and related these enzyme activities to the degree of involvement of the cells in resorption. Unlike other highly biosynthetic cells, such as chondrocytes and macrophage polykaryons, osteoclasts associated with bone resorption were deficient in G3PD, LDH, and G6PD activity. However, osteoclasts did demonstrate a capacity for fatty acid oxidation which increased in cells apposed to the bone surface. The lack of significant glycolytic and pentose shunt activity in the osteoclast provides good evidence that resorbing osteoclasts, unlike phagocytosing macrophage polykaryons, have the metabolic characteristics of cells with greatly reduced capabilities of de novo mRNA synthesis but which do maintain high rates of ATP production. The possibility that the loss of glycolytic activity is a prelude to cell death is discussed.
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PMID:Microcytophotometric analysis of human osteoclast metabolism: lack of activity in certain oxidative pathways indicates inability to sustain biosynthesis during resorption. 815 31

Controversial data have been obtained with direct cellular protection by prostaglandins and sulfhydryls. In the present studies, we compared the merits and liabilities of currently available cell viability assays, some of which have not been previously employed in studies of the gastric mucosa. We also tested the hypothesis that length of incubation of isolated cells with protective agents might influence the degree of cellular damage. Gastric mucosal cells were isolated from nonfasted rats and digested with various concentrations of pronase and/or EGTA. Cell viability was assessed by trypan blue and fast green exclusion, fluorescein diacetate hydrolysis, chromium release, LDH release, mitochondrial succinate dehydrogenase activity and nuclear fluorescence induced by ethidium bromide. The experiments revealed that both pronase and EGTA are needed to obtain mucosal cells with optimal yield and initial viability and that sequential additions of pronase (30 min) and EGTA (30 min), rather than their combination (60 min), increased viability without decreasing yield. Cell viability and yield were better when pronase was used in the first incubation. For LD50 determinations, a cell suspension was incubated with ethanol (0%-15%) for 5 min. For studying the effects of protective agents, the cells were pretreated with 16,16-dmPGE2 or cysteamine HCl at 37 degrees C for 30 min before a 5-min exposure to 7.5% or 15% ethanol. The LD50 value for ethanol injury was approximately 15% for all assays except LDH, where the LD50 value was 8.5%. Preincubating gastric mucosal cells for 30 min with 16,16-dmPGE2 or cysteamine resulted in no preservation of cell viability. However, when cells were preincubated with one of the protective agents for 60 min and then exposed to 8% or 10% ethanol for 5 min, partial protection was observed when assessed by succinate dehydrogenase activity and, in certain cases, by LDH release. We conclude that all seven cell viability assays yield a measurable LD50 value for ethanol-induced cell injury, but the results may vary by as much as 82%. Low concentrations of both pronase and EGTA are needed to obtain isolated mucosal cells with both high yield and initial viability. Biochemical measures of mitochondrial activity and nuclear damage provide reliable evidence of cell viability and should be used to complement membrane permeability assays. Long preincubation of cells (60 min) with protective agents resulted in only slight protection of mitochondrial function, in contrast to the rapid induction of gastroprotection seen with these compounds in vivo. We therefore surmise that processes that contribute to organ protection occur faster and more efficiently than those that control direct cell injury and protection.
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PMID:Isolated rat gastric mucosal cells: optimal conditions for cell harvesting, measures of viability and direct cytoprotection. 878 50

Five goat latissimus dorsi muscles (LDM) were submitted to a progressive chronic electrostimulation program to reach an integrated understanding of the fast-to-slow transformation process in large mammals. LDM were regularly sampled and followed during a period of 8 months. Each sample was simultaneously assessed for histoenzymological study, myosin and LDH isoforms and bioenergetic capacities [NADH dehydrogenase cytochrome c oxidoreductase (NADH Cyt c OR), succinate dehydrogenase cytochrome c oxidoreductase (Succ Cyt c OR), cytochrome c oxidase (Cyt c Ox) and LDH]. Such muscles were also tested with and without completion of II to I transformation for their mechanical properties in isometric and isotonic strain gauge testing. The conversion of fast-to-slow myosin monitored by heavy chain (HC I) and light chain slow component (LC2s) began a few days after stimulation and was almost 100% after 100 days. The H-LDH isoforms evolved similarly but did not reach 100% conversion after 200 days. The activity of respiratory chain oxidases increased within 36 h but to a variable extent and peaked after 32 days, corresponding to a 75% transformation of myosin compared to initial levels. NADH Cyt c OR, Succ Cyt c OR, and Cyt c Ox, respectively increased 10-, 5- and 5-fold. These activities then significantly decreased before the completion of the myofibrillar transformation and reached a plateau with stable activities that remained 2- to 3-fold higher than the unstimulated LDM. LDH activity sharply decreased until day 62 (5-fold) and then plateaued. Functionally, muscle showed a reduced speed of contraction and moderate reduction in power output but had become fatigue-resistant. This study documents the transformation process in large mammals and suggests the dynamic relation between workload, aerobic-anaerobic metabolism and the contractile myofibrillar system.
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PMID:Type II to type I transformation of chronically stimulated goat latissimus dorsi muscle: a histoenzymological, biochemical, bioenergetic, and functional study. 883 65

Nucleoside analogues can induce mitochondrial dysfunction leading to severe clinical syndromes. Lamivudine, a new nucleoside analogue, is an active inhibitor of hepatitis B viral replication without apparent clinical toxicity. To assess subclinical mitochondrial toxicity, we studied the morphology and function of the mitochondrial system in 15 patients treated with lamivudine. Morphology was investigated by routine histological evaluation and electron-microscopic studies of mitochondria in liver biopsy specimens. Mitochondrial function was assessed by 2-keto[1-14C] isocaproic acid decarboxylation (KICA breath test) and by measuring the activity in liver biopsy specimens of the mitochondrial enzymes encoded by nuclear and mitochondrial DNA (mt-DNA) (complex I and IV) as well as a mitochondrial and a cytosolic enzyme both encoded by nuclear DNA only (complex II and lactic dehydrogenase [LDH]). All 15 patients underwent a liver biopsy before treatment and a KICA breath test before and during treatment; 13 agreed to undergo a repeat liver biopsy during lamivudine treatment. Liver tissue with no or minimal fibrotic changes from 7 patients treated for 6 months with lamivudine was suitable for assessment of the mitochondrial enzyme activity. We observed no signs of toxicity by routine histological or electron-microscopic evaluation. KICA breath tests revealed no differences in either peak exhalation or the area under the curve from 0 to 60 minutes between healthy controls (3.0% and 19.3%), untreated patients with chronic hepatitis B (3.4% and 19.3%), and patients treated with lamivudine (3.1% and 20.6%). The activities of the mt-DNA-encoded enzymes remained normal after lamivudine therapy. Unexpectedly a significant decrease in the activity of nuclear-DNA-encoded enzymes in patients with chronic hepatitis B in comparison with normal controls was found. The mean activity of complex II dropped from 45.3 to 20.0 micromol x min(-1), that of lactic dehydrogenase from 106 to 44 micromol x min(-1) (Wilcoxon rank sum; P < .05). In conclusion, no subclinical signs of mitochondrial toxicity resulting from lamivudine therapy for 6 months were observed.
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PMID:Effect of lamivudine on morphology and function of mitochondria in patients with chronic hepatitis B. 921 72


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