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

---

Query: EC:1.15.1.1 (superoxide dismutase)
58,858 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The extensional growth rate of wild-type 74A8 N. crassa in the presence of various concentrations of 19 amino acid analogs was measured. Seven analogs were not inhibitory at concentrations in the range of one to 10mM. Of the remaining 12 analogs, nine inhibited growth in a novel way. The kinetics of growth in the presence of these analogs at 30 degrees were characterized by seven sequential phases: (1)lag; (2) acceleration of growth rate; (3) steady-state growth rate; (4) exponential rate of decline of growth rate; (5) no growth or growth rate less than or equal to 0.1 mm h-1; (6) accleration of growth rate; and (7) steady state. At 33 degrees, phases 6 and 7 did not occur and irreparable death of the clones occurred. The mechanism by which the clones acquired resistance at 30 degrees appeared to involve a combination of physiological adaptation and cellular selection. Dietary application of either free radical scavengers or surface-active membrane 'stabilizers' alleviated or prevented the inhibition and deterioration of growth rate which occurred in the presence of the nine amino acid analogs. Culture with either 4-fluorophenylalanine or ethionine led to an increase of the activities of antioxygenic enzymes glutathione peroxidase, glutathione reductase and superoxide dismutase. The amino acid analogs that cause senescence and death of growing cells are known to be incorporated into proteins and such proteins are generally abnormal. Because a substantial fraction of cellular protein occurs in membranes and the proteins synthesized by mitochondria are exclusively intrinsic membrane proteins, we suggest that a primary consequence of errors in protein synthesis is the production of faulty membranes. The deterioration of such membranes with associated lipid autoxidation and free radical production proceeding as a chain reaction at an exponential rate may in itself contribute to the exponential rate of cellular deterioration which is characteristic of the ageing process. According to this hypothesis, dietary membrane stabilizers, free radical scavengers and antioxygenic enzymes protect cells from error catastrophy arising from the chain of events leading from membrane deterioration.
...
PMID:Ageing of Neurospora crassa. IV. Induction of senescence in wild type by dietary amino acid analogs and reversal by antioxidants and membrane stabilizers. 0 15

The effects of dietary vitamin B-2 and vitamin E on delta9-desaturation of stearoyl-CoA, catalase, glutathione peroxidase, superoxide dismutase and electron transport components in rat liver microsomes have been investigated. delta9-desaturase activities were decreased on diets deficient of vitamin B-2, E and supplemented with E. Among the peroxide-scavenging enzymes, only the catalase activity in microsomes correlates significantly with delta9-desaturase activity. In vitro addition of bovine catalase had no effect on microsomal delta9-desaturase activity on control diet. However, it enhanced the delta9-desaturation in microsomes on vitamin B-2-deficient diet which contained low catalase and high superoxide dismutase activities, compared to those in microsomes of control diet. It is suggested that the hydrogen peroxide-generating and -decomposing systems may play an important role on the delta9-desaturase activity in microsomes.
...
PMID:Effects of dietary vitamin B-2 and vitamin E on the delta9-desaturase and catalase activities in the rat liver microsomes. 2 49

A recessive mutant of Neurospora crassa, called natural-death, is characterized by a decreasing clonal growth potential under all nutritional conditions and the irreversible cessation of growth. The primary molecular defect of this mutant is not known. Evidence presented here, based upon measurements of the activities and thermolabilities of several enzymes, suggests that faulty protein synthesis is probably not a cause of the senescence and death of the mutant, as suggested by Lewis and Holliday (Nature, 228 (1970) 877). Three lines of evidence indicate that lipid autoxidation and associated free radical reactions contribute to the senescence and death of this mutant: (1) The relative times before the onset of senescence and death of mutant clones in the last 40% of their chronological life-span were prolonged 2 to 3-fold by either dietary antioxidants or selenite and the total life-span was increased by 40% to 80%. These compounds also alleviated the senescent morphology and enhanced biomass production; (2) Senescing clones accumulated a green fluorescent pigment in situ, but dietary antioxidant nordihydroguaiaretic acid prevented this accumulation. The fluorescent pigment exhibited the spectral properties of lipofuscin, an end product of lipid autoxidation; (3) Relative to wild type, mycelial extracts of the mutant exhibited a 2 to 4-fold excess of activities of the antioxygenic enzymes superoxide dismutase, glutathione peroxidase and glutathione reductase. We briefly review: (1) the roles of antioxygenic enzymes and antioxidants in their protection against cellular damage from lipid autoxidation and free radical reactions; and (2) the major lines of evidence which appear to support a form of the free radical theory of ageing, encompassing the interrelated processes of membrane deterioration, lipid autoxidation and deleterious free radical reactions as the major causes of cellular deterioration.
...
PMID:Ageing of Neurospora crassa. I. Evidence for the free radical theory of ageing from studies of a natural-death mutant. 13 83

Cumene hydroperoxide and tert-butyl hydroperoxide at sublethal concentrations initially prevent growth of mycelia of wild-type Neurospora crassa, but after a time the cells grow at a subnormal steady-state rate. The antioxidant nordihydroguaiaretic acid protects unadapted cells from hydroperoxide inhibition, leading to a decrease in the time before growth begins, an increase in steady-state growth rate and an increase in biomass production. The results of growth transfer experiments and enzyme measurements indicated that the acquired resistance to the hydroperoxides is physiological and most likely involves the induction of the synthesis of the antioxygenic enzymes superoxide dismutase, glutathione peroxidase and glutathione reductase. Nordihydroguaiaretic acid normalizes the levels of activities of glutathione peroxidase and glutathione reductase during culture with hydroperoxide. Molecular-induced homolysis of the hydroperoxides, a process that is induced by unsaturated fatty acids of membrane lipids, leads to lipid autoxidation in a chain reaction which produces lipid hydroperoxides, which in turn decomposes to form more free radicals. Nordihydroguaiaretic acid, a well-known free radical scavenger, probably serves to minimize hydroperoxide decomposition, lipid autoxidation and molecular damage from free radicals, whereas the coupled enzyme system glutathione peroxidase and glutathione reductase minimizes these processes by decomposing the hydroperoxides to harmless alcohols. We suggest that either free radicals derived from these processes or some consequent non-radical products may serve as the inducers of this enzyme system, rather than the hydroperoxide substrates.
...
PMID:Ageing of Neurospora crassa. II. Organic hydroperoxide toxicity and the protective role of antioxidant and the antioxygenic enzymes. 13 84

Assays of the activity of chromosome 21 determined superoxide dismutase-1 (SOD-1) in lymphocytes and polymorphonuclear granulocytes have demonstrated 38% and 40% increases, respectively, in cells from individuals with trisomy 21. Similarly, SOD-1 activity in trisomic fibroblasts is increased by 81%, while cells monosomic for chromosome 21 have only 60% of normal activity. Taken together with the data on SOD-1 activities in trisomic erythrocytes and platelets, the present results firmly confirm the existence of a true dosage effect for this enzyme in cells aneuploid for chromosome 21. However, the results of assays of the activity of glutathione peroxidase in trisomic fibroblasts did not confirm the possibility previously reported of a chromosome 21 related dosage effect for this enzyme.
...
PMID:Dosage effects for superoxide dismutase-1 in nucleated cells aneuploid for chromosome 21. 14 79

Hyperoxia activates superoxide dismutase (SOD) while inactivating catalase and glutathione peroxidase in polymorphonuclear leucocytes (PMN) and alveolar marcophages (AM) obtained from guinea-pigs exposed to 85% oxygen for 90 h. The influence of these altered enzyme activities on the rate of oxygen consumption and release of superoxide anion (O--2) and hydrogen peroxide (H2O2) was investigated. By 18 h O--2 released from resting PMN increased two-fold and remained elevated through the entire periods of the study, whereas H2O2 release and oxygen consumption at the same time points remained normal. At 66 h PMN phagocytizing opsonized zymosan particles released additional quantities of O--2 and H2O2 and consumed significantly more oxygen compared to the usual increase noted at earlier time points. Although oxygen consumption was almost two-fold higher in AM than PMN, phagocytizing AM released three-fold less O--2 and five-fold less H2O2 than did PMN. Furthermore, AM of animals exposed to hyperoxia no longer exhibited enhanced O--2 production upon exposure to opsonized zymosan. Hydrogen peroxide release progressively decreased at rest but progressively increased during phagocytosis of opsonized zymosan during the 90 h exposure to hyperoxia. No changes in oxygen consumption of AM occurred during hyperoxia. The divergent oxidative responses in PMN and AM of guinea-pigs exposed to hyperoxia suggest different biochemical adaptive mechanisms.
...
PMID:Effect of hyperoxia on superoxide anion and hydrogen peroxide production of polymorphonuclear leucocytes and alveolar macrophages. 19 22

Environmental agents may enter the lung via the tracheobronchial tree or via the bloodstream. They can interact with lung cell metabolism and set in motion a sequence of events that leads to damage, adaptation, and repair. Biochemical signs of lung damage described include lipid peroxidation, decreased biosynthesis of macromolecules, depressed enzyme activities, and the binding of metabolites of the offending agent to tissue macromolecules. As a response to acute damage, lung can activate several biochemical pathways. The selenium-glutathione peroxidase system affords protection against lipid peroxidation and increased activity of superoxide dismutase provides oxygen tolerance. Biochemical adaptation occasionally occurs very quickly: the herbicides paraquat and diquat produce an acute loss of cellular NADPH in lung. This is accompanied by a sudden increase in pentose phosphate pathway activity. Biochemical events accompanying tissue repair following lung injury are increased synthesis of nucleic acids and of protein and enhanced enzymatic activity. The repair following lung damage caused by drugs may be inhibited by oxygen.
...
PMID:Environmental agents altering lung biochemistry. 32 Dec 51

It seems that superoxide dismutase plays the key role in protecting aerobes against O2 toxicity, but there is a whole range of ancillary mechanisms: enzymes to remove H2O2 (catalase, peroxidases) and hence to control formation of .OH from O2, which requires H2O2; antioxidants (ascorbate, GSH, alpha-tocopherol, carotenoids), which also react with singlet oxygen and/or .OH and often inhibit lipid peroxidation and last, but not least in animals, glutathione peroxidase, which controls the rate of lipid peroxidation. These mechanisms cope well at normal O2 concentrations but are insufficient at higher levels.
...
PMID:Biochemical mechanisms accounting for the toxic action of oxygen on living organisms: the key role of superoxide dismutase. 35 40

Administration of technical pentachlorophenol in drinking water (20 mg/l) to male Wistar rats caused significant liver concentration of tetrachlorophenol which remained stable during the exposure of 14 weeks. Pentachlorophenol and tetrachlorophenol accumulated to some extent in the perirenal fat whereas only pentachlorophenol could be found in brain. A period of four weeks of chlorophenol-free diet was sufficiently long to allow removal of the major part of the chlorophenol burden. The neurochemical effects included increased acid proteinase activity at the 8th week of exposure. It levelled off while superoxide dismutase activity increased to twice the control level. Glial glutathione peroxidase activity did not change whereas glial glutathione concentration was below the control range at the 12th week of exposure. Cerebral diaphorase activity was below the control range initially, and its activity increased above the control level during the recovery period whereas other biochemical changes levelled off.
...
PMID:Neurochemical effects of peroral administration of technical pentachlorophenol. 44 21

The activities of various peroxide-metabolizing enzymes were determined in homogenates of human liver excisions. The specific activity of selenium-dependent glutathione peroxidase was 41.1 +/- 23.7 (S.D.) mU/mg protein; non-selenium glutathione peroxidase showed a activity of 30.5 +/- 14.0 mU/mg protein. The catalase and superoxide dismutase concentrations were 4.72 +/- 0.58 and 1.87 +/- 0.68 microgram/mg protein, respectively. Total glutathione amounted to 12.9 +/- 7.4 nmol/mg. Malondialdehyde formation, used as the basis for the determination of lipid hydroperoxides, was 0.32 +/- 0.14 nmol/mg. The data indicate much lower enzyme and substrate levels compared to rats and mice. A positive correlation of r = 0.48 +/- 0.31 was found between the glutathione level and selenium-dependent peroxidase. Selenium-dependent and non-selenium-glutathione peroxidase correlate negatively (r = -0.71 +/- 0.18); superoxide dismutase concentration and lipid-hydroperoxides are also related by a negative correlation coefficient of r = 0.47 +/- 0.31. These data stress the major hepatoprotective role of these systems in human liver.
...
PMID:[The activity of the peroxide-metabolizing system in human liver (author's transl)]. 45 83


1 2 3 4 5 6 7 8 9 10 Next >>

---