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:1.9.3.1 (cytochrome oxidase)
8,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The five major antioxidants enzymes, cytochrome oxidase (COX), GSH, and GSSG, and endogenous and in vitro stimulated lipid peroxidation (TBA-RS) were assayed in the lung of old (28 months) and young (9 months) adult rats due to the almost total absence of data of this kind in this tissue, which is normally exposed to relatively high pO2 throughout life. Catalase, selenium (Se)-dependent GSH peroxidase (GPx), GSH reductase, GSH, GSSG, GSSG/GSH, and in vivo and in vitro TBA-RS showed similar values in old and young animals. The decrease observed for non Se-dependent GPx disappeared when the values were expressed in relation to COX activity. Only superoxide dismutase showed a clear decrease when referred both to protein and COX activity. These results suggest that lung aging is not accelerated in old age due to a decrease in the antioxidant capacity of the tissue. Nevertheless, they are compatible with a continuous damage of the lung tissue by free radicals throughout the life span.
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PMID:Aging and lung antioxidant enzymes, glutathione, and lipid peroxidation in the rat. 164 50

Old rats (28 months), when compared with young adults (9 months), did not show differences in activities of superoxide dismutase (SOD) or selenium-dependent and -independent glutathione peroxidases (GPx), or in levels of GSH, GSSG, GSSG/GSH and endogenous peroxidation in liver and brain. Rates of stimulated peroxidation in vitro were decreased in the livers of old rats. Old animals showed decreased levels of hepatic catalase and glutathione reductase. Nevertheless, when enzyme activities were referred to cytochrome oxidase activity these decreases disappeared, and GPx and SOD (brain) were even increased in old rats.
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PMID:Anti-oxidant defences and peroxidation in liver and brain of aged rats. 217 82

Investigation of the dietary interaction between cyanide and selenium in the chick, whereby cyanide alleviates selenium toxicity, suggests that cyanide alters metabolic reductive potential. Cyanide enhances the elimination of selenium as dimethyl selenide, the formation of which requires both reducing equivalents and methyl groups. Even when the methionine supply is adequate, meeting the need for the methyl groups, the interaction can be lost if there is a deficiency of certain micronutrients or an excess of vitamin K. Cyanide reduces liver glycogen, implying greater emphasis on anaerobic metabolism through inhibition of cytochrome oxidase. This may increase reductive potential but may also result in increased free radical production, processes that can be modified by levels of micronutrients. There is no evidence that an excess of sulphur amino acids can markedly enhance cyanide detoxification, although, for reasons that are not yet clear, cystine may be beneficial. However, the balance of dietary amino acids may be more critical than had been realized, because an excess of alanine appears to exacerbate cyanide toxicity.
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PMID:Nutritional and biochemical factors influencing the biological effects of cyanide. 307 58

Increased O2 metabolism imposed by physical exercise is likely to augment the production of active O2 species that have been shown to react with lipids, proteins, and DNA. Antioxidants and antioxidant enzymes, such as the selenium enzyme glutathione peroxidase, minimize or prevent such potentially toxic reactions. This study shows that selenium deficiency decreases glutathione peroxidase activity in liver and muscle (less than 80%, P less than 0.001), increases total glutathione in liver, muscle, and plasma (P less than 0.05) and increases muscle cytochrome oxidase activity, and ubiquinone content (P less than 0.05) but has no effect on endurance capacity. Exercise to exhaustion resulted in a significant (P less than 0.001) elevation of total and oxidized glutathione (GSSG) and a significant (P less than 0.05) decrease of vitamin E in plasma of control and selenium-deficient rats. Acute exercise also increased tissue GSSG levels in both control and selenium-deficient groups of rats. Hence, despite a large depletion of selenium-deficient glutathione peroxidase, pronounced oxidation of glutathione to GSSG can be produced by the increased oxidative metabolism during physical exercise. The results suggest that the residual glutathione peroxidase activity is sufficient to detoxify hydroperoxides in exercising selenium-deficient animals and to prevent the impairment of endurance capacity.
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PMID:Selenium deficiency, endurance exercise capacity, and antioxidant status in rats. 343 84

The effects of low-dose selenium and high-dose cadmium on myocardial injury were studied in weanling S.D. rats fed with feed containing controlled levels of selenium and cadmium. Results indicated low-dose selenium and high-dose cadmium could injure heart and myocardial cell membrane system to a certain extent, and cause focal necrosis and reduction in activities of glutathione peroxidase and cytochrome oxidase of heart muscle in rats. It suggested there were certain factors in the grain produced in the areas where Keshan disease was prevalent, which injured heart muscle in rats. So, selenium supplement could prevent from myocardial injury caused by the grain grown in those areas.
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PMID:[Studies on the effects of low-dose selenium and high-dose cadmium on myocardial injury]. 792 56

Sudden infant death syndrome (SIDS) occurs silently usually during sleep and, though remaining unexplained after autopsy, leaves footprints creating a pattern analogous to that which follows a flood of nitric acid (NO). These footprints in SIDS are associated with serious pathological changes, viz. elevated hepatic iron, bone marrow hyperplasia, hypomyelinated respiratory control centres, elevated lung immunoglobulins, cerebral hypoperfusion resembling lesions induced by chronic hypoxemia, ischemia, congenital heart disease and congenital myopathy. Hypoxia stimulates the immune response and the over-arousal of the immune response triggers a flood of NO. Adenosine triggers sleep. NO and adenosine are additive as dilators of coronary blood vessels. Blood pressure collapses. Selenium increases the activity of the enzyme ferrochelatase during incorporation of heme into cytochrome oxidase. NO binds to cytochrome oxidase, inhibiting respiration. When NO reaches dangerous levels, the cell turns on production of heme oxygenase. Heme is broken down to iron (Fe) carbon monoxide (CO) and bile pigments. NO has a huge affinity for hemoglobin which catalyses NO degradation to nitrate. Furthermore, NO is a product of smoke and SIDS incidence is higher in smoking mothers.
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PMID:Association of sudden infant death syndrome with grossly deranged iron metabolism and nitric oxide overload. 1079 Jul 39

Selenium-containing abzyme (m4G3) was prepared and its protection of myocardial mitochondria against oxidative damage was studied using the swelling of mitochondria, quantity of lipid peroxidation products, and change in cytochrome-c oxidase activity as a measure of mitochondrial damage. The results showed that m4G3 could inhibit mitochondrial damage caused by the hypoxanthine-xanthine oxidase system in vitro. Electronic spin resonance (ESR) studies demonstrated that m4G3 could decrease the amount of free radicals generated in the damage system.
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PMID:Protection of myocardial mitochondria against oxidative damage by selenium-containing abzyme m4G3. 1081 24

The antioxidant activity of a novel artificial glutathione peroxidase-like enzyme, selenium-containing glutathione 5-transferase from Lucilia cuprina (seleno-LuGST1-1), was studied by using a ferrous sulfate/ascorbate-induced mitochondrial damage model system. Swelling of mitochondria, lipid peroxidation, and cytochrome-c oxidase activity were selected to evaluate the preservation of mitochondrial integrity in this system. Seleno-LuGST1-1 could effectively protect the mitochondria against oxidative damage in a dose-dependent manner and exhibited both higher catalytic activity and greater antioxidant ability than the classic mimic, 2-phenyl-1,2-benziososelenazol-3(2H)-one (Ebselen). This novel artificial biocatalyst therefore may have great potential for pharmacologic application in the treatment of reactive oxygen species-related diseases.
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PMID:Protection of mitochondrial integrity from oxidative stress by selenium-containing glutathione transferase. 1625 90

A free radical is an unstable and highly-reactive chemical species capable of independent existence that contained one or more unpaired electrons in its outer orbital. A number of oxygen-derived free radicals (ODFRs) have been identified. However, superoxide (O(-)(2) and hydroxyl (OH*) radicals are extensively studied. The univalent reduction of oxygen to water produces a number of highly-reactive chemical intermediates such as O(-)2 and OH*, which are commonly-known as oxygen-derived free radicals. ODFRS may be formed from several sources as follows: a) mitochondrial cytochrome oxidase, b) xanthine oxidase, c) neutrophils and d) transitional metals. There are several important defense mechanisms to limit or to prevent the damage caused by excessive ODFRs activity. These antioxidant defenses can be divided into a) enzymatic defense mechanisms such as: superoxide dismutase (SOD): catalase: selenium-containing glutathione peroxidase and b) non-enzymatic defense mechanisms including: alpha-tocopherol; ascorbic acid; glutathione and any sulfhydryl-containing compounds.
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PMID:Role of oxygen-derived free radicals on gastric mucosal injury induced by ischemia-reperfusion. 1986 38

Selenite has been a touted cancer chemopreventative agent but generates conflicting outcomes. Multiple mechanisms of selenite cytotoxicity in cancer cells are thought to be induced by metabolites of selenite. We observed that intracellular metabolism of selenite generates endogenous selenium nanoparticles (SeNPs) in cancer cells. Critical proteins that bind with high affinity to elemental selenium during SeNPs self-assembly were identified through proteomics analysis; these include glycolytic enzymes, insoluble tubulin, and heat shock proteins 90 (HSP90). Sequestration of glycolytic enzymes by SeNPs dramatically inhibits ATP generation, which leads to functional and structural disruption of mitochondria. Transcriptome sequencing showed tremendous down-regulation of mitochondrial respiratory NADH dehydrogenase (complex I), cytochrome c oxidase (complex IV), and ATP synthase (complex V) in response to glycolysis-dependent mitochondrial dysfunction. Sequestration of insoluble tubulin led to microtubule depolymerization, altering microtubule dynamics. HSP90 sequestration led to degradation of its downstream effectors via autophagy, ultimately resulting in a cell-signaling switch to apoptosis. Additionally, the surface effects of SeNPs generated oxidative stress, thus contributing to selenite cytotoxicity. Herein, we reveal that the multiple mechanisms of selenite-induced cytotoxicity are caused by endogenous protein-assisted self-assembly of SeNPs and suggest that endogenous SeNPs could potentially be the primary cause of selenite-induced cytotoxicity.
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PMID:Selenite-induced toxicity in cancer cells is mediated by metabolic generation of endogenous selenium nanoparticles. 2556 70


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