Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P30044 (antioxidant enzyme)
 8,037 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Membrane associated thioredoxin reductase has been previously shown to reduce free radicals on the outer plasma membranes of human keratinocytes and melanocytes to provide a possible first line of defense against free radical damage at the surface of the skin. Preliminary experiments with cell cultures of human keratinocytes and melanocytes grown in serum-free medium showed that the enzyme activity depends on extracellular calcium concentration in the medium. Thioredoxin reductase activity at the surface of the skin, at the surface of human keratinocytes and melanocytes, and purified thioredoxin reductase from E. coli and adult human keratinocytes all exhibited calcium-dependent allosteric control. Since thioredoxin reductase contains two extremely reactive thiolate groups at the active site with pK values close to neutrality, both of these anions can form covalent complexes with N-ethylmaleimide by nucleophilic attack on the double bond. In our experiments we used spin-labeled maleimide [4-maleimido-tempo] to examine the local environment in the active site of thioredoxin reductase in the presence and absence of calcium. Both spin-labeled thioethers are distinguishable by EPR spectroscopy, with one site being significantly more immobilized than the other. Hence, it has been possible to observe direct evidence for active site closure by calcium. These results suggest that extracellular calcium may play an important role in regulation of thioredoxin reductase activity for the defense mechanism against UV-mediated free radical damage at the surface of human skin.
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PMID:The role of calcium in the regulation of free radical reduction by thioredoxin reductase at the surface of the skin. 243 92

The aim of our research was the study of the intensity of the oxidative homeostasis of the organism during the mechanical jaundice. From the results of our study it follows that during the cholestasis the violation of the balance between pro-and antioxidant blood system takes place in the patient's blood. The latter is manifested in the blood EPR spectrum in the considerable increase (about 47%) of the intensity of the EPR oxidated ceruloplazmin signal, in the decrease of the intensity of the EPR signal Fe3+ transferin (on 16%), in the increase of the contents of promoters of the free-radical oxidation of ions Fe2+ and Mn2+. As it follows from the results of our researches, the considerable increase of the contents of the free nitrogen oxide is observed during the mechanical jaundice. So it can be concluded, that the intensification of the free-radical processes and the emanation of the protective antioxidant enzyme systems takes place in the organism. Consequently, activation of the peroxide oxidation processes takes place, which disrupts cell membrane integrity and leads to the development of the irreversible tissue injuries.
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PMID:[Oxidative homeostasis of organism during mechanical jaundice]. 1678 84

Aluminium (Al) is reported to promote free radical production, decrease the antioxidant enzyme status and disturb the enzyme activity involved in acetylcholine metabolism leading to cognitive dysfunction that are strongly associated with Alzheimer's disease (AD) pathogenesis. This work aimed at investigating the effect of Al-toxicity on synaptosomal membrane biophysical properties and lipid peroxidation during 65 days. We utilized ATR-IR spectroscopy to study the changes in membrane biochemical structure and biophysical properties of isolated rat cortical synaptosomes, and EPR spin trapping and labeling to follow NADPH oxidase activity and changes of membrane order parameter, respectively. The results showed increase in membrane fluidity and disorder in early 21d of AlCl3 treatment, while after 42d the membrane rigidity, packing, and order increased. The late (65d) an increase in the amount of unsaturated fatty acids, the accumulation of lipid peroxide end products, and ROS production were detected in rat cortex synaptosomes mediated by Al toxicity and oxidative stress (OS). A dramatic increase was also detected in Ca2+ level, synaptic membrane polarity, and EPR-detected order S-parameter. These outcomes strongly suggest that the synaptosomal membrane phospholipids underwent free radical attacks mediated by AlCl3 due to greater NOX activity, and the release of synaptic vesicles into synaptic cleft might be hindered. The adopted spectroscopic techniques have shed light on the biomolecular structure and membrane biophysical changes of isolated cortical synaptosomes for the first time, allowing researchers to move closer to a complete understanding of pathological tissues.
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PMID:ATR-IR and EPR spectroscopy for detecting the alterations in cortical synaptosomes induced by aluminium stress. 3174 52