Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04179 (MnSOD)
 2,777 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Male Wistar rats received an aqueous solution of ammonium metavanadate (AMV) of 0.15 mg/V/ml concentration instead of water for 14 days. The erythrocyte count and haemoglobin level in blood were not changed; the haematocrit index was slightly increased. The spontaneous lipid peroxidation in kidney and liver homogenates was increased. The Fe(II)- or ascorbate-induced lipid peroxidation was more pronounced in the kidney than in the liver. No changes in lipid peroxidation were observed in erythrocytes after AMV treatment. The AMV treatment resulted in a decrease in the activity of the antioxidant enzymes, catalase and glutathione peroxidase in the kidney and liver; the cytosolic Cu,Zn-SOD and mitochondrial Mn-SOD were unchanged. The activity of the enzymes in blood was not changed. The results are discussed with a view to the participation of lipid peroxidation in vanadium toxicity.
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PMID:Lipid peroxidation and antioxidant enzymes in vanadate-treated rats. 806 48

The effect of sodium metavanadate (NaVO3) consumption on trace element metabolism, components of the antioxidant defense system and lipid oxidative damage were studied in control (CON) and streptozotocin-induced diabetic (DIAB) rats. Ten days after injection, CON and DIAB rats received either 0 mM NaVO3/80 mM NaCl (0 group) or 1.2 mM NaVO3/80 mM NaCl (1.2V group) in their drinking water. DIAB groups had higher food and fluid intakes than the CON groups; vanadium (V) groups had lower food and fluid intakes than the saline groups. Vanadium therapy lowered plasma glucose concentrations of DIAB rats. The following parameters were similar among the groups: plasma Zn, Cu and Fe concentrations, plasma ceruloplasmin activity, liver Zn, Cu, Mn and Fe concentrations, kidney Mn and Fe concentrations, liver non-Se-dependent glutathione peroxidase (GSH-Px), glutathione reductase (GSH-Red) and Mn-SOD activities, liver reduced glutathione (GSH) and oxidized glutathione (GSSG) concentrations and kidney non-Se-dependent GSH-Px activity. Kidney Zn and Cu concentrations were higher in DIAB rats than in CON rats. The CON-1.2V and DIAB-1.2V groups had V accumulation in the liver and kidney. Liver CuZn-SOD and Se-dependent GSH-Px and kidney CuZn-SOD and GSH-Red activities were lower in DIAB rats compared to CON rats; kidney Mn-SOD and kidney Se-dependent GSH-Px activities were higher in DIAB rats than CON rats. Vanadium treatment did not cause significant alterations in the antioxidant defense system; however, tissue vanadium concentrations were positively correlated to TBARS production. These results show that diabetes caused significant alterations in the antioxidant defense system and that V therapy was associated with a marked deterioration in health of both control and diabetic rats.
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PMID:Vanadium treatment of diabetic Sprague-Dawley rats results in tissue vanadium accumulation and pro-oxidant effects. 824 40

Vanadium is a metal that under physiological conditions can exist in two oxidation states, V(IV) (vanadyl ion) and V(V) (vanadate ion). Here, it was demonstrated that both ions can form complexes with siderophores. Pseudomonas aeruginosa produces two siderophores under iron-limiting conditions, pyoverdine (PVD) and pyochelin (PCH). Vanadyl sulfate, at a concentration of 1-2 mM, strongly inhibited growth of P. aeruginosa PAO1, especially under conditions of severe iron limitation imposed by the presence of non-utilizable Fe(III) chelators. PVD-deficient mutants were more sensitive to vanadium than the wild-type, but addition of PVD did not stimulate their growth. Conversely, PCH-negative mutants were more resistant to vanadium than the wild-type strain. Both siderophores could bind and form complexes with vanadium after incubation with vanadyl sulfate (1:1, in the case of PVD; 2:1, in the case of PCH). Although only one complex with PVD, V(IV)-PVD, was found, both V(IV)- and V(V)-PCH were detected. V-PCH, but not V-PVD, caused strong growth reduction, resulting in a prolonged lag phase. Exposure of PAO1 cells to vanadium induced resistance to the superoxide-generating compound paraquat, and conversely, exposure to paraquat increased resistance to V(IV). Superoxide dismutase (SOD) activity of cells grown in the presence of V(IV) was augmented by a factor of two. Mutants deficient in the production of Fe-SOD (SodB) were particularly sensitive to vanadium, whilst sodA mutants deficient for Mn-SOD were only marginally affected. In conclusion, it is suggested that V-PCH catalyses a Fenton-type reaction whereby the toxic superoxide anion O(2)- is generated, and that vanadium compromises PVD utilization.
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PMID:Vanadium interferes with siderophore-mediated iron uptake in Pseudomonas aeruginosa. 1102 19

Oxygen-free radicals, more generally known as reactive oxygen species (ROS) along with reactive nitrogen species (RNS) are well recognised for playing a dual role as both deleterious and beneficial species. The "two-faced" character of ROS is substantiated by growing body of evidence that ROS within cells act as secondary messengers in intracellular signalling cascades, which induce and maintain the oncogenic phenotype of cancer cells, however, ROS can also induce cellular senescence and apoptosis and can therefore function as anti-tumourigenic species. The cumulative production of ROS/RNS through either endogenous or exogenous insults is termed oxidative stress and is common for many types of cancer cell that are linked with altered redox regulation of cellular signalling pathways. Oxidative stress induces a cellular redox imbalance which has been found to be present in various cancer cells compared with normal cells; the redox imbalance thus may be related to oncogenic stimulation. DNA mutation is a critical step in carcinogenesis and elevated levels of oxidative DNA lesions (8-OH-G) have been noted in various tumours, strongly implicating such damage in the etiology of cancer. It appears that the DNA damage is predominantly linked with the initiation process. This review examines the evidence for involvement of the oxidative stress in the carcinogenesis process. Attention is focused on structural, chemical and biochemical aspects of free radicals, the endogenous and exogenous sources of their generation, the metal (iron, copper, chromium, cobalt, vanadium, cadmium, arsenic, nickel)-mediated formation of free radicals (e.g. Fenton chemistry), the DNA damage (both mitochondrial and nuclear), the damage to lipids and proteins by free radicals, the phenomenon of oxidative stress, cancer and the redox environment of a cell, the mechanisms of carcinogenesis and the role of signalling cascades by ROS; in particular, ROS activation of AP-1 (activator protein) and NF-kappaB (nuclear factor kappa B) signal transduction pathways, which in turn lead to the transcription of genes involved in cell growth regulatory pathways. The role of enzymatic (superoxide dismutase (Cu, Zn-SOD, Mn-SOD), catalase, glutathione peroxidase) and non-enzymatic antioxidants (Vitamin C, Vitamin E, carotenoids, thiol antioxidants (glutathione, thioredoxin and lipoic acid), flavonoids, selenium and others) in the process of carcinogenesis as well as the antioxidant interactions with various regulatory factors, including Ref-1, NF-kappaB, AP-1 are also reviewed.
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PMID:Free radicals, metals and antioxidants in oxidative stress-induced cancer. 1643 Aug 79