Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Selenium Oxides”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 757 records · Page 42Linked to original sources
PubMed2003

Preparation of 9-hydroxy grayanotoxin derivatives and their acute toxicity in mice.

Novel 9alpha and 9beta-hydroxy grayanotoxin II derivatives were prepared by photo-sensitized oxygenation of iso-grayanotoxin II and oxidation of grayanotoxin II tetraacetate with selenium dioxide respectively. The lethal dosage of 9alpha and 9beta-hydroxy grayanotoxin II were lower than that of grayanotoxin II. In addition, the lethal dosage of 9beta-hydroxy-dihydro grayanotoxin II was higher than that of dihydro grayanotoxin II.

Animals↗
PubMed1984

Inhibition of cellular antioxidants: a possible mechanism of toxic cell injury.

Cells that utilize molecular oxygen generate highly reactive oxygen-derived free radicals. Endogenous cellular oxidants inactivate oxidant free radicals and protect aerobic cells from oxidant injury. Glutathione, glutathione reductase, and superoxide dismutase are key components of this antioxidant defense. Inhibition of antioxidant components would be expected to result in cell injury. Using exposure to oxygen at high pressure to increase the level of oxidant free radicals, evidence is presented to support the hypothesis that inhibition of cellular antioxidants renders organisms more susceptible to oxygen toxicity. Diethyldithiocarbamate at doses of 250, 500 and 1000 mg/kg inhibited rat brain superoxide dismutase activity and shortened onset time to seizures in a dose-related manner in 4 ATA oxygen. Carmustine at doses of 12.5, 25 and 50 mg/kg inhibits glutathione reductase activity in rat brain in proportion to the dose. Time to onset of seizures of rats pretreated with carmustine prior to exposure to 4 ATA oxygen was shortened, and oxidized glutathione levels were increased in the cortex and subcortex. These data suggest that inhibition of antioxidant components results in organisms becoming more sensitive to oxygen toxicity. Compounds that inhibit cellular antioxidants may produce toxic cell injury by permitting intracellular oxidant free radicals to attack essential cell constituents.

Aerobiosis↗
PubMed2004

Oxygen free radical and antioxidant defense mechanism in cancer.

The reactive oxygen species (ROS) can damage the nucleic acids. The oxidative modification of the DNA constitutes the fundamental molecular event in carcinogenesis and that is why the interest in the study of the involvement of ROS in that process. On the other hand, oxidative DNA damage-induced mutagenesis is widely hypothesized to be a frequent event in the normal human cell. The enormous evidence suggests an important role of ROS in the expansion and progression of tumor clones, being considered a relevant class of carcinogens. In addition, the use of immunohistochemical techniques has showed that the various types of cancer examined to date manifest an imbalance in their antioxidant mechanisms to respect the primary cell. In the near future new insights in cancer therapies, based on modulation of cellular redox status, may lead the way to additional tools against carcinogenesis from ROS.

Animals↗
PubMedDate not supplied

[Therapeutic-preventive effect of sodium selenite on the course of experimental myocardial infarct].

An occlusion of the left coronary artery in rats tends to signally raise the intensity of free radical oxidation of myocardial-lipids, which is revealed by the chemofluorescent method. A direct correlational link between the intensity of the lipids peroxidation and the extent of the myocardial damage was established. Subcutaneous injection of sodium selenite in a dose of 30 gamma/kg 2 hours prior to ligation and once daily for a space of 7 days produces a distincly reduced intensity of free-radical processes in the myocardium, decreases the extent of infarction and prevents the appearance of gross changes on the ECG.

Animals↗
PubMed1976

Purification and properties of proline reductase from Clostridium sticklandii.

Proline reductase of Clostridium sticklandii is a membrane-bound protein and is released by treatment with detergents. The enzyme has been purified to homogeneity and is estimated by gel filtration and sedimentation equilibrium centrifugation to have a molecular weight of 298,000 to 327,000. A minimum molecular weight of 30,000 to 31,000 was calculated on the basis of sodium dodecyl sulfate-acrylamide gel electrophoresis and amino acid composition. Amino acid analysis showed a preponderance of acidic amino acids. No tryptophan was detected in the protein either spectrophotometrically or by amino acid analysis. A total of 20 sulfhydryl groups measured by titration of the reduced protein with 5,5'-dithiobis(2-nitrobenzoic acid) is in agreement with 20 cystic acid residues determined in hydrolysates of performic acid-oxidized protein. No molybdenum, iron, or selenium was found in the pure protein. Although NADH is the physiological electron donor for the proline reductase complex, the purified 300,000 molecular weight reductase component is inactive in the presence of NADH in vitro. Dithiothreitol, in contrast, can serve as electron donor both for unpurified (putative proline reductase complex) and purified proline reductase in vitro.

Amino Acid Oxidoreductases↗
PubMed1991

Effects of dietary factors on antioxidant enzymes in rats exposed to hyperbaric oxygen.

To delineate the effect of dietary supplementation with vitamin E (Vit E) alone or in combination with riboflavin (Rib) or selenium (Se) or both, on biological oxidative damage in rat brain and lungs we exposed rats to hyperbaric oxygen (HBO) and measured the activities of glutathione reductase (GSSG-R), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and glucose-6-phosphate dehydrogenase (G-6-PD) prior to or 48 h after exposure. Rats fed the dietary supplements, and a control group maintained on an unsupplemented diet, for 30 d, were each divided into 2 subgroups, of which 1 was exposed to 4.5 absolute atmospheres (ATA) of 100% oxygen for 30 min, hereafter referred to as "exposed". The remaining subgroups were left unexposed. Pre-exposure GSSG-R activity in brain was elevated in all experimentally fed groups (ranging from 23 to 84%) compared with the unexposed control, whereas GSH-Px, G-6-PD and SOD activities were unchanged. The lungs showed significant increases in pre-exposure GSSG-R, ranging from 15 to 28%, and GSH-Px, ranging from 13 to 23%, activities in all the groups fed the supplemental nutrients, except those on Vit E alone. Increases in G-6-PD activity were observed only in those fed supplements of Rib. In most cases exposure to oxygen caused an increase in GSSG-R, GSH-Px and G-6-PD activities. However the increases were higher in the supplemented groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Effects of selenium on cell proliferation in rat liver and mammalian cells as indicated by cytokinetic and biochemical analysis.

Studies were conducted in vivo with regenerating liver and in vitro with mammalian cells to determine the effects of selenium on cell proliferation and the stages of the cell cycle affected by selenium. Six ppm selenium as Na2SeO3 fed to weanling male F344 rats for 6 wk significantly reduced the percentage of 3H-labeled hepatocyte nuclei by one-half compared to 0.1 ppm selenium when [methyl-3H]thymidine was injected at 23 h post-two-thirds hepatectomy. Sampling was done at 30 h post-hepatectomy. A trend towards decreased 3H per DNA per labeled cell was also observed, suggesting that selenium decreased the rate of DNA synthesis as well as delaying the entry of cells into S phase (i.e., increasing the duration of G0-G1). Studies in vitro with H-4 "minimal deviation" hepatomas and 3T3 mouse fibroblasts demonstrated that selenium decreased the growth of these cells in a dose-dependent manner, and this inhibition was reversible upon removal of selenium from the growth medium. Cytokinetic analysis using fluorescence flow cytometry and microscopic techniques indicated that selenium treatment increased the duration of G1, S, and G2 phases of the cell cycle, while having no effect on mitosis under the conditions of our experiments. Biochemical analyses of H-4 cells demonstrated that selenium treatment caused a significant dose-dependent increase in oxidized and reduced glutathione (GSSG and GSH) as well as in the GSSG:GSH ratio as was previously observed in liver in vivo. In addition, glutathione reductase activity as well as the oxidized nicotinamide adenine dinucleotide phosphate:reduced nicotinamide adenine dinucleotide phosphate ratio was significantly increased with selenium treatment. These results indicate that selenium affects all "synthetic" stages of the cell cycle, and elevated GSSG or the GSSG:GSH ratio may explain the antiproliferative effects of selenium on cells.

Animals↗
PubMedDate not supplied

The role of trace elements in juvenile diabetes mellitus.

There is accumulating evidence that the metabolism of several trace elements is altered in insulin-dependent diabetes mellitus and that these nutrients might have specific roles in the pathogenesis and progress of this disease. Magnesium deficiency is the most evident disturbance of metal metabolism in diabetes mellitus. Hypomagnesemia might increase the risk of ischemic heart disease and severe retinopathy. Increased urinary loss of zinc is a commonly encountered feature of diabetes. High-dose oral zinc might enhance wound healing, although data regarding diabetes are lacking. Chromium increases tissue sensitivity to insulin and tends to raise high-density lipoprotein (HDL) cholesterol and the HDL:low-density lipoprotein ratio. Selenium is involved in processes which protect the cell against oxidative damage by peroxides produced from lipid metabolism. There is one report of elevated serum selenium in diabetic children although the clinical significance of this finding is still unclear. An insulin-like effect has recently been attributed to vanadium in experimental animals, a finding of potential interest to man. Current knowledge does not implicate iron, iodine, manganese, cobalt, nickel, silicone, fluoride, molybdenum or tin in the pathophysiology of diabetes. Appropriate trace element supplementation might prove beneficial in ameliorating some physiological deficiencies associated with diabetes and prevent or retard secondary complications. However, properly designed and well-documented trials, especially on magnesium supplementation, need to be performed before rationales for such supplementation are developed. The potential roles of vanadium, chromium and selenium in diabetes constitute challenging areas for further experimental and clinical research.

Animals↗
PubMedDate not supplied

Carboxymethyl-selenopyruvic acid as the product of the oxidative deamination of carboxymethyl-selenocysteine.

CMSeC labeled with 14C in the carboxymethyl moiety was incubated with snake venom L-aminoacid oxidase. As the product of the reaction only one ketoacid was detected, which retained all the radioactivity of the oxidized substrate. This clearly shows that no breakdown of the C-Se bond of CMSeC occurs during its oxidation, and confirms previously reported data indicating that the ketoacid arising from CMSeC is CMSeP.

Amino Acid Oxidoreductases↗