Showing papers on "Oxidative stress published in 1981"
01 Feb 1981
TL;DR: It is demonstrated that the cytosolic factor protects membranous organelles from oxidative damage to the lipids by preventing peroxidation from occurring at all, and may constitute a ubiquitous membrane-stabilizing system in that it is also present in other tissues.
Abstract: Both enzymic and nonenzymic lipid peroxidation in membranes are inhibited by a)certain chelating compounds, b)some metal ion (Mn2+, Co2+, and Ce3+), and c)lipid soluble antioxidants. The commonalities suggest that the processes of oxidative lipid degradation in the two types of systems may be similar, differing only in the mechanism of initiation. This is further borne out by studies with a glutathione-dependent, heat-labile cytosolic factor that inhibits malondialdehyde formation (a product of lipid peroxidation) in both systems. Studies in the authors' laboratory, however, have demonstrated that the cytosolic factor protects membranous organelles from oxidative damage to the lipids by preventing peroxidation from occurring at all. Analyses of the fatty acid composition of the membranes demonstrate that the polyunsaturated fatty acid content remains stable when the membranes are subjected to peroxidizing conditions in the presence of the cytosolic factor and GSH. Both the cytosolic factor and GSH are required for the protective action since neither can provide this marked stabilizing effects by itself. High concentrations of GSH reduce lipid peroxidation to some extent, but low concentrations are not effective without the addition of the cytosolic factor. The mechanism of this inhibition of peroxidative attack is unknown. Partial purification of rat liver cytosolic glutathione peroxidase demonstrated that the heat-labile cytosolic factor was not glutathione peroxidase. The cytosolic factor may be a glutathione transferase, but that is not known with certainty. Possibly more than one cytosolic protein possesses this GSH-dependent property for inhibiting lipid peroxidation under conditions of oxidative stress. The conditions for the functioning of this protective system in intact cells appear to be optimum and it may constitute a ubiquitous membrane-stabilizing system in that it is also present in other tissues (heart and lung, for example).
69 citations
TL;DR: The increase in glutathione observed upon exposure to NO2 may be a protective reaction of the erythrocyte to meet the oxidative stress.
Abstract: The biochemical response to controlled exposures of nitrogen dioxide (NO/sub 2/) was studied in 19 human subjects exposed to 0.2 ppM NO/sub 2/ for 2 h and compared to 15 control subjects exposed to filtered air for 2 h. Seven biochemical blood parameters, including glutathione, red blood cell glutathione reductase, 2,3-diphosphoglycerate, methemoglobin, vitamin E, complement C/sub 3/, and IgA were measured prior to exposure, immediately after exposure, and 22 h following exposure. The only variable that showed significant change due to NO/sub 2/ exposure was glutathione. Glutathione is known to protect the erythrocyte from oxidative stress. The increase in glutathione observed upon exposure to NO/sub 2/ may be a protective reaction of the erythrocyte to meet the oxidative stress.
9 citations