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Reactive oxygen species kidneys

Fandrey J, Frede S, Ehleben W, Porwol T, Acker H, et al. 1997. Cobalt chloride and desferrioxamine antagonize the inhibition of erythropoietin production by reactive oxygen species. Kidney Int 51 492-496. [Pg.290]

Delayed respiratory distress, fibrosis, and atelectasis Gastrointestinal, liver, and kidney toxicity Formation of reactive oxygen species Block tricarboxylic acid cycle (fluoroacetates)... [Pg.69]

In other publications single-walled carbon nanotubes were shown to promote neoplasm formation in kidneys [22, 23], Contrary to [20], other authors found that carbon nanostructures were capable of inducing reactive oxygen species (oxygen radicals) that could damage cellular structures [24-26],... [Pg.31]

Figure 7.35 The uptake and elimination of cephaloridine by proximal tubular cells in the kidney and possible mechanisms of toxicity. The uptake can be inhibited (probenicid) and the elimination also inhibited (mepiphenidol). Abbreviations OAT 1, organic anion transporter OCT, organic cation transporter ROS, reactive oxygen species. Figure 7.35 The uptake and elimination of cephaloridine by proximal tubular cells in the kidney and possible mechanisms of toxicity. The uptake can be inhibited (probenicid) and the elimination also inhibited (mepiphenidol). Abbreviations OAT 1, organic anion transporter OCT, organic cation transporter ROS, reactive oxygen species.
R9. Ricardo, S. D., Bertram, J. F., and Ryan, G. B., Reactive oxygen species in puromycin aminonu-cleoside nephrosis In vitro studies. Kidney Int. 45,1057—1069 (1994). [Pg.215]

It is possible to measure the formation of various radicals such as reactive oxygen species in cells. Reactive oxygen species (ROS) activate the nuclear factor of activated T cell transcription factor (NFAT), which is associated with its dephosphorylation, nuclear translocation, and increased affinity for DNA binding. Vanadium activation of nuclear factor of activated T cells (NFAT) was found to correlate with formation of the ROS H202 and was dependent upon the activity of calcium channels [39], In activated human neutrophiles, vanadium(II), (III), and (IV) increased hydroxyl radical formation and attenuation of myeloperoxidase activity, whereas V(V) did not show these effects. Similar results were seen in a cell-free system [40], Increased lipid peroxidation in liver but not in kidneys was found in normal rats treated with vanadate [41]. [Pg.175]

Pallet MS, Neumann TV Reactive oxygen species and rat renal epithelial cells during hypoxia and reoxygenation. Kidney Int 40 1041-1049,1991... [Pg.218]

Oxidation of cellular components by reactive oxygen species (ROS) and free radicals is involved in a variety of serious acute and chronic diseases inflammation [56], ischemia-reperfusion damage [57,58], limg disease [59], kidney damage [60], atherosclerosis, diabetes, allergies, cancer and aging [61]. [Pg.714]

The mechanism of acute acetaminophen nephrotoxicity is related to the bioactivation of acetaminophen and/or its metabolites to highly reactive species which are capable of arylating renal macromolecules or generating reactive oxygen species. Acetaminophen hepatotoxicity is the result of conversion of acetaminophen to the reactive intermediate N-acetyl-p-benzoquinoneimine (NAPQI), which can covalently bind to hepatic macromolecules. It is less clear what role formation of NAPQI in the kidney plays in acetaminophen nephrotoxicity. In some species (e.g., the Fischer 344 rat) deacetylation appears to be an important biotransformation step in acetaminophen nephrotoxicity, while in other species (e.g., the CD-I mouse), bioactivation does not appear to require deacetylation of acetaminophen before the ultimate nephrotoxicant species is produced. Therefore, the role of NAPQI in acute acetaminophen nephrotoxicity might be species dependent. [Pg.1486]

Gobe G, Crane D (2010) Mitochondria, reactive oxygen species and cadmium toxicity in the kidney. Toxicol Lett 198(1 ) 49-55. doi 10.1016/j.toxlet.2010.04.013... [Pg.454]

The nature of the metal-ions in the active site also varies between species. Whereas the purple acid phosphatase isolated from red kidney beans (rkbPAP) contains Fe and Zn", the tartrate-resistant acid phosphatase isolated from rat osteoclasts (TRAcP) contains two iron atoms in different oxidation states, an stabilized Fe ion and a redox-active Fe ion. In this way, the ability of the ferrous ion to act as an electron donor confers to the enzyme an alternative function as generator of reactive oxygen species (ROS) [20, 21]. The enzyme may appear in an inactive purple form when the redox-active iron is oxidized to the ferric state, or it can be in an active pink form where the redox-active iron is reduced to the ferrous state [22]. In particular, the tartrate-resistant acid phosphatase isolated from osteoclasts is synthetized as a precursor which is activated by cysteine proteinases resulting in an active two subunit enzyme [23]. [Pg.160]


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See also in sourсe #XX -- [ Pg.428 ]




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