scholarly journals Action of hypochlorous acid on the antioxidant protective enzymes superoxide dismutase, catalase and glutathione peroxidase

1987 ◽  
Vol 248 (3) ◽  
pp. 973-976 ◽  
Author(s):  
O I Aruoma ◽  
B Halliwell
Keyword(s):  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Reperfusion Injury ◽  
Hypochlorous Acid ◽  
Low Concentration ◽  
Inflammatory Agent ◽  
Cuzn Superoxide Dismutase ◽  
Protective Enzymes ◽  
Anti Inflammatory

The neutrophil enzyme myeloperoxidase generates hypochlorous acid (HOCl) at sites of inflammation. Glutathione peroxidase is very quickly inactivated by low concentration of HOCl. Inactivation of catalase is also rapid, but requires higher HOCl concentrations and the haem appears to be degraded. Inactivation of bovine CuZn superoxide dismutase is slower. Hence superoxide dismutase should not be easily inactivated by HOCl at sites of inflammation, which may contribute to its effectiveness as an anti-inflammatory agent and in minimizing reperfusion injury.

scholarly journals Glutathione Peroxidase-1 Contributes to the Neuroprotection Seen in the Superoxide Dismutase-1 Transgenic Mouse in Response to Ischemia/Reperfusion Injury

2003 ◽  
Vol 23 (1) ◽  
pp. 19-22 ◽  
Author(s):  
Peter J. Crack ◽  
Juliet M. Taylor ◽  
Judy B. de Haan ◽  
Ismail Kola ◽  
Paul Hertzog ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Focal Cerebral Ischemia ◽  
Infarct Volume ◽  
Ischemia Reperfusion ◽  
Wild Type Mouse ◽  
Superoxide Dismutase 1 ◽  
Glutathione Peroxidase 1

The authors hypothesized that glutathione peroxidase-1 (Gpx-1) contributes to the neuroprotection seen in the superoxide dismutase-1 transgenic (Sod-1 tg) mouse. To investigate this hypothesis, they crossed the Gpx-1 -/- mouse with the Sod-1 tg and subjected the cross to a mouse model of ischemia/reperfusion. Two hours of focal cerebral ischemia followed by 24 hours of reperfusion was induced via intraluminal suture. The Sod-1 tg/Gpx-1 -/- cross exhibited no neuroprotection when infarct volume was measured; indeed, infarct volume increased in the Sod-1 tg/Gpx-1 -/- cross compared with the wild-type mouse. Our results suggest that Gpx-1 plays an important regulatory role in the protection of neural cells in response to ischemia/reperfusion injury.

Radiation Resistance and the CuZn Superoxide Dismutase, Mn Superoxide Dismutase, Catalase, and Glutathione Peroxidase Activities of Seven Human Cell Lines

1984 ◽  
Vol 100 (1) ◽  
pp. 115 ◽  
Author(s):  
Stefan L. Marklund ◽  
N. Gunnar Westman ◽  
Göran Roos ◽  
Jörgen Carlsson ◽  
Goran Roos ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Cell Lines ◽  
Human Cell ◽  
Radiation Resistance ◽  
Human Cell Lines ◽  
Cuzn Superoxide Dismutase

scholarly journals CuZn-superoxide dismutase, Mn-superoxide dismutase, catalase and glutathione peroxidase in pancreatic islets and other tissues in the mouse

1981 ◽  
Vol 199 (2) ◽  
pp. 393-398 ◽  
Author(s):  
K Grankvist ◽  
S L Marklund ◽  
I B Täljedal
Keyword(s):  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Pancreatic Islets ◽  
Islet Cells ◽  
Blood Contamination ◽  
Tissue Samples ◽  
Mouse Islets ◽  
Cuzn Superoxide Dismutase ◽  
Endogenous Enzymes

Exogenous superoxide dismutase, catalase and scavengers of the hydroxyl radical protect pancreatic-islet cells against the toxic actions of alloxan in vitro [Grankvist et al. (1979) Biochem. J. 182, 17--25]. To test whether the extraordinary sensitivity of islet cells to alloxan is due to a deficiency of endogenous enzymes protecting against oxygen-reduction products, we assayed CuZn-superoxide dismutase, Mn-superoxide dismutase, catalase and glutathione peroxidase in mouse islets and other tissues. To correct for any blood contamination, haemoglobin was also measured in the tissue samples. Pancreatic islets were found to belong to tissues with relatively little activity of the protective enzymes. However, the deviation from other tissues in this respect is probably not large enough to explain the especially great susceptibility of islet cells to alloxan.

Sign in / Sign up

Export Citation Format

Share Document