Uncoupling of mitochondrial oxidative phosphorylation alters lipid peroxidation-derived free radical production but not recovery of postischemic rat hearts and post-hypoxic endothelial cells

1996 ◽  
Vol 160-161 (1) ◽  
pp. 167-177 ◽  
Author(s):  
I. E. Blasig ◽  
B. F. Dickens ◽  
W. B. Weglicki ◽  
J. H. Kramer
Keyword(s):  
Lipid Peroxidation ◽  
Endothelial Cells ◽  
Free Radical ◽  
Oxidative Phosphorylation ◽  
Mitochondrial Oxidative Phosphorylation ◽  
Free Radical Production ◽  
Radical Production ◽  
Rat Hearts

scholarly journals Direct evidence of iNOS-mediated in vivo free radical production and protein oxidation in acetone-induced ketosis

2008 ◽  
Vol 295 (2) ◽  
pp. E456-E462 ◽  
Author(s):  
Krisztian Stadler ◽  
Marcelo G. Bonini ◽  
Shannon Dallas ◽  
Danielle Duma ◽  
Ronald P. Mason ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Free Radical ◽  
Nadph Oxidase ◽  
Knockout Mice ◽  
Protein Oxidation ◽  
Ketone Bodies ◽  
Free Radical Production ◽  
Radical Production ◽  
Inos Knockout Mice

Diabetic patients frequently encounter ketosis that is characterized by the breakdown of lipids with the consequent accumulation of ketone bodies. Several studies have demonstrated that reactive species are likely to induce tissue damage in diabetes, but the role of the ketone bodies in the process has not been fully investigated. In this study, electron paramagnetic resonance (EPR) spectroscopy combined with novel spin-trapping and immunological techniques has been used to investigate in vivo free radical formation in a murine model of acetone-induced ketosis. A six-line EPR spectrum consistent with the α-(4-pyridyl-1-oxide)- N-t-butylnitrone radical adduct of a carbon-centered lipid-derived radical was detected in the liver extracts. To investigate the possible enzymatic source of these radicals, inducible nitric oxide synthase (iNOS) and NADPH oxidase knockout mice were used. Free radical production was unchanged in the NADPH oxidase knockout but much decreased in the iNOS knockout mice, suggesting a role for iNOS in free radical production. Longer-term exposure to acetone revealed iNOS overexpression in the liver together with protein radical formation, which was detected by confocal microscopy and a novel immunospin-trapping method. Immunohistochemical analysis revealed enhanced lipid peroxidation and protein oxidation as a consequence of persistent free radical generation after 21 days of acetone treatment in control and NADPH oxidase knockout but not in iNOS knockout mice. Taken together, our data demonstrate that acetone administration, a model of ketosis, can lead to protein oxidation and lipid peroxidation through a free radical-dependent mechanism driven mainly by iNOS overexpression.

scholarly journals Free-radical production triggered by hyperthermia contributes to heat stress-induced cardioprotection in isolated rat hearts

2002 ◽  
Vol 135 (7) ◽  
pp. 1776-1782 ◽  
Author(s):  
Claire Arnaud ◽  
Marie Joyeux ◽  
Catherine Garrel ◽  
Diane Godin-Ribuot ◽  
Pierre Demenge ◽  
...  
Keyword(s):  
Heat Stress ◽  
Free Radical ◽  
Free Radical Production ◽  
Radical Production ◽  
Rat Hearts ◽  
Isolated Rat

scholarly journals Effect of the 21-Aminosteroid U74389G on Oxygen-Induced Free Radical Production, Lipid Peroxidation, and Inhibition of Lung Growth in Neonatal Rats

1999 ◽  
Vol 46 (2) ◽  
pp. 215-223 ◽  
Author(s):  
Xiaoping Luo ◽  
Larisa Sedlackova ◽  
Rose Belcastro ◽  
Judy Cabacungan ◽  
Stephen J Lye ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Free Radical ◽  
Neonatal Rats ◽  
Lung Growth ◽  
Free Radical Production ◽  
Radical Production
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