Electron transfer reactions in endoplasmic reticulum: Free radical production, lipid peroxidation, covalent binding and cell division

2009 ◽  
Vol 18 (S7) ◽  
pp. 347-356
Author(s):  
Trevor F. Slater ◽  
Mustaq Ahmed ◽  
Chiara Benedetto ◽  
Kevin Cheeseman ◽  
John E. Packer ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Endoplasmic Reticulum ◽  
Electron Transfer ◽  
Cell Division ◽  
Free Radical ◽  
Covalent Binding ◽  
Transfer Reactions ◽  
Electron Transfer Reactions ◽  
Free Radical Production ◽  
Radical Production

Carbon tetrachloride toxicity as a model for studying free-radical mediated liver injury

1985 ◽  
Vol 311 (1152) ◽  
pp. 633-645 ◽  
Keyword(s):  
Lipid Peroxidation ◽  
Endoplasmic Reticulum ◽  
Cell Division ◽  
Free Radical ◽  
Tissue Injury ◽  
Biological Activities ◽  
Covalent Binding ◽  
Liver Tumours

A single dose of CC1 4 when administered to a rat produces centrilobular necrosis and fatty degeneration of the liver. These hepatotoxic effects of CC1 4 are dependent upon its metabolic activation in the liver endoplasmic reticulum to reactive intermediates, including the trichloromethyl free radical. Positive identification of the formation of this free radical in vivo, in isolated liver cells and in microsomal suspensions in vitro has been achieved by e.s.r. spin-trapping techniques. The trichloromethyl radical has been found to be relatively unreactive in comparison with the secondarily derived peroxy radical CCl 3 O 2 , although each free radical species contributes significantly to the biological disturbances that occur. Major early perturbations produced to liver endoplasmic reticulum by exposure in vivo or vitro to CC1 4 include covalent binding and lipid peroxidation; studies of these processes occurring during CC1 4 intoxication have uncovered a number of concepts of general relevance to free-radical mediated tissue injury. Lipid peroxidation produces a variety of substances that have high biological activities, including effects on cell division; many liver tumours have a much reduced rate of lipid peroxidation compared with normal liver. A discussion of this rather general feature of liver tumours is given in relation to the liver cell division that follows partial hepatectomy.

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 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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