Methionine restriction decreases mitochondrial oxygen radical generation and leak as well as oxidative damage to mitochondrial DNA and proteins

2006 ◽  
Vol 20 (8) ◽  
pp. 1064-1073 ◽  
Author(s):  
Alberto Sanz ◽  
Pilar Caro ◽  
Victoria Ayala ◽  
Manuel Portero-Otin ◽  
Reinald Pamplona ◽  
...  
Keyword(s):  
Mitochondrial Dna ◽  
Oxidative Damage ◽  
Oxygen Radical ◽  
Methionine Restriction ◽  
Radical Generation

On the oxidative damage by cadmium to kidney mitochondrial functions

2019 ◽  
Vol 97 (2) ◽  
pp. 187-192 ◽  
Author(s):  
Natalia Pavón ◽  
Mabel Buelna-Chontal ◽  
Arturo Macías-López ◽  
Francisco Correa ◽  
Cristina Uribe-Álvarez ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heavy Metals ◽  
Mitochondrial Dna ◽  
Oxidative Damage ◽  
Mitochondrial Dysfunctions ◽  
Mitochondrial Functions ◽  
Electrical Gradient ◽  
Radical Generation ◽  
Parameters Of Interest ◽  
Stimulation Of

In the kidney, the accumulation of heavy metals such as Cd2+ produces mitochondrial dysfunctions, i.e., uncoupling of the oxidative phosphorylation, inhibition of the electron transport through the respiratory chain, and collapse of the transmembrane electrical gradient. This derangement may be due to the fact that Cd2+ induces the transition of membrane permeability from selective to nonselective via the opening of a transmembrane pore. In fact, Cd2+ produces this injury through the stimulation of oxygen-derived radical generation, inducing oxidative stress. Several molecules have been used to avoid or even reverse Cd2+-induced mitochondrial injury, for instance, cyclosporin A, resveratrol, dithiocarbamates, and even EDTA. The aim of this study was to explore the possibility that the antioxidant tamoxifen could protect mitochondria from the deleterious effects of Cd2+. Our results indicate that the addition of 1 μmol/L Cd2+ to mitochondria collapsed the transmembrane electrical gradient, induced the release of cytochrome c, and increased both the generation of H2O2 and the oxidative damage to mitochondrial DNA (among other measured parameters). Of interest, these mitochondrial dysfunctions were ameliorated after the addition of tamoxifen.

scholarly journals The Amyloid β Protein Induces Oxidative Damage of Mitochondrial DNA

1997 ◽  
Vol 56 (12) ◽  
pp. 1356-1362 ◽  
Author(s):  
PETER BOZNER ◽  
VALENTINA GRISHKO ◽  
SUSAN P. LEDOUX ◽  
GLENN L. WILSON ◽  
Y-C CHYAN ◽  
...  
Keyword(s):  
Mitochondrial Dna ◽  
Oxidative Damage ◽  
Amyloid Β ◽  
Amyloid Β Protein ◽  
Β Protein

Free-oxygen radical generation in ischaemic rat intestine using a tissue section chemiluminescent assay

1987 ◽  
Vol 15 (2) ◽  
pp. 289-289 ◽  
Author(s):  
JOHN P. LAVELLE ◽  
PATRICK B. COLLINS ◽  
ALAN H. JOHNSON ◽  
THOMAS F. GOREY
Keyword(s):  
Tissue Section ◽  
Oxygen Radical ◽  
Rat Intestine ◽  
Free Oxygen Radical ◽  
Free Oxygen ◽  
Radical Generation

scholarly journals Inhibition of kinases impairs neutrophil activation and killing of Staphylococcus aureus

1998 ◽  
Vol 331 (2) ◽  
pp. 489-495 ◽  
Author(s):  
Bruno SCHNYDER ◽  
Paul C. MEUNIER ◽  
Bruce D. CAR
Keyword(s):  
Staphylococcus Aureus ◽  
Map Kinases ◽  
Specific Inhibitor ◽  
Neutrophil Function ◽  
Oxygen Radical ◽  
Polymorphonuclear Neutrophils ◽  
Detectable Effect ◽  
Phosphatidylinositol 3 Kinase ◽  
Radical Generation ◽  
Phosphatidylinositol 3

Intracellular phosphorylations polymorphonuclear neutrophils are mediated by kinases, including mitogen activated-protein (MAP) kinases and phosphatidylinositol 3-kinase. In the present study we demonstrate their effector functions upon both ligation of cell-surface seven-transmembrane-spanning receptors by bacterial peptide formylmethionyl-leucylphenylalanine as well as in the process of destruction of Staphylococcus aureus. To regulate neutrophil MAP kinases p38 and p44/42, specifically, we made use of their specific inhibitors 10 µM SK&F 86002 (for p38) and PD 098059 (for activating kinase of p44/42). SK&F 86002 was a potent inhibitor (by 70%) of induced antimicrobial oxygen-radical generation compared with PD 098059 (by 20%). SK&F 86002 and PD 098059 inhibited mobilization of a dominant neutrophil adhesion molecule, β2 integrin, from cytoplasmic granules to the plasma membrane by 40 and 10% respectively, and the combination of the two drugs resulted in a 90% effect. The combined effect of both drugs was moderate inhibition of bacterial destruction, despite the fact that neither compound had detectable effect on bactericidal activity if applied individually. Bacterial destruction was also inhibited by wortmannin (0.1 µM), the specific inhibitor of phosphatidylinositol 3-kinase, which had previously been described to target various other activations of the neutrophil, including oxygen-radical generation. Although the relative contribution of p38 and p44/42 MAP kinases varied, the marked effects of the combined inhibition of the kinases revealed their concerted actions to be critical for normal neutrophil function.

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