نتایج جستجو برای: mitochondrial permeability

تعداد نتایج: 179091  

Journal: :Journal of cell science 2002
Julia V Gerasimenko Oleg V Gerasimenko Altaf Palejwala Alexei V Tepikin Ole H Petersen Alastair J M Watson

In normal pancreatic acinar cells, the oxidant menadione evokes repetitive cytosolic Ca(2+) spikes, partial mitochondrial depolarisation, cytochrome c release and apoptosis. The physiological agonists acetylcholine and cholecystokinin also evoke cytosolic Ca(2+) spikes but do not depolarise mitochondria and fail to induce apoptosis. Ca(2+) spikes induced by low agonist concentrations are confin...

Journal: :Toxicological sciences : an official journal of the Society of Toxicology 1998
J B Custodio C M Palmeira A J Moreno K B Wallace

Acrylic acid (AA) is used widely in the synthesis of esters essential in the production of paints, adhesives, plastics, and coatings. The minimal systemic toxicity of AA is attributed to its rapid oxidation to acetyl-CoA and CO2 via the vitamin B12-independent beta-oxidation pathway. This oxidation is localized to the mitochondria and preliminary evidence suggests a possible inhibition of mitoc...

2012
A Sesso JE Belizário MM Marques ML Higuchi RI Schumacher A Colquhoun E Ito J Kawakami

Outer mitochondrial membrane (OMM) rupture was first noted in isolated mitochondria in which the inner mitochondrial membrane (IMM) had lost its selective permeability. This phenomenon referred to as mitochondrial permeability transition (MPT) refers to a permeabilized inner membrane that originates a large swelling in the mitochondrial matrix, which distends the outer membrane until it rupture...

Journal: :Circulation 2011
Jan Horstkotte Tamara Perisic Manuela Schneider Philipp Lange Melanie Schroeder Claudia Kiermayer Rabea Hinkel Tilman Ziegler Pankaj K Mandal Robert David Sabine Schulz Sabine Schmitt Julian Widder Fred Sinowatz Bernhard F Becker Johann Bauersachs Michael Naebauer Wolfgang M Franz Irmela Jeremias Markus Brielmeier Hans Zischka Marcus Conrad Christian Kupatt

BACKGROUND Excessive formation of reactive oxygen species contributes to tissue injury and functional deterioration after myocardial ischemia/reperfusion. Especially, mitochondrial reactive oxygen species are capable of opening the mitochondrial permeability transition pore, a harmful event in cardiac ischemia/reperfusion. Thioredoxins are key players in the cardiac defense against oxidative st...

2011
Jae-Sung Kim Jin-Hee Wang John J. Lemasters

42 Onset of the mitochondrial permeability transition (MPT) is the penultimate event 43 leading to lethal cellular ischemia/reperfusion injury, but the mechanisms precipitating 44 the MPT after reperfusion remain unclear. Here, we investigated the role of 45 mitochondrial free Ca and reactive oxygen species (ROS) in pHand MPT-dependent 46 reperfusion injury to hepatocytes. Cultured rat hepatocy...

Journal: :Circulation 2005
Laurent Argaud Odile Gateau-Roesch Olivier Raisky Joseph Loufouat Dominique Robert Michel Ovize

BACKGROUND Brief periods of ischemia performed just at the time of reperfusion can reduce infarct size, a phenomenon called "postconditioning." After reflow, opening of the mitochondrial permeability transition pore (mPTP) has been involved in lethal reperfusion injury. We hypothesized that postconditioning may modulate mPTP opening. METHODS AND RESULTS Anesthetized open-chest rabbits underwe...

Journal: :Biochemical Society symposium 1999
M Crompton S Virji V Doyle N Johnson J M Ward

This chapter reviews recent advances in the identification of the structural elements of the permeability transition pore. The discovery that cyclosporin A (CsA) inhibits the pore proved instrumental. Various approaches indicate that CsA blocks the pore by binding to cyclophilin (CyP)-D. In particular, covalent labelling of CyP-D in situ by a photoactive CsA derivative has shown that pore ligan...

Journal: :Biochimica et Biophysica Acta (BBA) - Bioenergetics 2010

Journal: :Journal of the American College of Cardiology 2006
Jérome Larche Steve Lancel Sidi Mohamed Hassoun Raphael Favory Brigitte Decoster Philippe Marchetti Claude Chopin Remi Neviere

OBJECTIVES The purpose of this study was to test whether mitochondrial dysfunction is causative of sepsis sequelae, a mouse model of peritonitis sepsis induced by cecal ligation and perforation. Inhibition of mitochondrial permeability transition was achieved by means of pharmacological drugs and overexpression of the antiapoptotic protein B-cell leukemia (Bcl)-2. BACKGROUND Sepsis is the lea...

نمودار تعداد نتایج جستجو در هر سال

با کلیک روی نمودار نتایج را به سال انتشار فیلتر کنید