Mitochondrial Membrane Fluidity is Consistently Increased in Different Models of Huntington Disease: Restorative Effects of Olesoxime

2014 ◽  
Vol 50 (1) ◽  
pp. 107-118 ◽  
Author(s):  
Janett Eckmann ◽  
Laura E. Clemens ◽  
Schamim H. Eckert ◽  
Stephanie Hagl ◽  
Libo Yu-Taeger ◽  
...  
Keyword(s):  
Membrane Fluidity ◽  
Huntington Disease ◽  
Mitochondrial Membrane ◽  
Mitochondrial Membrane Fluidity

scholarly journals Remote Ischemic Preconditioning of the Heart: Protective Responses in Functional and Biophysical Properties of Cardiac Mitochondria

2014 ◽  
pp. S469-S478 ◽  
Author(s):  
M. FERKO ◽  
I. KANCIROVÁ ◽  
M. JAŠOVÁ ◽  
S. ČARNICKÁ ◽  
M. MURÁRIKOVÁ ◽  
...  
Keyword(s):  
Membrane Fluidity ◽  
Ischemic Preconditioning ◽  
Mitochondrial Membrane ◽  
Ischemia Reperfusion ◽  
Remote Ischemic Preconditioning ◽  
Membrane Properties ◽  
Myocardial Energetics ◽  
Male Wistar Rats ◽  
The Right ◽  
Mitochondrial Membrane Fluidity

Remote ischemic preconditioning (RIP)-induced protection of myocardial energetics was well documented on the level of tissue, but data concerning the involvement of mitochondria were missing. We aimed at the identification of changes in membrane properties and respiratory functions induced in rat heart mitochondria by RIP. Experiments were performed on 46 male Wistar rats divided into control and RIP-treated groups of 21 animals each. Blood flow in the occluded area was recorded by MRI angiography in four animals. RIP protocol comprised of three successive 5-min occlusions each followed by 5-min reperfusions of descending branches of the right hind limb femoral artery. The efficacy of RIP was evaluated as the extent of RIP-induced protection against damage to the functions of mitochondria isolated by differential centrifugation after 30-min global ischemia followed by 40-min reperfusion of the hearts in Langendorff mode. Assessments: mitochondrial membrane fluidity with a fluorescent probe DPH, CoQ9 and CoQ10 with HPLC, mitochondrial respiration with the Oxygraph-2k (Oroboros). Results revealed that RIP was affecting the mitochondria. The immediate protection conferred by RIP involves beneficial and prognostically significant effects: a total elimination of ischemia/reperfusion-induced depression of mitochondrial membrane fluidity and a trend for better preservation of mitochondrial state 3 respiration.

scholarly journals Participation of Heart Mitochondria in Myocardial Protection Against Ischemia/Reperfusion Injury: Benefit Effects of Short-Term Adaptation Processes

2015 ◽  
pp. S617-S625 ◽  
Author(s):  
M. FERKO ◽  
I. KANCIROVÁ ◽  
M. JAŠOVÁ ◽  
I. WACZULÍKOVÁ ◽  
S. ČARNICKÁ ◽  
...  
Keyword(s):  
Infarct Size ◽  
Reperfusion Injury ◽  
Membrane Fluidity ◽  
Mitochondrial Membrane ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Favorable Effect ◽  
Ischemic Reperfusion Injury ◽  
Ischemic Reperfusion ◽  
Mitochondrial Membrane Fluidity

Acute streptozotocin diabetes mellitus (DM) as well as remote ischemic preconditioning (RPC) has shown a favorable effect on the postischemic-reperfusion function of the myocardium. Cardioprotective mechanisms offered by these experimental models involve the mitochondria with the changes in functional properties of membrane as the end-effector. The aim was to find out whether separate effects of RPC and DM would stimulate the mechanisms of cardioprotection to a maximal level or whether RPC and DM conditions would cooperate in stimulation of cardioprotection. Experiments were performed on male Wistar rats divided into groups: control, DM, RPC and DM treated by RPC (RPC+DM). RPC protocol of 3 cycles of 5-min hind limb ischemia followed by 5-min reperfusion was used. Ischemic-reperfusion injury was induced by 30-min ischemia followed by 40-min reperfusion of the hearts in Langendorff mode. Mitochondria were isolated by differential centrifugation, infarct size assessed by staining with 1 % 2,3,5-triphenyltetrazolium chloride, mitochondrial membrane fluidity with a fluorescent probe DPH, CoQ9 and CoQ10 with HPLC. Results revealed that RPC as well as DM decreased the infarct size and preserved mitochondrial function by increasing the mitochondrial membrane fluidity. Both used models separately offered a sufficient protection against ischemic-reperfusion injury without an additive effect of their combination.

Protective Effects of the Antioxidant 4b,5,9b,10-Tetrahydroindeno[1,2-b]indole Against TCDD Toxicity in C57BL/6J Mice

2009 ◽  
Vol 29 (1) ◽  
pp. 40-48 ◽  
Author(s):  
Howard G. Shertzer
Keyword(s):  
Body Weight ◽  
Membrane Fluidity ◽  
Mitochondrial Respiration ◽  
Mitochondrial Membrane ◽  
Body Weight Gain ◽  
Concomitant Administration ◽  
Protective Effects ◽  
Percentage Body Fat ◽  
Production Of Hydrogen ◽  
Mitochondrial Membrane Fluidity

The protection against 2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD; 5 µg/kg body weight) toxicity by the antioxidant 4b,5,9b,10-tetrahydroindeno[1,2- b]indole (THII) was examined in female C57BL/6J mice. TCDD produced increases in the levels of hepatic lipid-derived aldehydes, rates of mitochondrial production of hydrogen peroxide and superoxide, and the oxidation state of cytosolic GSH. In contrast, mitochondrial GSH increased in reduction state, correlating with an increase in mitochondrial membrane potential. Systemically, TCDD lowered body weight gain, percentage body fat, and hepatic ATP levels, parameters prevented by concomitant administration of 100 µM THII in drinking water. However, TCDD-induced increases in mitochondrial respiration and decreased mitochondrial membrane fluidity were not prevented by THII. These results suggest that TCDD-mediated oxidative stress was not responsible for changes in mitochondrial respiration or membrane fluidity. Furthermore, although TCDD produced a large increase in mitochondrial oxygen consumption, this was not associated with the poor gain in weight produced by TCDD.

scholarly journals Stimulation of Mitochondrial ATP Synthase Activity – a New Diazoxide-Mediated Mechanism of Cardioprotection

2016 ◽  
pp. S119-S127 ◽  
Author(s):  
M. JAŠOVÁ ◽  
I. KANCIROVÁ ◽  
M. MURÁRIKOVÁ ◽  
V. FARKAŠOVÁ ◽  
I. WACZULÍKOVÁ ◽  
...  
Keyword(s):  
Membrane Fluidity ◽  
Atp Synthase ◽  
Mitochondrial Membrane ◽  
Isolated Heart ◽  
Myocardial Infarct ◽  
Direct Interaction ◽  
Myocardial Infarct Size ◽  
Mitochondrial Atp Synthase ◽  
Mitochondrial Membrane Fluidity

Pharmacological preconditioning by diazoxide and a model of experimental streptozotocin-induced acute diabetes mellitus (STZ-DM) provided similar levels of cardioprotection assessed as limiting myocardial infarct size. The aim was to explore the possibility of existence of another in vitro mechanism, which could be contributory to cardioprotection mediated by diazoxide treatment. Mitochondrial membrane fluidity and ATP synthase activity in isolated heart mitochondria were determined under the influence of two factors, STZ-DM condition and treatment with diazoxide. Both factors independently increased the ATP synthase activity (p<0.05), as no interaction effect was observed upon the combination of STZ-DM with diazoxide. On the other hand, the mitochondrial membrane fluidity was significantly increased by STZ-DM only; no significant main effect for diazoxide was found. Based on the results from measurements of enzyme kinetics, we assume a direct interaction of diazoxide with the molecule of ATP synthase stimulated its activity by noncompetitive activation. Our present work revealed, for the first time, that cardioprotection induced by diazoxide may not be caused exclusively by mitochondrial KATP opening, but presumably also by a direct interaction of diazoxide with ATP synthase, although the mechanisms for achieving this activation cannot be fully delineated.

Mitochondrial membrane fluidity and oxidative damage to mitochondrial DNA in aged and AD human brain

1997 ◽  
Vol 31 (1) ◽  
pp. 53-64 ◽  
Author(s):  
Patrizia Mecocci ◽  
M. Flint Beal ◽  
Roberta Cecchetti ◽  
Maria Cristina Polidori ◽  
Antonio Cherubini ◽  
...  
Keyword(s):  
Mitochondrial Dna ◽  
Oxidative Damage ◽  
Human Brain ◽  
Membrane Fluidity ◽  
Mitochondrial Membrane ◽  
Mitochondrial Membrane Fluidity

Altered mitochondrial membrane fluidity in AD brain

1996 ◽  
Vol 207 (2) ◽  
pp. 129-132 ◽  
Author(s):  
Patrizia Mecocci ◽  
Antonio Cherubini ◽  
M.Flint Beal ◽  
Roberta Cecchetti ◽  
Fausto Chionne ◽  
...  
Keyword(s):  
Membrane Fluidity ◽  
Mitochondrial Membrane ◽  
Mitochondrial Membrane Fluidity
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