Opposite modulation of time course of quantal release in two parts of the same synapse by reactive oxygen species

Neuroscience ◽  
2011 ◽  
Vol 189 ◽  
pp. 93-99 ◽  
Author(s):  
A. Tsentsevitsky ◽  
E. Nikolsky ◽  
R. Giniatullin ◽  
E. Bukharaeva
Keyword(s):  
Reactive Oxygen Species ◽  
Time Course ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Quantal Release

Abstract 633: Aerobic Training Induces Time-course Changes Of Ace2-Ang(1-7)-Mas Receptor Axis And Reactive Oxygen Species In The Heart Of Spontaneously Hypertensive Rats

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Sebastião D Silva junior ◽  
Dulce E Casarini ◽  
Lisete C Michelini
Keyword(s):  
Reactive Oxygen Species ◽  
Time Course ◽  
Reactive Oxygen ◽  
Receptor Expression ◽  
Ros Production ◽  
Oxygen Species ◽  
Hypertensive Rats ◽  
Sequential Effects ◽  
Spontaneously Hypertensive ◽  
Mas Receptor

Objective: Since we showed recently that T causes time-dependent changes on brain RAS and oxidative stress of hypertensive rats, we sought now to investigate the sequential effects of T on ACE2-Ang(1-7)-MasR axis and reactive oxygen species (ROS) production in the left ventricle (LV) of SHRs. Methods: Male SHR and WKY aged 12 weeks underwent maximal exercise test (ET) and were allocated to T (50-60% of maximum exercise capacity, 1 h/day, 5 days/week) or sedentary (S) groups for 8 weeks. Subgroups of rats were cannulated at weeks 0 (S0), 1 (T1), 2 (T2), 4 (T4) and 8 (S8 and T8) for measurement of resting pressure (AP) and heart rate (HR), followed by saline perfusion and harvesting of the heart. ACE2 and MasR expression (Western Blotting) and ROS production (Dihydroethidium staining) were measured in the LV. Results: At the beginning of protocols SHR vs WKY exhibited higher MAP and HR (169±1 mmHg, 351±9 b/min, corresponding to 44% and 7% increases), elevated MasR (1,22±0,03 vs 1,00± 0,01 AU) but similar ACE2 expression (1,06±0,04 AU). ROS production was higher in SHR vs WKY (78±4 x 103 vs 66±1 x 103 AU). T increased treadmill performance (+0,87±0.10 km/h) and decreased resting HR (-15% at T4-T8) in both groups; MAP was only reduced in SHR (-10% at T8). T caused no change in the WKY group but increased ACE2 expression in the SHR (~1.14±0.03 au, T1-T4 P<0.05 vs WKY), with a biphasic response in Mas receptor expression: an early fall and a late increase (1,02±0,07 AU at T2-T4 and 1,20±0,04 AU at T8, respectively, P<0.05). In the SHR, T also caused an early normalization in ROS production (65±1 x 103 AU at T2) which was maintained up to T8. Again T did not change ROS production in the WKY group. Conclusions: Augmented ACE2 expression and reduced ROS production in the heart of the SHR are early responses to training, which are followed by a late increase in MasR expression. Data suggest that the prompt normalization of ROS production is mediated by ACE2-induced reduction of angiotensin II content in the LV of the trained SHR.

scholarly journals Chondrocyte cell death mediated by reactive oxygen species-dependent activation of PKC-βI

2006 ◽  
Vol 290 (3) ◽  
pp. C802-C811 ◽  
Author(s):  
Marcello DelCarlo ◽  
Richard F. Loeser
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Cell Survival ◽  
Time Course ◽  
Reactive Oxygen ◽  
Specific Protein ◽  
Ros Production ◽  
Oxygen Species ◽  
Secondary Messenger ◽  
Promote Cell Survival

Signals generated by the extracellular matrix (ECM) promote cell survival. We have shown that chondrocytes detached from their native ECM and plated without serum at low density on poly-l-lysine undergo significant cell death that is associated with the production of reactive oxygen species (ROS). No cell death or ROS production was observed when cells were plated on fibronectin under the same conditions. Cell death on poly-l-lysine could be completely inhibited with the addition of either antioxidants or inhibitors of specific protein kinase C (PKC) isoforms including PKC-βI. PKC-βI was noted to translocate from the cytosol to the particulate membrane after plating on poly-l-lysine, and this translocation was inhibited by the addition of an antioxidant. Time-course analyses implicated endogenous ROS production as a secondary messenger leading to PKC-βI activation and subsequent chondrocyte cell death. Cell survival on poly-l-lysine was significantly improved in the presence of oligomycin or DIDS, suggesting that ROS production occurred via complex V of the electron transport chain of the mitochondria and that ROS were released to the cytosol via voltage-dependent anion channels. Together, these results represent a novel mechanism by which ROS can initiate cell death through the activation of PKC-βI.

Mitochondria as a source of reactive oxygen species

2009 ◽  
pp. c3 ◽  
Author(s):  
Helena M. Cochemé ◽  
Michael P. Murphy
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Oxygen Species

Clinical aspects of reactive oxygen and nitrogen species

2004 ◽  
Vol 71 ◽  
pp. 121-133 ◽  
Author(s):  
Ascan Warnholtz ◽  
Maria Wendt ◽  
Michael August ◽  
Thomas Münzel
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Risk Factor ◽  
Endothelial Dysfunction ◽  
Vascular Tissue ◽  
Rapid Development ◽  
Reactive Oxygen ◽  
Clinical Aspects ◽  
No Production ◽  
Oxygen Species

Endothelial dysfunction in the setting of cardiovascular risk factors, such as hypercholesterolaemia, hypertension, diabetes mellitus and chronic smoking, as well as in the setting of heart failure, has been shown to be at least partly dependent on the production of reactive oxygen species in endothelial and/or smooth muscle cells and the adventitia, and the subsequent decrease in vascular bioavailability of NO. Superoxide-producing enzymes involved in increased oxidative stress within vascular tissue include NAD(P)H-oxidase, xanthine oxidase and endothelial nitric oxide synthase in an uncoupled state. Recent studies indicate that endothelial dysfunction of peripheral and coronary resistance and conductance vessels represents a strong and independent risk factor for future cardiovascular events. Ways to reduce endothelial dysfunction include risk-factor modification and treatment with substances that have been shown to reduce oxidative stress and, simultaneously, to stimulate endothelial NO production, such as inhibitors of angiotensin-converting enzyme or the statins. In contrast, in conditions where increased production of reactive oxygen species, such as superoxide, in vascular tissue is established, treatment with NO, e.g. via administration of nitroglycerin, results in a rapid development of endothelial dysfunction, which may worsen the prognosis in patients with established coronary artery disease.

Fas ligand expression in rat kupffer cells in response to lipopolysaccharide is mediated by reactive oxygen species

2001 ◽  
Vol 120 (5) ◽  
pp. A361-A361
Author(s):  
K UCHIKURA ◽  
T WADA ◽  
Z SUN ◽  
S HOSHINO ◽  
G BULKLEY ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Kupffer Cells ◽  
Fas Ligand ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Ligand Expression
Sign in / Sign up

Export Citation Format

Share Document