Acute infusion of nicotine impairs nNOS-dependent reactivity of cerebral arterioles via an increase in oxidative stress

2007 ◽  
Vol 103 (6) ◽  
pp. 2062-2067 ◽  
Author(s):  
Denise M. Arrick ◽  
William G. Mayhan
Keyword(s):  
Oxidative Stress ◽  
Superoxide Anion ◽  
Potential Role ◽  
Acute Exposure ◽  
Cerebral Microcirculation ◽  
Superoxide Anion Production ◽  
Anion Production ◽  
Cerebral Arterioles ◽  
Oxide Synthase

Our goals were to determine whether acute exposure to nicotine alters neuronal nitric oxide synthase (nNOS)-dependent reactivity of cerebral arterioles and to identify a potential role for oxidative stress in nicotine-induced impairment in nNOS-dependent responses of cerebral arterioles. We measured in vivo diameter of cerebral arterioles to nNOS-dependent ( N-methyl-d-aspartate and kainate) and -independent (nitroglycerin) agonists before and during acute treatment with nicotine. We found that nNOS-dependent, but not -independent, vasodilatation was impaired during treatment with nicotine. In addition, treatment of the cerebral microcirculation with tempol (1 h before infusion of nicotine) prevented nicotine-induced impairment in nNOS-dependent vasodilatation. Furthermore, the production of superoxide anion (lucigenin chemiluminescence) was increased in parietal cortex tissue of rats by treatment with nicotine, and this increase in superoxide anion production could be inhibited by tempol. Our findings suggest that acute exposure to nicotine impairs nNOS-dependent dilatation of cerebral arterioles by a mechanism that appears to be related to the formation of superoxide anion.

scholarly journals Exercise training restores impaired dilator responses of cerebral arterioles during chronic exposure to nicotine

2010 ◽  
Vol 109 (4) ◽  
pp. 1109-1114 ◽  
Author(s):  
William G. Mayhan ◽  
Denise M. Arrick ◽  
Hong Sun ◽  
Kaushik P. Patel
Keyword(s):  
Exercise Training ◽  
Superoxide Anion ◽  
Chronic Exposure ◽  
Superoxide Dismutase 1 ◽  
Superoxide Anion Production ◽  
Cerebral Microvessels ◽  
Anion Production ◽  
Pial Arterioles ◽  
Cerebral Arterioles ◽  
Oxide Synthase

Our goal was to determine whether exercise training (ExT) alleviates impaired nitric oxide synthase (NOS)-dependent dilation of pial arterioles during chronic exposure to nicotine. We measured dilation of cerebral (pial) arterioles in sedentary and exercised control and nicotine-treated (2 mg·kg−1·day−1 for 4 wk via an osmotic minipump) rats to an endothelial NOS (eNOS)-dependent (ADP), a neuronal NOS (nNOS)-dependent [ N-methyl-d-aspartic acid (NMDA)], and a NOS-independent (nitroglycerin) agonist. In addition, we harvested brain tissue from sedentary and exercised control and nicotine-treated rats to measure the production of superoxide anion and measured superoxide dismutase-1 (SOD-1) protein in cerebral microvessels using Western blot. We found that eNOS-and nNOS-dependent, but not NOS-independent, vasodilation was impaired in nicotine-treated compared with control rats. In addition, the production of superoxide anion (lucigenin chemiluminescence) was increased, and SOD-1 protein decreased, in rats treated with nicotine compared with control rats. Further, although ExT did not significantly affect eNOS- or nNOS-dependent vasodilation in control rats, ExT restored impaired eNOS- and nNOS-dependent responses in nicotine-treated rats. In addition, the increase in superoxide anion production observed in nicotine-treated rats was reduced by ExT, and SOD-1 protein was increased in nicotine-treated rats by ExT. We suggest that ExT restores impaired NOS-dependent dilation of pial arterioles during chronic exposure to nicotine by a mechanism related to the formation of superoxide anion.

Mitochondrial Adenosine Triphosphate–regulated Potassium Channel Opening Acts as a Trigger for Isoflurane-induced Preconditioning by Generating Reactive Oxygen Species

2003 ◽  
Vol 98 (4) ◽  
pp. 935-943 ◽  
Author(s):  
Katsuya Tanaka ◽  
Dorothee Weihrauch ◽  
Lynda M. Ludwig ◽  
Judy R. Kersten ◽  
Paul S. Pagel ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Infarct Size ◽  
Adenosine Triphosphate ◽  
Superoxide Anion ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Superoxide Anion Production ◽  
Channel Opening ◽  
Anion Production

Background Whether the opening of mitochondrial adenosine triphosphate-regulated potassium (K(ATP)) channels is a trigger or an end effector of anesthetic-induced preconditioning is unknown. We tested the hypothesis that the opening of mitochondrial K(ATP) channels triggers isoflurane-induced preconditioning by generating reactive oxygen species (ROS) in vivo. Methods Pentobarbital-anesthetized rabbits were subjected to a 30-min coronary artery occlusion followed by 3 h reperfusion. Rabbits were randomly assigned to receive a vehicle (0.9% saline) or the selective mitochondrial K(ATP) channel blocker 5-hydroxydecanoate (5-HD) alone 10 min before or immediately after a 30-min exposure to 1.0 minimum alveolar concentration (MAC) isoflurane. In another series of experiments, the fluorescent probe dihydroethidium was used to assess superoxide anion production during administration of 5-HD or the ROS scavengers N-acetylcysteine or N-2-mercaptopropionyl glycine (2-MPG) in the presence or absence of 1.0 MAC isoflurane. Myocardial infarct size and superoxide anion production were measured using triphenyltetrazolium staining and confocal fluorescence microscopy, respectively. Results Isoflurane (P < 0.05) decreased infarct size to 19 +/- 3% (mean +/- SEM) of the left ventricular area at risk as compared to the control (38 +/- 4%). 5-HD administered before but not after isoflurane abolished this beneficial effect (37 +/- 4% as compared to 24 +/- 3%). 5-HD alone had no effect on infarct size (42 +/- 3%). Isoflurane increased fluorescence intensity. Pretreatment with N-acetylcysteine, 2-MPG, or 5-HD before isoflurane abolished increases in fluorescence, but administration of 5-HD after isoflurane only partially attenuated increases in fluorescence produced by the volatile anesthetic agent. Conclusions The results indicate that mitochondrial K(ATP) channel opening acts as a trigger for isoflurane-induced preconditioning by generating ROS in vivo.

Exposure of surfactant protein A to ozone in vitro and in vivo impairs its interactions with alveolar cells

1992 ◽  
Vol 262 (1) ◽  
pp. L63-L68 ◽  
Author(s):  
R. S. Oosting ◽  
J. F. Van Iwaarden ◽  
L. Van Bree ◽  
J. Verhoef ◽  
L. M. Van Golde ◽  
...  
Keyword(s):  
Superoxide Anion ◽  
Protein A ◽  
Surfactant Protein ◽  
Surfactant Protein A ◽  
Alveolar Type ◽  
Type Ii ◽  
Superoxide Anion Production ◽  
Anion Production

This study focused on the question of whether exposure of surfactant protein A (SP-A) to ozone affected properties of this protein that may be involved in regulating alveolar type II cell and alveolar macrophage functions. In vitro exposure of human or canine SP-A to ozone reduced the ability of this protein to inhibit phorbol-ester induced secretion of [3H]phosphatidylcholine by alveolar type II cells in culture. Ozone-exposed human SP-A showed a decreased ability to enhance phagocytosis of herpes simplex virus and to stimulate superoxide anion production by alveolar macrophages. Experiments with elastase showed that ozone-exposed canine SP-A was more susceptible to proteolysis. A conformational change of the protein could underlie this phenomenon. Surfactant isolated from ozone-exposed rats (0.4 ppm ozone for 12 h) was also less able to stimulate superoxide anion production by alveolar macrophages than surfactant from control rats, which suggested that SP-A in vivo was also susceptible to ozone. The results of this study suggest that SP-A-alveolar cell interactions can be inhibited by ozone exposure, which may contribute to the toxicity of ozone in the lungs.

scholarly journals Mechanism of Preconditioning by Isoflurane in Rabbits: A Direct Role for Reactive Oxygen Species

2002 ◽  
Vol 97 (6) ◽  
pp. 1485-1490 ◽  
Author(s):  
Katsuya Tanaka ◽  
Dorothee Weihrauch ◽  
Franz Kehl ◽  
Lynda M. Ludwig ◽  
John F. LaDisa ◽  
...  
Keyword(s):  
Infarct Size ◽  
Superoxide Anion ◽  
Myocardial Infarct ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Myocardial Infarct Size ◽  
Oxygen Species ◽  
Superoxide Anion Production ◽  
Anion Production

Background Reactive oxygen species (ROS) contribute to myocardial protection during ischemic preconditioning, but the role of the ROS in protection against ischemic injury produced by volatile anesthetics has only recently been explored. We tested the hypothesis that ROS mediate isoflurane-induced preconditioning in vivo. Methods Pentobarbital-anesthetized rabbits were instrumented for measurement of hemodynamics and were subjected to a 30 min coronary artery occlusion followed by 3 h reperfusion. Rabbits were randomly assigned to receive vehicle (0.9% saline), or the ROS scavengers N-acetylcysteine (NAC; 150 mg/kg) or N-2-mercaptopropionyl glycine (2-MPG; 1 mg. kg(-1).min(-1)), in the presence or absence of 1.0 minimum alveolar concentration (MAC) isoflurane. Isoflurane was administered for 30 min and then discontinued 15 min before coronary artery occlusion. A fluorescent probe for superoxide anion production (dihydroethidium, 2 mg) was administered in the absence of the volatile anesthetic or 5 min before exposure to isoflurane in 2 additional groups (n = 8). Myocardial infarct size and superoxide anion production were assessed using triphenyltetrazolium staining and confocal fluorescence microscopy, respectively. Results Isoflurane (P < 0.05) decreased infarct size to 24 +/- 4% (mean +/- SEM; n = 10) of the left ventricular area at risk compared with control experiments (43 +/- 3%; n = 8). NAC (43 +/- 3%; n = 7) and 2-MPG (42 +/- 5%; n = 8) abolished this beneficial effect, but had no effect on myocardial infarct size (47 +/- 3%; n = 8 and 46 +/- 3; n = 7, respectively) when administered alone. Isoflurane increased superoxide anion production as compared with control experiments (28 +/- 12 -6 +/- 9 fluorescence units; P < 0.05). Conclusions The results indicate that ROS produced following administration of isoflurane contribute to protection against myocardial infarction in vivo.

scholarly journals In vitro characterisation of fresh and frozen sex-sorted bull spermatozoa

2017 ◽  
Vol 29 (7) ◽  
pp. 1415 ◽  
Author(s):  
Shauna A. Holden ◽  
Craig Murphy ◽  
Juan F. Moreno ◽  
Stephen T. Butler ◽  
Andrew R. Cromie ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Superoxide Anion ◽  
Superoxide Anion Production ◽  
Holstein Friesian ◽  
Anion Production ◽  
And Oxidative Stress

This study sought to compare the in vitro characteristics of fresh and frozen non-sorted (NS) and sex-sorted (SS) bull spermatozoa. Experiment 1: Holstein–Friesian ejaculates (n = 10 bulls) were split across four treatments and processed: (1) NS fresh at 3 × 106 spermatozoa, (2) X-SS frozen at 2 × 106 spermatozoa, (3) X-SS fresh at 2 × 106 spermatozoa and (4) X-SS fresh at 1 × 106 spermatozoa. NS frozen controls of 20 × 106 spermatozoa per straw were sourced from previously frozen ejaculates (n = 3 bulls). Experiment 2: Aberdeen Angus ejaculates (n = 4 bulls) were split across four treatments and processed as: (1) NS fresh 3 × 106 spermatozoa, (2) Y-SS fresh at 1 × 106 spermatozoa, (3) Y-SS fresh at 2 × 106 spermatozoa and (4) X-SS fresh at 2 × 106 spermatozoa. Controls were sourced as per Experiment 1. In vitro assessments for progressive linear motility, acrosomal status and oxidative stress were carried out on Days 1, 2 and 3 after sorting (Day 0 = day of sorting. In both experiments SS fresh treatments had higher levels of agglutination in comparison to the NS fresh (P < 0.001), NS frozen treatments had the greatest PLM (P < 0.05) and NS spermatozoa exhibited higher levels of superoxide anion production compared with SS spermatozoa (P < 0.05). Experiment 1 found both fresh and frozen SS treatments had higher levels of viable acrosome-intact spermatozoa compared with the NS frozen treatments (P < 0.01).

Endothelial Dysfunction Coincides With an Enhanced Nitric Oxide Synthase Expression and Superoxide Anion Production

Hypertension ◽  
1997 ◽  
Vol 30 (4) ◽  
pp. 934-941 ◽  
Author(s):  
Anne Bouloumié ◽  
Johann Bauersachs ◽  
Wolfgang Linz ◽  
Bernward A. Schölkens ◽  
Gabriele Wiemer ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Dysfunction ◽  
Nitric Oxide Synthase ◽  
Superoxide Anion ◽  
Superoxide Anion Production ◽  
Anion Production ◽  
Oxide Synthase

Anemia associated with extraerythrocytic oxidative stress damage mediated by neutrophil superoxide anion production in chronic renal failure patients undergoing hemodialysis

2012 ◽  
Vol 19 (4) ◽  
pp. 261-268 ◽  
Author(s):  
Jair Tonon ◽  
Flávia Alessandra Guarnier ◽  
Alessandra Lourenço Cecchini ◽  
Rubens Cecchini
Keyword(s):  
Oxidative Stress ◽  
Renal Failure ◽  
Chronic Renal Failure ◽  
Superoxide Anion ◽  
Superoxide Anion Production ◽  
Anion Production ◽  
Neutrophil Superoxide ◽  
Stress Damage
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