scholarly journals THE STUDY OF NITRIC OXIDE ACTION IN VIVO ON NA+ , K+ -ÀÒPASE IN RAT AORTA

2009 ◽  
Vol 55 (1) ◽  
pp. 27-35
Author(s):  
O.V. Akopova ◽  
◽  
O.N. Kharlamova ◽  
A.V. Kotsiuruba ◽  
Yu.P. Korkach ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Free Radical ◽  
Atpase Activity ◽  
Rat Aorta ◽  
Radical Reactions ◽  
Hypotensive Action ◽  
No Donor ◽  
Free Radical Reactions ◽  
Stimulation Of

The influence of nitric oxide on Na+,K+-ATPase activity in rat aorta was studied by means of stimulation of endogenous NO synthesis after injections of bacterial lipopolysaccharide (LPS) and pharmacological NO donor nitroglycerine (NG). It was shown that NO action on Na+,K+-ATPase in vivo is dose-de­pendent. Stimulation of the endogenous NO synthesis by LPS as well as the administration of low doses of NG lead to the activation of Na+,K+-ATPase and favor the conclusion that NO-dependent Na+,K+-ATPase stimulation mediates vasodilatory and hypotensive action of nitric oxide. The Na+,K+-ATPase activity in rat aorta depends on the balance between the level of reactive oxygen and nitrogen species (ROS and RNS), forma­tion of NO depots in the tissue of aorta as high- and low mo­lecular weight nitrosothiols, and also on the intensity of free-radical reactions resulting in the generation of hydroperoxide radicals. The results obtained suggest that NOS- and cGMP-dependent pathway takes part in Na+,K+-ATPase activation by LPS and NG, but the enzyme inhibition by nitric oxide in vivo is not cGMP-dependent and is determined by the activation of free-radical reactions and dramatic enhancement of nitrosylation level in rat aorta tissue.

Further studies on free-radical pathology in the major central nervous system disorders: effect of very high doses of methylprednisolone on the functional outcome, morphology, and chemistry of experimental spinal cord impact injury

1982 ◽  
Vol 60 (11) ◽  
pp. 1415-1424 ◽  
Author(s):  
H. B. Demopoulos ◽  
E. S. Flamm ◽  
M. L. Seligman ◽  
D. D. Pietronigro ◽  
J. Tomasula ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Nervous System ◽  
Free Radical ◽  
Tissue Injury ◽  
Functional Restoration ◽  
Radical Reactions ◽  
Free Radical Reactions ◽  
Cord Injury

The hypothesis that pathologic free-radical reactions are initiated and catalyzed in the major central nervous system (CNS) disorders has been further supported by the current acute spinal cord injury work that has demonstrated the appearance of specific, cholesterol free-radical oxidation products. The significance of these products is suggested by the fact that: (i) they increase with time after injury; (ii) their production is curtailed with a steroidal antioxidant; (iii) high antioxidant doses of the steroidal antioxidant which curtail the development of free-radical product prevent tissue degeneration and permit functional restoration. The role of pathologic free-radical reactions is also inferred from the loss of ascorbic acid, a principal CNS antioxidant, and of extractable cholesterol. These losses are also prevented by the steroidal antioxidant. This model system is among others in the CNS which offer distinctive opportunities to study, in vivo, the onset and progression of membrane damaging free-radical reactions within well-defined parameters of time, extent of tissue injury, correlation with changes in membrane enzymes, and correlation with readily measurable in vivo functions.

Measuring free radical reactions in vivo

1993 ◽  
Vol 49 (3) ◽  
pp. 494-505 ◽  
Author(s):  
A E Holley ◽  
K H Cheeseman
Keyword(s):  
Free Radical ◽  
Radical Reactions ◽  
Free Radical Reactions

In Vivo ESR Measurement of Free Radical Reactions in Living Mice

1998 ◽  
pp. 13-22
Author(s):  
Hideo Utsumi ◽  
Keizo Takeshita ◽  
Kazuhiro Ichikawa ◽  
Hiroaki Sano ◽  
Toshiki Masumizu ◽  
...  
Keyword(s):  
Free Radical ◽  
Radical Reactions ◽  
Free Radical Reactions

Intensity of free-radical reactions in metastasizing cervical cancer.

2021 ◽  
Vol 39 (15_suppl) ◽  
pp. e17508-e17508
Author(s):  
Natalia V. Chernikova ◽  
Irina A. Goroshinskaya ◽  
Elena M. Frantsiyants ◽  
Ekaterina V. Verenikina ◽  
Yuriy A. Poryvaev ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cervical Cancer ◽  
Lipid Peroxidation ◽  
Free Radical ◽  
Blood Plasma ◽  
Plasma Proteins ◽  
Oxidative Modification ◽  
Radical Reactions ◽  
Free Radical Reactions ◽  
Blood Plasma Proteins

e17508 Background: Cervical cancer (CC) is one of the main causes of death among patients with gynecological tumors. As a rule, patients die from relapses and metastases which rates reach 30-45%. According to research data, treatment of patients with distant metastases is ineffective, and half of them die within 9.7 months, while the average survival is 15.9±0.26 months. The development of many pathological processes is considered to be associated with an increase in free-radical reactions leading to oxidative damage to various biomolecules. The purpose of the study was to analyze some characteristics of the free-radical oxidation and antioxidant defence in metastasizing CC. Methods: The study included 56 patients aged 29-73 years with stage IIB-IV CC after antitumor treatment. The main group – 27 patients who developed metastases within 4 months to 8 years after the CC diagnosis; controls – 29 patients with non-metastatic CC; donors – 19 healthy women aged 27-61 years. The accumulation of carbonyl derivatives in blood plasma proteins was detected in the reaction with 2, 4-dinitrophenylhydrazine. The induced oxidative modification of proteins was stimulated with Fenton's reagent. Free-radical processes was evaluated by the intensity of peroxide-induced luminol-dependent plasma chemiluminescence and the content of nitric oxide metabolites; the intensity of lipid peroxidation - by the content of malondialdehyde (MDA); the activity of catalase and ceruloplasmin was also studied. Results: CC progression was accompanied by increasing lipid peroxidation and spontaneous oxidation of blood plasma proteins. MDA levels in patients with metastases increased by 57.8% compared to donors and by 34.3% compared to patients without metastases (p < 0.05). The concentration of 2, 4-dinitrophenylhydrozones increased on average by 4 times compared to donors and by almost 2 times compared to patients without metastases. Patients with metastasizing CC demonstrated elevated levels of products of the interaction of nitric oxide and its derivatives with proteins and peptides - 3-nitrotyrosine and nitrosoglutathione, compared to both donors (by 31.4% and 55.3%) and patients in remission (by 38.1% and 34.5%). Chemiluminescence activity increased by 54.5% compared to donors (p < 0.05) and by 93% (p < 0.01) compared to controls. Catalase activity in the blood plasma of patients with metastases increased by 54.1% compared to donors, but was lower than the values in the control group (by 22.1%). Ceruloplasmin activity was increased only in patients without metastases (by 33%). Conclusions: The process of CC metastasis is accompanied by a greater intensity of oxidative processes of both proteins and lipids, as well as depletion of the adaptive capabilities of the body's antioxidant system.

scholarly journals Measurement of allantoin and uric acid in human body fluids. A potential index of free-radical reactions in vivo?

1987 ◽  
Vol 243 (3) ◽  
pp. 803-808 ◽  
Author(s):  
M Grootveld ◽  
B Halliwell
Keyword(s):  
Uric Acid ◽  
Free Radical ◽  
Human Body ◽  
Body Fluids ◽  
Radical Reactions ◽  
Free Radical Reactions ◽  
Potential Index ◽  
Free Radical Attack ◽  
Radical Attack

Free-radical attack upon uric acid generates allantoin [Ames, Cathcart, Schwiers & Hochstein (1981) Proc. Natl. Acad. Sci. U.S.A. 78, 6858-6862]. Methods are described for the accurate measurement of uric acid and allantoin in human body fluids. The concentrations of uric acid and allantoin in human serum and synovial fluid are reported. It is suggested that measurement of changes in allantoin concentration may be a useful index of free-radical reactions taking place in vivo.

Effects of intravenous methylprednisolone on spinal cord lipid peroxidation and (Na+ + K+)-ATPase activity

1982 ◽  
Vol 57 (2) ◽  
pp. 247-253 ◽  
Author(s):  
Edward D. Hall ◽  
J. Mark Braughler
Keyword(s):  
Spinal Cord ◽  
Lipid Peroxidation ◽  
Free Radical ◽  
Atpase Activity ◽  
Cyclic Gmp ◽  
Radical Reactions ◽  
Spinal Segment ◽  
Free Radical Reactions ◽  
Content Type ◽  
Neurochemical Changes

✓ The present study was undertaken to examine the ability of a single large intravenous dose of methylprednisolone (15, 30, or 60 mg/kg) to attenuate lipid peroxidation and enhance (Na+ + K+)-ATPase activity during the 1st hour after a 400 gm-cm injury to the cat spinal cord. The contusion injury was associated with a rise in the concentration of fluorescent lipid peroxy products in the injured segment at 1 hour. In addition, the accumulation of cyclic guanosine 3″,5″-monophosphate (cyclic GMP), which was used as a new index of injury-induced free radical reactions, in the injured spinal segment was twice control levels. The injury-induced increase in fluorescence and cyclic GMP content in the contused spinal segment at 1 hour was completely prevented by the administration of 15 or 30 mg/kg of methylprednisolone at 30 minutes after injury. A 60-mg/kg dose, however, did not prevent the elevation in cyclic GMP. A concomitant examination of the acute effects of glucocorticoid administration on (Na+ + K+)-ATPase activity in the injured cord revealed a striking increase of enzyme activity after the 30-mg/kg dose, but a depression in activity with the 60-mg/kg dose. These results demonstrate that a single massive dose of methylprednisolone can beneficially reduce free-radical reactions and lipid peroxidation as well as enhance the activity of neuronal (Na+ + K+)-ATPase during the early phase after spinal cord contusion. The requirement for doses to be in the range of 15 to 30 mg/kg in order to produce these neurochemical changes is consistent with other studies that have demonstrated significantly greater recovery and tissue preservation in spinal cord-injured animals treated with comparable doses of methylprednisolone soon after injury. These findings suggest the need for a rigorous approach to glucocorticoid therapy in central nervous system trauma.

scholarly journals Nitric oxide increases carbon monoxide production by piglet cerebral microvessels

2005 ◽  
Vol 289 (4) ◽  
pp. H1442-H1447 ◽  
Author(s):  
Charles W. Leffler ◽  
Liliya Balabanova ◽  
Alexander L. Fedinec ◽  
Helena Parfenova
Keyword(s):  
Nitric Oxide ◽  
Carbon Monoxide ◽  
Catalytic Activity ◽  
Excitatory Amino Acid ◽  
Gas Chromatography Mass Spectrometry ◽  
No Production ◽  
No Donor ◽  
Cerebral Microvessels ◽  
Stimulation Of

Carbon monoxide (CO) and nitric oxide (NO) can be involved in the regulation of cerebral circulation. Inhibition of production of either one of these gaseous intercellular messengers inhibits newborn pig cerebral arteriolar dilation to the excitatory amino acid glutamate. Glutamate can increase NO production. Therefore, the present study tests the hypothesis that NO, which is increased by glutamate, stimulates the production of CO by cerebral microvessels. Experiments used freshly isolated cerebral microvessels from piglets that express only heme oxygenase-2 (HO-2). CO production was measured by gas chromatography-mass spectrometry. Although inhibition of nitric oxide synthase (NOS) with Nω-nitro-l-arginine (l-NNA) did not alter basal HO-2 catalytic activity or CO production, l-NNA blocked glutamate stimulation of HO-2 activity and CO production. Furthermore, the NO donor sodium nitroprusside mimicked the actions of glutamate on HO-2 and CO production. The action of NO appears to be via cGMP because 8-bromo-cGMP mimics and 1 H-[1,2,4]oxadiazole-[4,3- a]quinoxalin-1-one (ODQ) blocks glutamate stimulation of CO production and HO-2 catalytic activity. Inhibitors of neither casein kinase nor phosphotidylinositol 3-kinase altered HO-2 catalytic activity. Conversely, inhibition of calmodulin with calmidazolium chloride blocked glutamate stimulation of CO production and reduced HO-2 catalytic activity. These data suggest that glutamate may activate NOS producing NO that leads to CO synthesis via a cGMP-dependent elevation of HO-2 catalytic activity. These results are consistent with the findings in vivo that either HO or NOS inhibition blocks cerebrovascular dilation to glutamate in piglets.

Iron-mediated radical reactions upon reperfusion contribute to myocardial "stunning"

1990 ◽  
Vol 259 (6) ◽  
pp. H1901-H1911 ◽  
Author(s):  
R. Bolli ◽  
B. S. Patel ◽  
M. O. Jeroudi ◽  
X. Y. Li ◽  
J. F. Triana ◽  
...  
Keyword(s):  
Free Radical ◽  
Myocardial Stunning ◽  
Time Window ◽  
Contractile Function ◽  
Myocardial Dysfunction ◽  
Venous Blood ◽  
Radical Reactions ◽  
Free Radical Reactions ◽  
Group I

Recent evidence suggests that postischemic myocardial dysfunction ("stunning") is mediated by iron-catalyzed free radical reactions, but the exact time window during which the critical iron-mediated damage develops remains unknown. Furthermore, the evidence that iron promotes free radical reactions in vivo is indirect. Thus open-chest dogs undergoing a 15-min coronary occlusion and 4 h of reperfusion were given one of the following intracoronary infusions: desferrioxamine (DF) beginning 2 min before reperfusion (group I), DF beginning 1 min after reperfusion (group II), iron-loaded DF in dosage identical to group I (group III), or vehicle (controls, group IV). Recovery of contractile function was substantially greater in group I than in controls, whereas in groups II and III it was indistinguishable from controls. To determine whether the protection afforded by DF was due to inhibition of free radical reactions, myocardial production of free radicals was directly assessed by intracoronary infusion of the spin trap alpha-phenyl N-tert-butyl nitrone (PBN). In controls (group VI), radical adducts of PBN were released in the coronary venous blood after reperfusion. DF given as in group I (group V) markedly suppressed myocardial production of PBN adducts. These results strongly suggest that a substantial portion of the damage responsible for myocardial stunning is caused by iron-catalyzed free radical reactions that develop in the initial seconds of reperfusion and can be prevented by administration of iron chelators started just before reflow. Furthermore, the results demonstrate that attenuation of postischemic dysfunction by DF is associated with attenuation of free radical reactions in vivo, thereby providing direct evidence for a pathogenetic role of iron-catalyzed free radical reactions in myocardial stunning in the intact animal.

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