Interaction of Pro- and Antioxidant Factors, Nitric Oxide Metabolites in Blood and Gingival Tissues during Experimental Chronic Gastritis and Duodenitis

2016 ◽  
Vol 28 ◽  
pp. 85-88
Author(s):  
Y.G. Romanenko
Keyword(s):  
Nitric Oxide ◽  
Superoxide Dismutase ◽  
Blood Plasma ◽  
Malonic Dialdehyde ◽  
Gingival Tissue ◽  
Antioxidant Protection ◽  
Leading Role ◽  
Protein Molecules ◽  
Nitric Oxide Metabolites

The stable metabolites rate of nitric oxide is reduced three times compared with the rate in the group of control animals in homogenates of rats’ gingival tissue with gastritis and duodenitis. Increasing of the catalase rate with simultaneous increasing of lipids and proteins oxidation was accompanied by decreasing activity of superoxide dismutase. Decreasing of the malonic dialdehyde content and indices protein molecules fragmentation in the blood plasma with simultaneous increasing of catalase and nitric oxide metabolites levels indicates the leading role of nitric oxide in antioxidant protection of the organism in conditions of disease.

Level of Nitrogen Oxide and Indicators of Oxidative-Antioxidative Status in the Gingival Tissues, Blood Plasma in Experimental Chronic Gastritis and Duodenitis and Drug Correction

2017 ◽  
Vol 31 ◽  
pp. 83-90
Author(s):  
Y.G. Romanenko
Keyword(s):  
Nitric Oxide ◽  
Calcium Carbonate ◽  
Blood Plasma ◽  
Chronic Gastritis ◽  
Gingival Tissue ◽  
Control Group ◽  
Treatment Level ◽  
Antioxidative Status ◽  
Nitric Oxide Metabolites

model of chronic gastritis and duodenitis was conducted in 48 immature Wistar rats both gender by intragastric injection of medical bile. Control group consisted of 10 animals. After approximation model of the gastritis and duodenitis rats were divided into five subgroups: the 1st subgroup (before treatment, 9 rats), subgroup 2 (10 animals) received the antioxidant, subgroup 3 (11 animals) – received NO donator, subgroup 4 (10 animals) - received an antioxidant and NO donator, subgroup 5 (8 animals) – received the antioxidant, NO donator and calcium carbonate. In rats with gastritis and duodenitis was observed redistribution of stable metabolites of nitric oxide: decreasing level in the gingival homogenates and increasing in the blood plasma. Level of malondialdehyde and aldehyddehydrogenase in the gingival tissue increased, and in the blood plasma decreased, on a background of catalase activation; content of ketone phenilhydrazone remained in the level of control group. Decreasing markers of oxidation lipids and proteins in the blood plasma, on a background of increasing levels of catalase and nitric oxide metabolites (in 14 times), indicates about a key role of NO in the antioxidant protection of organism in a case of disease.Application of antioxidant could not impact on the indicators of oxidation lipids and proteins. It had been shown decreasing content of the nitric oxide metabolites in the gingival tissues and blood plasma. Drug correction with donator of nitric oxide have to increase markers of oxidation lipids and proteins in the gingival tissues, on a background of high catalase activity and low levels of nitric oxide metabolites. In the blood plasma content of nitric oxide metabolites was higher, which indicated about an active inflammatory process in the stomach and duodenum mucosa. Indicators of the protein molecules fragmentation and malondialdehyde were not differ from those before treatment. Level of catalase was in two times higher, than in the control group, but level of superoxide dismutase was decreased. Complex of antioxidant and donator of nitric oxide helped to stabilise the indicators of oxidation lipids and proteins, although level of nitric oxide metabolites in the gingiva was significantly decreased. Application complex from the antioxidant, donator of nitric oxide and calcium carbonate at the treatment of chronic gastritis and duodenitis restored an oxidative-antioxidative status in the blood plasma and gingival tissues, increasing the production of nitric oxide to a level in the control group.

scholarly journals Features of antioxidant system in patients with obstructive jaundice of benign and malignant origin in dynamics

2018 ◽  
Vol 99 (6) ◽  
pp. 919-923
Author(s):  
N G Elmanova
Keyword(s):  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Antioxidant Enzymes ◽  
Antioxidant System ◽  
Surgical Intervention ◽  
Reduced Glutathione ◽  
Malonic Dialdehyde ◽  
Antioxidant Protection ◽  
High Level

Aim. Study of the features of changes of antioxidant protection in patients with mechanical jaundice of benign and malignant origin in dynamics. Methods. The author studied the role of antioxidant system in the progression of mechanical jaundice of various origins in 104 patients. Groups of patients with a syndrome of mechanical jaundice of benign (62 patients) and malignant origin (42 patients) were isolated. The material of the study was blood from the ulnar vein, which was taken in the morning on an empty stomach before surgery. In the dynamics (on the 7th day after the operation), 53 patients were examined. To assess the state of antioxidant protection, a spectrophotometric method of investigation was used. Results. A high level of malonic dialdehyde, the product of lipid peroxidation, was determined in all patients regardless of origin. There was also a depression of the enzymatic link of antioxidant protection (a decrease in the activity of superoxide dismutase and catalase). After surgical intervention in patients with mechanical jaundice of benign origin, correction of the level of reduced glutathione was observed. In patients with mechanical jaundice of malignant origin in dynamics, the activity of antioxidant enzymes did not differ significantly from the norm (p1-3 = 0,23; p1-3 = 311). Conclusion. After surgical intervention, partial improvement of the condition of patients with mechanical jaundice of benign origin was observed, and dysfunction of antioxidant protection persisted in patients with mechanical jaundice of malignant origin.

scholarly journals The state of antioxidant protection system in cows under the influence of heavy metals

2020 ◽  
Vol 11 (2) ◽  
pp. 237-242
Author(s):  
L. G. Slivinska ◽  
A. R. Shcherbatyy ◽  
B. O. Lukashchuk ◽  
B. V. Gutyj
Keyword(s):  
Heavy Metals ◽  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Malonic Dialdehyde ◽  
Protection System ◽  
Lipid Hydroperoxides ◽  
Technogenic Pollution ◽  
Antioxidant Protection ◽  
Diene Conjugates ◽  
Antioxidant Protection System

A highly relevant problem of modern veterinary science is the study of features and mechanisms of combined action of the most common heavy metals – cadmium and plumbum and their influence on the body of humans and animals in the regions of Ukraine under technogenic pollution. The purpose of the work was to study the influence of heavy metals on the state of the antioxidant protection system of cows, in particular on the content of lipid peroxidation products (malonic dialdehyde, lipid hydroperoxides and diene conjugates), and activity of antioxidant enzymes (glutathione peroxidase and superoxide dismutase), depending on the distance to the heaps of mines in the coal basin. The study objects were cows of black-and-white breed at the age of 3–7 years. It was established that this parameter in the place with the highest concentration of diene conjugates in the blood of cows was by 25.8 % higher compared to the place of low concentration and 12.1 % higher compared to the place with medium concentration. In the place with the highest content of lipid hydroperoxides in the blood of cows the parameter was 23.7 % higher compared to the cows from the place with the low content. The concentration of lipid hydroperoxides in the blood of cows from the place with the medium content was 16.7% higher compared to the cows from the place with the low content. The parameter from the place with the lowest content of lipid hydroperoxides in the blood of cows was 12.1% lower compared to the place with the highest content. The level of malonic dialdehyde in the blood of cows from the technogenic pollution zone in the place with the largest amount was higher by 36.2; 34.0 and 18.8 % – compared to places with medium and low levels, respectively. The activity of superoxide dismutase in the blood of cows in the place with its highest activity was 0.284 ± 0.0099 % block. reac/g Hb, and in the place with the lowest activity – 0.23 ± 0.0051 % block. reac/g Hb. The activity of glutathione peroxidase in the blood of cows in farms of the technogenic pollution zone depended on the distance to the mine. These researches will further develop effective methods of treating cows under the influence of heavy metals, in particular regarding the antioxidant system.

scholarly journals Biochemical criteria for the development mechanisms of various reproduction disorders in dairy cows

2021 ◽  
Vol 22 (11) ◽  
Author(s):  
Inna Ventsova ◽  
VLADIMIR SAFONOV
Keyword(s):  
Oxidative Stress ◽  
Dairy Cows ◽  
Malonic Dialdehyde ◽  
Antioxidant Protection ◽  
Factors Analysis ◽  
Gonadal Dysfunction ◽  
Vitamins E And C ◽  
Endocrine Status ◽  
Nitric Oxide Metabolites ◽  
Uterine Diseases

Abstract. Ventsova I, Safonov V. 2021. Biochemical criteria for the development mechanisms of various reproduction disorders in dairy cows. Biodiversitas 22: 4997-5002. The article presents the evaluation of peroxide, antioxidant, and hormonal conditions of high-producing red-and-white dairy cows in the physiological and pathological course of pregnancy and the postpartum period. The blood concentration of malonic dialdehyde, stable nitric oxide metabolites, S-nitrosothiols, vitamins E and C, carotin, gonadal, corticosteroid, and thyroid hormones, as well as activity of GPx, GR, SOD, catalase, and ceruloplasmin, were estimated to define major disorder-provoking factors. Analysis of the data shows that ketosis-gestosis syndrome during pregnancy, postpartum metritis, and gonadal dysfunction occur mainly because of oxidative stress in the context of unbalanced peroxide responses and antioxidant protection. Levels of malonic dialdehyde compared to healthy animals increased by 42.3%, 75%, 56.6%, respectively, as also enzyme activities of GR by 26%, 68.1%, 30.1% and catalase by 17.3%, 45.1%, and 23.9%, correspondingly. The endocrine status indicators in the animals with ketosis-gestosis syndrome changed as follows: progesterone levels were 29.5% lower in cows, 17?-estradiol and cortisol were 20.8% and 14.7% lower, respectively. In animals with inflammatory uterine diseases and depressing reproductive glands, progesterone level was 2 and 3 times lower than in healthy animals, the content of cortisol was 17.6% and 25.1% lower, and testosterone decreased by 21.4% and 75.1%, respectively.

scholarly journals Enhancement of myocardial reactive hyperemia with manganese-superoxide dismutase: role of endothelium-derived nitric oxide

1996 ◽  
Vol 31 (4) ◽  
pp. 537-545 ◽  
Author(s):  
R. Tsunoda ◽  
K. Okumura ◽  
H. Ishizaka ◽  
T. Matsunaga ◽  
T. Tabuchi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Superoxide Dismutase ◽  
Manganese Superoxide Dismutase ◽  
Reactive Hyperemia ◽  
Manganese Superoxide

scholarly journals Overexpression of CuZn superoxide dismutase protects RAW 264.7 macrophages against nitric oxide cytotoxicity

1999 ◽  
Vol 338 (2) ◽  
pp. 295-303 ◽  
Author(s):  
Florian BROCKHAUS ◽  
Bernhard BRÜNE
Keyword(s):  
Nitric Oxide ◽  
Cell Death ◽  
Superoxide Dismutase ◽  
Uric Acid ◽  
No Synthase ◽  
Raw 264.7 ◽  
Down Regulation ◽  
Raw 264.7 Macrophages ◽  
Inducible No Synthase

Initiation of nitric oxide (NO•)-mediated apoptotic cell death in RAW 264.7 macrophages is associated with up-regulation of mitochondrial manganese superoxide dismutase (MnSOD; SOD2) and down-regulation of cytosolic copper zinc superoxide dismutase (CuZnSOD; SOD1) at their individual mRNA and protein levels. To evaluate the decreased CuZnSOD expression and the initiation of apoptosis we stably transfected macrophages to overexpress human CuZnSOD. Individual clones revealed a 2-fold increase in CuZnSOD activity. Expression of a functional and thus protective CuZnSOD was verified by attenuated superoxide (O2•-)-mediated apoptotic as well as necrotic cell death. In this study we showed that SOD-overexpressing macrophages (R-SOD1-12) were also protected against NO•-initiated programmed cell death. Protection was substantial towards NO• derived from exogenously added NO donors or when NO• was generated by inducible NO synthase activation, and was evident at the level of p53 accumulation, caspase activation and DNA fragmentation. Stimulation of parent and SOD-overexpressing cells with a combination of lipopolysaccharide and murine interferon γ produced equivalent amounts of nitrite/nitrate, which ruled out attenuated inducible NO• synthase activity during protection. Because protection by a O2•--scavenging system during NO•-intoxication implies a role of NO• and O2•- in the progression of cell damage, we used uric acid to delineate the role of peroxynitrite during NO•-elicited apoptosis. The peroxynitrite scavenger uric acid left S-nitrosoglutathione or spermine-NO-elicited apoptosis unaltered, blocking only 3-morpholinosydnonimine-mediated cell death. As a result we exclude peroxynitrite from contributing, to any major extent, to NO•-mediated apoptosis. Therefore protection observed with CuZnSOD overexpression is unlikely to stem from interference with peroxynitrite formation and/or action. Unequivocally, the down-regulation of CuZnSOD is associated with NO• cytotoxicity, whereas CuZnSOD overexpression protects macrophages from apoptosis.

Hyperglycemia increases endothelial superoxide that impairs smooth muscle cell Na+-K+-ATPase activity

2002 ◽  
Vol 282 (3) ◽  
pp. C560-C566 ◽  
Author(s):  
Sandeep Gupta ◽  
Eugene Chough ◽  
Jennifer Daley ◽  
Peter Oates ◽  
Keith Tornheim ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Superoxide Dismutase ◽  
Smooth Muscle ◽  
Steady State ◽  
Atpase Activity ◽  
Rabbit Aorta ◽  
Enhanced Chemiluminescence ◽  
Arterial Tissue ◽  
Reciprocal Change

Nitric oxide (NO) plays an important role in the control of numerous vascular functions including basal Na+-K+-ATPase activity in arterial tissue. Hyperglycemia inhibits Na+-K+-ATPase activity in rabbit aorta, in part, through diminished bioactivity of NO. The precise mechanism(s) for such observations, however, are not yet clear. The purpose of this study was to examine the role of superoxide in modulating NO-mediated control of Na+-K+-ATPase in response to hyperglycemia. Rabbit aorta incubated with hyperglycemic glucose concentrations (44 mM) demonstrated a 50% reduction in Na+-K+-ATPase activity that was abrogated by superoxide dismutase. Hyperglycemia also produced a 50% increase in steady-state vascular superoxide measured by lucigenin-enhanced chemiluminescence that was closely associated with reduced Na+-K+-ATPase activity. Specifically, the hyperglycemia-induced increase in vascular superoxide was endothelium dependent, inhibited by l-arginine, and stimulated by N ω-nitro-l-arginine. Aldose reductase inhibition with zopolrestat also inhibited the hyperglycemia-induced increase in vascular superoxide. In each manipulation of vascular superoxide, a reciprocal change in Na+-K+-ATPase activity was observed. Finally, a commercially available preparation of Na+-K+-ATPase was inhibited by pyrogallol, a superoxide generator. These data suggest that hyperglycemia induces an increase in endothelial superoxide that inhibits the stimulatory effect of NO on vascular Na+-K+-ATPase activity.

Nicotine impairs histamine-induced increases in macromolecular efflux: role of oxygen radicals

1998 ◽  
Vol 84 (5) ◽  
pp. 1589-1595 ◽  
Author(s):  
William G. Mayhan ◽  
Glenda M. Sharpe
Keyword(s):  
Nitric Oxide ◽  
Superoxide Dismutase ◽  
Smokeless Tobacco ◽  
Oxygen Radicals ◽  
Cheek Pouch ◽  
Hamster Cheek Pouch ◽  
Macromolecular Transport ◽  
Before And After ◽  
Oxide Synthase

Nicotine, a major component of cigarettes and smokeless tobacco, has toxic effects on endothelium and impairs reactivity of resistance arterioles in response to agonists that stimulate the synthesis and/or release of nitric oxide. However, the effect of nicotine on nitric oxide synthase-dependent increases in macromolecular transport is not known. Thus our first goal was to determine the effect of nicotine on histamine-induced increases in macromolecular efflux. We used intravital microscopy and FITC dextran (mol wt 70,000) (FITC-dextran-70K) to examine macromolecular extravasation from postcapillary venules in response to histamine before and after intravenous infusion of vehicle or nicotine. Extravasation of macromolecules was quantitated by counting venular leaky sites and calculating clearance (ml/s × 10−6) of FITC-dextran-70K. Histamine elicited reproducible increases in venular leaky sites and clearance in hamsters infused with vehicle. In contrast, nicotine infusion inhibited histamine-induced increases in macromolecular efflux. Histamine (1.0 and 5.0 μM) elicited 19 ± 2 and 34 ± 4 vs. 3 ± 1 and 11 ± 5 leaky sites per 0.11 cm2, before vs. after nicotine infusion, respectively ( P < 0.05). Histamine-induced clearance of FITC-dextran-70K was also impaired after infusion of nicotine. Our second goal was to examine whether alterations in histamine-induced increases in macromolecular efflux by nicotine may be related to the production of oxygen radicals. Application of superoxide dismutase (150 U/ml) to the hamster cheek pouch restored histamine-induced increases in venular leaky sites and clearance of FITC-dextran-70K during infusion of nicotine. Thus nicotine alters agonist-induced increases in microvascular permeability, via the formation of oxygen radicals, to presumably inactivate nitric oxide.

Increased urinary nitric oxide metabolites in patients with multiple sclerosis correlates with early and relapsing disease

1999 ◽  
Vol 5 (5) ◽  
pp. 335-341 ◽  
Author(s):  
Gavin Giovannoni ◽  
N C Silver ◽  
J O'Riordan ◽  
R F Miller ◽  
S J.R. Heales ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Progressive Disease ◽  
Demyelinating Disease ◽  
Neuronal Loss ◽  
Clinical Relapse ◽  
Potential Mediator ◽  
Relapsing Remitting ◽  
Nitric Oxide Metabolites ◽  
Nitrate And Nitrite

Nitric oxide (•NO) has been implicated in the immunopathogenesis of MS as a potential mediator of neuronal loss. To investigate the role of .NO in the development of progressive disease we measured the .NO metabolites (nitrate and nitrite) and neopterin, in the urine of 129 patients with demyelinating disease (DD): 23 with clinically isolated syndromes compatible with demyelination and in 46 relapsing remitting (RR) and 60 patients with progressive MS. Eighty-nine of these 129 patients underwent Gd-enhanced MRI. In addition 58 normal control subjects (NC), 19 AIDS and 35 rheumatoid arthritis (RA) patients were studied. Patients with DD, AIDS and RA had significantly elevated urinary nitrate plus nitrite (nit: creat.urine) and neopterin (neopt: creat.urine) to creatinine ratios compared to NC subjects. (Median[25th-75th%] nit: creat.urine: NC=1183[962-1365] vs DD=1245[875-2403], AIDS=1686[1231-2531], and RA=1950[1214-2726] mmol/mol, P50.001 and median[25th-75th%] neopt: creat.urine: NC=99[76-151] vs DD=163[119-266], AIDS=972[653-1456], and RA=389[257-623] mmol/mol, P50.001). Patients with early DD and RR MS had significantly elevated nit: creat.urine compared to patients with progressive MS (nit: creat.urine: 1612[1020-2733] vs 1159[790-1641] mmol/mol, P=0.006). The nit: creat.urine and neopt: creat.urine did not correlate with clinical relapse or MRI activity. Excretion of .NO metabolites is increased in patients with early or relapsing-remitting disease. .NO appears to be a double-edged sword, mediating tissue damage and modulating complex immunological functions which may be protective in MS.

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