scholarly journals Peculiarities of disorders of nitrogen oxide system in the blood at adrenalin-induced myocardial injury in conditions of immobilization stress and their correction by L-arginine

2021 ◽  
pp. 24-28
Author(s):  
Oksana Lys ◽  
Mykhailo Reheda ◽  
Nataliya Sementsiv ◽  
Mariana Reheda-Furdychko ◽  
Stepan Reheda
Keyword(s):  
Nitric Oxide ◽  
Myocardial Injury ◽  
Immobilization Stress ◽  
Total Activity ◽  
Oxide System ◽  
Scientific Data ◽  
Corrective Effect ◽  
Food Content ◽  
Oxide Synthase

The aim: of the study was to elucidate the changes to nitric oxide activity in the blood during adrenaline-induced myocardial injury under immobilization stress and to establish the corrective effect of L-arginine. Methods: determination of free arginine was conducted by the method of Aleinikova T.L., total nitric oxide products in the blood by the method of Schmidt H.H., the total activity of nitric oxide synthase by the method of Sumbaiev V.V.. Immobilization stress was reproduced by the method of Horizontov P.D. Adrenaline-induced myocardial injury was reproduced by the method of Markova O.O. L-arginine was injected based on scientific data by Kiryanova N.A. Results. Studies have shown that on days 1 and 3 with adrenaline-induced myocardial injury under immobilization stress there was an increase in nitric oxide products in the blood, respectively, according to control. The use of L-arginine on the 5th day, led to a decrease in levels of NO products in the blood by less than, lower against the group of animals with MI and IS, to treatment. Conclusions. Thus, biochemical studies of NO system in the dynamics of IS and MI showed an increase in food content and total synthase activity of NO on the background of reduced levels of L-arginine, which were detected at all stages of the study and especially expressed on the 1st day before treatment. The use of the drug L-arginine, made it possible to identify its corrective effect on impaired metabolic processes in MI and IS

Inducible nitric oxide synthase augments injury elicited by oxidative stress in rat cardiac myocytes

1998 ◽  
Vol 274 (1) ◽  
pp. C245-C252 ◽  
Author(s):  
Junsuke Igarashi ◽  
Masashi Nishida ◽  
Shiro Hoshida ◽  
Nobushige Yamashita ◽  
Hiroaki Kosaka ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Cardiac Myocytes ◽  
Myocardial Injury ◽  
No Production ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
No Donor ◽  
Oxide Synthase ◽  
Gpx Activity

The effects of nitric oxide (NO) produced by cardiac inducible NO synthase (iNOS) on myocardial injury after oxidative stress were examined. Interleukin-1β induced cultured rat neonatal cardiac myocytes to express iNOS. After induction of iNOS,l-arginine enhanced NO production in a concentration-dependent manner. Glutathione peroxidase (GPX) activity in myocytes was attenuated by elevated iNOS activity and by an NO donor, S-nitroso- N-acetyl-penicillamine (SNAP). Although NO production by iNOS did not induce myocardial injury, NO augmented release of lactate dehydrogenase from myocyte cultures after addition of H2O2(0.1 mM, 1 h). Inhibition of iNOS with Nω-nitro-l-arginine methyl ester ameliorated the effects of NO-enhancing treatments on myocardial injury and GPX activity. SNAP augmented the myocardial injury induced by H2O2. Inhibition of GPX activity with antisense oligodeoxyribonucleotide for GPX mRNA increased myocardial injury by H2O2. Results suggest that the induction of cardiac iNOS promotes myocardial injury due to oxidative stress via inactivation of the intrinsic antioxidant enzyme, GPX.

Testosterone production in mice lacking inducible nitric oxide synthase expression is sensitive to restraint stress

2007 ◽  
Vol 292 (2) ◽  
pp. E615-E620 ◽  
Author(s):  
Ben A. Weissman ◽  
Chantal M. Sottas ◽  
Ping Zhou ◽  
Costantino Iadecola ◽  
Matthew P. Hardy
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Restraint Stress ◽  
Immobilization Stress ◽  
Male Mice ◽  
Wild Type ◽  
Basal Plasma ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Immobilization stress (IMO) induces a rapid increase in glucocorticoid secretion [in rodents, corticosterone CORT)] and this is associated with decreased circulating testosterone (T) levels. Nitric oxide (NO), a reactive free radical and neurotransmitter, has been reported to be produced at higher rates in tissues such as brain during stress. The biosynthesis of T is also known to be dramatically suppressed by NO. Specifically, the inducible isoform of nitric oxide synthase (iNOS) was directly implicated in this suppression. To assess the respective roles of CORT and NO in stress-mediated inhibition of T production, adult wild-type (WT) and inducible nitric oxide synthase knockout (iNOS−/−) male mice were evaluated. Animals of each genotype were assigned to either basal control or 3-h IMO groups. Basal plasma and testicular T levels were equivalent in both genotypes, whereas testicular weights of mutant mice were significantly higher compared with WT animals. Exposure to 3-h IMO increased plasma CORT and decreased T concentrations in mice of both genotypes. Testicular T levels were also affected by stress in WT and mutant males, being sharply reduced in both genotypes. However, the concentrations of nitrite and nitrate, the stable metabolites of NO measured in testicular extracts, did not differ between control and stressed WT and iNOS−/− mice. These results support the hypothesis that CORT, but not NO, is a plausible candidate to mediate rapid stress-induced suppression of Leydig cell steroidogenesis.

201 ROLE OF THE NITRIC OXIDE SYSTEM IN EFFECTS OF PROLACTIN AND GROWTH HORMONE ON METAPHASE-II CHROMOSOMES IN BOVINE OOCYTES AGING IN VITRO

2016 ◽  
Vol 28 (2) ◽  
pp. 231
Author(s):  
I. Lebedeva ◽  
G. Singina ◽  
E. Shedova ◽  
A. Lopukhov ◽  
N. Zinovieva
Keyword(s):  
Nitric Oxide ◽  
Growth Hormone ◽  
Cumulus Cells ◽  
Total Activity ◽  
Inhibitory Effect ◽  
Pituitary Hormones ◽  
Oxide System ◽  
Nos Inhibitors ◽  
Bovine Oocytes

Aging of mammalian oocytes is the time-dependent process of cytological and molecular transformations leading to a decline in the ovum quality and developmental capacity. We have previously shown that 2 related pituitary hormones, prolactin (PRL) and growth hormone (GH), may decelerate abnormal changes in the morphology of metaphase II (MII) chromosomes in bovine cumulus-enclosed oocytes (CEO) aging in vitro. The goal of the present research was to examine the involvement of different isoforms of nitric oxide synthase (NOS) in the actions of PRL and GH on MII chromosomes in aging bovine oocytes. Bovine CEO were matured for 20 h in TCM 199 containing 10% FCS, 10 μg mL–1 porcine FSH, and 10 μg mL–1 ovine LH. After IVM, CEO or denuded oocytes (DO) were cultured for 24 h in the aging medium of TCM 199 supplemented with 10% FCS (control). In experimental groups, the medium contained either 50 ng mL–1 bovine PRL or 10 ng mL–1 bovine GH and/or NOS inhibitors. The following inhibitors were applied: (1) N-propyl-l-arginine (NPLA; an inhibitor of neuronal NOS (nNOS), 5 μM) and (2) L-NAME (an effective inhibitor of both endothelial NOS (eNOS) and nNOS, 20 μM). Destructive changes of MII chromosomes in oocytes were assessed by the following morphological signs: decondensation, partial adherence, chromosome clumping into a single mass, and fragmentation. The total activity of NOS in oocytes was determined by NADPH-diaphorase staining. The data from 4–5 replicates were analysed by ANOVA. During CEO aging in the control medium, the rate of MII oocytes with destructive changes of chromosomes rose from 16.8 ± 2.1% to 58.5 ± 1.4% (P < 0.001), whereas both PRL and GH reduced this rate up to 42.0 ± 1.3% and 46.5 ± 1.6%, respectively (P < 0.001). The nNOS inhibitor NPLA abolished (P < 0.001) the inhibitory effect of PRL on abnormal modifications of chromosomes in CEO but did not affect the frequency of these modifications in the control or GH-treated groups. In the absence of the hormones, L-NAME (the eNOS+nNOS inhibitor) decreased the rate of aging CEOs with chromosome abnormalities from 58.5 ± 1.4% to 41.2 ± 2.5% (P < 0.001), acting unidirectionally with PRL and GH. Meanwhile, L-NAME enhanced (P < 0.05) the suppressing effect of PRL on destructive changes of MII chromosomes but did not influence the similar effect of GH. At the same time the chromosome morphology in senescent DOs was unaffected by the hormones or NOS inhibitors. Furthermore, the total activity of NOS in oocytes separated of cumulus after 24 h of aging was similar in the control and experimental groups. Thus, the inhibitory effect of GH on abnormal modifications of MII chromosomes in aging bovine oocytes may be related to a reduction of the eNOS activity in cumulus cells, whereas the respective effect of PRL is likely to be achieved by both inactivation of eNOS and activation of nNOS. This research was supported by RFBR (No. 13–04–01888).

scholarly journals Regulation of nitric oxide synthase isoforms and role of nitric oxide during prostaglandin F2alpha-induced luteolysis in rabbits

Reproduction ◽  
2003 ◽  
pp. 807-816 ◽  
Author(s):  
C Boiti ◽  
G Guelfi ◽  
D Zampini ◽  
G Brecchia ◽  
A Gobbetti ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Time Course ◽  
Plasma Concentrations ◽  
Physiological Role ◽  
Total Activity ◽  
Corpora Lutea ◽  
Prostaglandin F ◽  
Oxide Synthase

Total activity of nitric oxide synthase (NOS) and the gene expression of both endothelial NOS (eNOS) and inducible NOS (iNOS) isoforms in corpora lutea of pseudopregnant rabbits were examined during prostaglandin F(2alpha) (PGF(2alpha))-induced luteolysis. Corpora lutea were collected at 0, 6, 12, 24 and 48 h after an injection of PGF(2alpha) at day 9 of pseudopregnancy. At 12 h after PGF(2alpha) administration, luteal mRNA encoding eNOS decreased (P0.05) by 40% and remained low throughout the subsequent 36 h, whereas eNOS protein increased (P0.05) two- to threefold. By contrast, expression of mRNA encoding iNOS was poor and remained fairly constant, but transcription increased eightfold (P0.01) within 6 h after PGF(2alpha) treatment and then decreased to values similar to those of controls. Total NOS activity increased twofold (P0.01) at 6 h after treatment and remained high thereafter, whereas progesterone concentrations in explanted corpora lutea decreased (P0.01) from 302.4+/-42.3 pg x mg(-1) at day 9 to 58.6+/-8.3 at 48 h later, and peripheral plasma concentrations of progesterone declined too. Long-term administration of Nomega-nitro-L-arginine methyl ester (0.6 g l(-1) per os) from day 2 of pseudopregnancy onward partially blocked the luteolytic action of PGF(2alpha) administered at day 9 of pseudopregnancy. In nitric oxide (NO)-deficient rabbits, progesterone concentrations remained higher (P0.01) than in controls at 24-48 h after PGF(2alpha) administration (4.5 to 3.2 ng x ml(-1), respectively). These data are the first to characterize NOS activity. The time course of expression of eNOS and iNOS in rabbit corpora lutea during PGF(2alpha)-induced luteolysis gives additional support to a physiological role of NO in the regulation of regression of corpora lutea in rabbits.

scholarly journals Plaunol A from Croton stellatopilosus Inhibits Inducible Nitric Oxide Synthase and Cyclooxygenase-2 in Macrophage RAW264.7 Cells

2018 ◽  
Vol 13 (7) ◽  
pp. 1934578X1801300
Author(s):  
Charoenwong Premprasert ◽  
Supinya Tewtrakul ◽  
Juraithip Wungsintaweekul
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Cyclooxygenase 2 ◽  
Raw264.7 Cells ◽  
Mrna Levels ◽  
Chromatographic Techniques ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

A clerodane diterpene (plaunol A) and three flavonoids (vitexin; luteolin-7-O-β-D-glucoside and luteolin-4'-O-glucoside) were isolated from stems and leaves of Croton stellatoliosus Ohba, using series of chromatographic techniques. Evaluation for anti-inflammatory activity in LPS-induced RAW264.7 cells revealed that, only plaunol A exhibited the inhibitory activity on nitric oxide production with the IC50 of 11.69 μM. This was no cytotoxic effect to the cells at a concentration of 100 μM, by MTT assay. Determination of mRNA levels by qRT-PCR, indicated that plaunol A suppressed the expressions of inducible nitric oxide synthase and cyclooxygenase-2 in lipopolysaccharide-induced RAW264.7 cells.

scholarly journals New Modified Method for Determination of Nitric Oxide Synthase Activity in Plasma of Vitiligo Patients

2018 ◽  
Vol 34 (5) ◽  
pp. 2502-2509
Author(s):  
Jwan Abdulmohsin Zainulabdeen ◽  
Aymen Abdulsattar Al-kinani
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Healthy Individuals ◽  
Modified Method ◽  
Oxide Concentration ◽  
Nitric Oxide Concentration ◽  
And Gender ◽  
Oxide Synthase

Vitiligo is a non-contagious skin disorder that characterized by depigmentation of skin due to melanocyte impairment which may be caused to increase levels of free radicals (such as superoxide and nitric oxide) that causing an increase in oxidative stress. The purpose of this study was measured by the activity of oxide synthase (NOS) by our modified method and nitric oxide concentration in plasma of vitiligo patients. The activity of nitric oxide synthase was determined via a modified method by coupling two methods; the first method was based on converting L-arginine to L-citrulline and nitric oxide and the second was used to measure the concentration of nitric oxide. This modified method was applied to patients with vitiligo disease and healthy individuals who matched in age and gender with patients. The condition of this modified method was optimized and the results revealed the following: the activity of NOS was higher in a solution that contains: Tris buffer (50mM), arginine (100mM), calcium chloride (20mM), and NADPH (5mM) during 30 minutes, meanwhile the precision of this method was 2.03. In the current study, the results show that the levels of NOS activity and nitric oxide were affected by the disease in which both parameters appeared highly significant increases in vitiligo patients (p=0.000 and 0.002 respectively) in comparison with the healthy individuals. Results of the experiments proved that it is possible to depend on the modified method to measure the activity of nitric oxide synthase (NOS). Also, the increased levels of NOS activity and nitric oxide concentration in vitiligo patients support the autocytotoxic hypothesis which suggests that oxidative stress may have a role in melanocyte impairment.

Relationships between caveolae and eNOS: everything in proximity and the proximity of everything

2002 ◽  
Vol 283 (1) ◽  
pp. F1-F10 ◽  
Author(s):  
Michael S. Goligorsky ◽  
Hong Li ◽  
Sergey Brodsky ◽  
Jun Chen
Keyword(s):  
Nitric Oxide ◽  
Fluid Shear Stress ◽  
Central Element ◽  
Endothelial Permeability ◽  
Inflammatory Cells ◽  
Oxide System ◽  
Fluid Shear ◽  
Caveolin 1 ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Caveolae, flask-shaped invaginations of the plasma membrane occupying up to 30% of cell surface in capillaries, represent a predominant location of endothelial nitric oxide synthase (eNOS) in endothelial cells. The caveolar coat protein caveolin forms high-molecular-weight, Triton-insoluble complexes through oligomerization mediated by interactions between NH2-terminal residues 61–101. eNOS is targeted to caveolae by cotranslational N-myristoylation and posttranslational palmitoylation. Caveolin-1 coimmunoprecipitates with eNOS; interaction with eNOS occurs via the caveolin-1 scaffolding domain and appears to result in the inhibition of NOS activity. The inhibitory conformation of eNOS is reversed by the addition of excess Ca2+/calmodulin and by Akt-induced phosphorylation of eNOS. Here, we shall dissect the system using the classic paradigm of a reflex loop: 1) the action of afferent elements, such as fluid shear stress and its putative caveolar sensor, on caveolae; 2) the ways in which afferent signals may affect the central element, the activation of the eNOS-nitric oxide system; and 3) several resultant well-established and novel physiologically important effector mechanisms, i.e., vasorelaxation, angiogenesis, membrane fluidity, endothelial permeability, deterrance of inflammatory cells, and prevention of platelet aggregation.

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