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1

Immunohistochemical evaluation of caspase 3 expression in rats' hepatocytes after L-arginine therapy

100%

Pedrycz A., Kot K., Olesinski I.

Bulletin of the Veterinary Institute in Puławy

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2010

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tom 54

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nr 1

101-103

The apoptotical effect of nitric oxide on effector apoptotical caspase 3 in rats' hepatocytes was examined. The experiment was performed on 16 white Wistar female rats divided into two equal groups. The rats from the experimental group received orally L-arginine in a dose of 40 mg/kg b.w. every other day for 2 weeks. The rats from the control group received orally 2 ml of distilled water in the same manner as the experimental group. All the rats were decapitated after 3 weeks of the experiment. After decapitation, specimens from the liver were collected, fixed in 10% formalin, and then embedded in paraffin blocks. Protein caspase 3 on slides was detected using the standard three-step immunohistochemical method. The quantitative evaluation of caspase 3 expression showed that the area occupied by positive caspase 3 reaction in the liver of the experimental group (128.11 µm²±96.54) was comparable to that in the control group (212.18 µm² ±1 16.59) (P=0.25). The dose of L-arginine used was similar to that applied in pregnant women treated for gestosis. The study shows that L-arginine as a donor of exogenous nitric oxide has no an apoptotic effect on rats' hepatocytes.

2

Duodenocutaneous fistula in rats as a model for "wound healing-therapy" in ulcer healing: the effect of pentadecapeptide BPC 157, L-nitro-arginine methyl ester and L-arginine

100%

Skorjanec S., Kokot A., Drmic D., Radic B., Sever M., Klicek R., Kolenc D., Zenko A., Lovric Bencic M., Belosic Halle Z., Situm A., Zivanovic Posilovic G., Masnec S., Suran J., Aralica G., Seiwerth S., Sikiric P.

Journal of Physiology and Pharmacology

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2015

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tom 66

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nr 4

3

Enhanced expression of endothelial nitric oxide synthase in the myocardium ameliorates the progression of left ventricular hypertrophy in L-arginine treated Wistar-Kyoto rats

100%

Ahmad A., Sattar M. A., Rathore H. A., Abdulla M. H., Khan S. A., Abdullah N. A., Johns E. J.

Journal of Physiology and Pharmacology

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2016

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tom 67

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nr 1

4

Nitric oxide mediates antinociceptive effect of leucopyrokinin active analog [2-8]-leucopyrokinin [[2-8]-LPK]

100%

Rykaczewska-Czerwinska M., Konopinska D., Plech A.

Pestycydy

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2005

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nr 4

65-70

5

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Effect of L-arginine on lead induced oxidative stress in the blood of rats with different resistance to hypoxia

100%

Tkachenko H., Kurhalyuk N., Khabrovska L., Kminski P.

Polish Journal of Food and Nutrition Sciences

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2007

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tom 57

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nr 3

387-393

The aim of the study was to estimate beneficial effects of L-arginine, a nitric oxide precursor, on antioxidant enzymes activity (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, ceruloplasmine), the lipid peroxidation processes level and parameters of membrane erythrocytes resistance before and after lead intoxication in rats with different resistance to hypoxia. Our results suggest that the antioxidant system enzymes activity and lipid peroxidation processes level in animals which differ in sensitiveness to hypoxia, are higher in animals with low resistance to hypoxia in the control group. We have shown that the amino acid, L-arginine, is an efficient antioxidant capable of reducing the level of lipid peroxidation processes in blood of lead-preexposed rats. L-arginine treatment under lead intoxication caused alteration in antioxidant enzymes activity due to increasing the enzymes activity of glutathione system, especially in animals with low resistance to hypoxia. The influence of L-arginine under lead intoxication was investigated to ascertain whether this amino acid possesses antioxidant properties before lead injection (preventive effect) and whether L-arginine has therapeutic effects by treatment after lead intoxication. We have shown a significant protective effect of L-arginine under treatment with a preventive effect before lead intoxication. These studies suggest that L-arginine may be a useful drug in treatment under lead intoxication.

6

Dietary vitamin E and selenium yeast supplemented with L-arginine enhanced laying performance and egg quality attributes of guinea fowl (Numida meleagris)

100%

Johnson A. A., Oso A. O., John M. O., Adedeji A. S., Ibrahim A. O., Adeniji O. A., Sulyman A., Adetona A., Ajibade F. P.

Animal Science and Genetics

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2022

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tom 18

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nr 4

7

The effect of a selective inhibition of potassium channels on the relaxation induced by nitric oxide in the human pregnant myometrium

100%

Modzelewska B., Kleszczewski T., Kostrzewska A.

Cellular and Molecular Biology Letters

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2002

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tom 07

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nr Suppl.

8

Administration of L-arginine stimulates oxygen consumption during hypoxia in mice

100%

Lach H., Srebro Z., Sura P., Mindur I.

Acta Biologica Cracoviensia. Series Zoologia

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2001

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tom 43

9

Antithrombotic effect of L-arginine in hypertensive rats

100%

Cylwik D., Mogielnicki A., Kramkowski K., Stokowski J., Buczko W.

Journal of Physiology and Pharmacology

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2004

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tom 55

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nr 3

The aim of the study was to evaluate the effect of L-arginine (L-Arg) on haemostasis in stasis model of venous thrombosis in renal hypertensive rats. The effect of the single dose (i.v.300 mg/kg bolus+300 mg/kg/h) and of the 10-day application (p.o. 1 g/kg, once daily) of L-Arg was determined. L-Arg reduced the blood pressure both in the acute and long-term application. The single dose of L-Arg decreased the occurrence rate of the thrombus whereas long-term administration reduced significantly the thrombus weight. There were no differences in prothrombin time and activated partial thromboplastin time while the fibrinogen concentration decreased both in the acute and the long-term experiment. L-Arg shortened euglobulin clot lysis time and bleeding time in the long-term application. The chronic L-Arg treatment also inhibited significantly collagen-induced platelet aggregation. The overall haemostasis and coagulation potentials were inhibited and the fibrinolysis potential was higher in the group receiving this amino-acid. The results show that L-Arg, in a complex way, evokes the antithrombotic effect in the model of venous thrombosis in hypertensive rats.

10

Mitochondria recycle nitrite back to the bioregulator nitric monoxide

100%

Nohl H., Staniek K., Sobhian B., Bahrami S., Redl H., Kozlov A. V.

Acta Biochimica Polonica

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2000

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tom 47

|

nr 4

Nitric monoxide (NO) exerts a great variety of physiological functions. L-Arginine supplies amino groups which are transformed to NO in various NO-synthase-active isoenzyme complexes. NO-synthesis is stimulated under various conditions increasing the tissue of stable NO-metabolites. The major oxidation product found is nitrite. Elevated nitrite levels were reported to exist in a variety of diseases including HIV, reperfusion injury and hypovolemic shock. Denitrifying bacteria such as Paracoccus denitrificans have a membrane bound set of cytochromes (cyt cd1, cyt bc) which were shown to be involved in nitrite reduction activities. Mammalian mitochondria have similar cytochromes which form part of the respiratory chain. Like in bacteria quinols are used as reductants of these types of cytochromes. The observation of one-e- divergence from this redox-couple to external dioxygen made us to study whether this site of the respiratory chain may also recycle nitrite back to its bioactive form NO. Thus, the aim of the present study was therefore to confirm the existence of a reductive pathway which reestablishes the existence of the bioregulator NO from its main metabolite NO2-. Our results show that respiring mitochondria readily reduce added nitrite to NO which was made visible by nitrosylation of deoxyhemoglobin. The adduct gives characteristic triplet-ESR-signals. Using inhibitors of the respiratory chain for chemical sequestration of respiratory segments we were able to identify the site where nitrite is reduced. The results confirm the ubiquinone/cyt bc1 couple as the reductant site where nitrite is recycled. The high affinity of NO to the heme-iron of cytochrome oxidase will result in an impairment of mitochondrial energy-production. "Nitrite tolerance" of angina pectoris patients using NO-donors may be explained in that way.

11

Homocysteine induces endothelial dysfunction via inhibition of arginine transport

100%

Jin L., Caldwell R. B., Li-Masters T., Caldwell R. W.

Journal of Physiology and Pharmacology

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2007

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tom 58

|

nr 2

Hyperhomocysteinemia is an independent risk factor for cardiovascular diseases. High levels of plasma homocysteine (HCY) increase oxidative stress and reduce endothelial-dependent relaxation. We determined whether hyperhomocysteinemia-induced endothelial dysfunction is mediated through inhibition of cellular transport of L-arginine. In endothelial cells, HCY had a biphasic effect on arginine transport. HCY treatment for 6 hr increased L-arginine uptake by 34%; however, uptake was decreased by 25% after 24 h. HCY caused membrane hyperpolarization during both 6 and 24 h incubation periods, indicating that the negative charge facilitating arginine uptake was maintained. HCY significantly reduced expression of cellular arginine transporter protein (CAT-1) after 24 h treatment; whereas endothelial nitric oxide synthase (eNOS) protein levels and basal eNOS activity were not altered. Nevertheless, nitric oxide (NO) formation was significantly decreased. The antioxidant ascorbic acid prevented the effect of HCY on arginine transport. HCY induced formation of the peroxynitrite biomarker nitrotyrosine, which was blocked by supplemental L-arginine. HCY treatment of aortic rings caused decreased vasorelaxation to acetylcholine, which was prevented by supplemental arginine. In conclusion, HCY decreased NO formation and induced endothelial dysfunction without altering protein level or basal activity of eNOS, but through decreases in function and protein expression of the CAT-1 transporter. Reduced arginine supply may lead to eNOS uncoupling and generation of superoxide, contributing to HCY-induced oxidative stress.

12

Carboxyebselen a potent and selective inhibitor of endothelial nitric oxide synthase

100%

Hatchett R. J., Gryglewski R. J., Mlochowski J., Zembowicz A., Radziszewski W.

Journal of Physiology and Pharmacology

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1994

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tom 45

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nr 1

13

Flavonoids and nitric oxide synthase

100%

Olszanecki R., Gebska A., Kozlovski V. I., Gryglewski R. J.

Journal of Physiology and Pharmacology

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2002

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tom 53

|

nr 4,1

Induction of NOS-2 in macrophages and smooth muscles within vascular wall with concomittant suppression of endothelial NOS-3 activity is considered to be a hallmark of vascular inflammation that triggers atherogenesis. Accordingly, drugs designed to reverse these changes should not only support vaning function of NOS-3 but also suppress proinflammatory NO production by NOS-2. It means that using selective inhibitors of induction of NOS-2 (they spare ex definitione constitutive activity of NOS-3) is a more rational approach than using isselectivel. inhibitors of activity of previously induced NOS-2. First of all, those drugs are never sufficiently selective. In our work we tried to identify inhibitors of NOS-2 induction within the group of flavonoids, known stimulators of NOS-3 with putative antiatherogenic effects. Representatives of four main groups of flavonoids: flavonols (kaempferol, quercetin, rutin), flavones (apigenin, primuletin), flavanols (catechine) and flavanones (hesperetin, hesperidin, naringenin) were tried on NOS-2 induction and activity in the in vitro model of LPS-treated macrophages (cell line J774.2). While none of these compounds inhibited activity of NOS-2, all with unexpectedly scattered potencies inhibited induction of NOS-2 protein in LPS-treated J774.2 cells, as evidenced by Western blotting technique. Subsequently, RT-PCR and Northern blotting methods revealed that so far the most potent compounds, kaempferol and apigenin, at micromolar concentrations did inhibit NOS-2 induction at the level of NOS-2 gene transcription. We conclude that some of flavonoids are potent inhibitors of NOS-2 induction. At the same time they may increase endothelial NOS-3 activity. Could these flavonoids become natural parents of future drugs, which will be used for reversal of inflammatory component of atherothrombosis?

14

Biochemical targets of nitric oxide-induced toxicity

100%

Grudzinski I. P.

Roczniki Państwowego Zakładu Higieny

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2003

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tom 54

|

nr 1

Nitric oxide (NO) has become one of the most intensively studied molecules in recent years. Although its beneficial role has been well established, a large body of adverse effects was also attributed to NO and/or its red-ox derivatives in biological systems. Peroxynitrite (ONO-), a product of reaction between NO and superoxide anion (O2•-) was recognized as a potent pro-oxidant endogenous toxicant. The agent was found to induce DNA and protein oxidative damages leading to increased risk(s) of severe human pathologies including cancer. In this review, the discrete chemical aspects of both nitric oxide and peroxynitrite have been discussed in an attempt to elucidate the major biochemical target(s) of NO-and/or peroxynitrite-induced toxicity.

15

Immunohistochemical assessment of the effects of L-arginine as a nitric oxide [NO] substrate on caspase 3 expression in rats' renal tubular cells

84%

Pedrycz A., Boratynski Z., Krasowski A.

Bulletin of the Veterinary Institute in Puławy

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2010

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tom 54

|

nr 3

The study was performed on 16 albino Wistar female rats divided into two equal groups: experimental and control. The rats from the experimental group received per os, every second day for 2 weeks 40 mg/kg b.w. of L-arginine. The rats from the control group received, in the same manner, 2 ml of distilled water. The animals were decapitated after 3 weeks of the experiment. After decapitation specimens from the kidneys were collected, fixed in 10% formalin, and then embedded in paraffin blocks. Protein caspase 3 was detected using the standard three step immunohistochemical method. Additionally, the apoptotic index was evaluated. The study shows that L-arginine, as a donor of exogenous nitric oxide, induced the apoptotic signal in normal renal tubular cells of the rats. The apoptotic index statistically significantly increased in the epithelial cells of the treated renal tubules compared to the control. The immunohistochemical reaction for the executing caspase 3 in the renal tubular cells, although increased in comparison with the control, was statistically insignificant.

16

Ontogeny regulates creatine metabolism in rat small and large intestine

84%

Garcia-Miranda P., Garcia-Delgado M., Peral M. J., Calonge M. L., Ilundain A. A.

Journal of Physiology and Pharmacology

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2009

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tom 60

|

nr 3

127-133

The ontogeny of intestinal CRT, AGAT and GAMT was investigated in foetuses, newborn, suckling, weaning and adult rats. In the colon, CRT mediates creatine transport because it was Na+- and Cl- dependent and inhibited by creatine and GPA. In addition, Northern assays showed two CRT transcripts (2.7-kb and 4.2-kb) and the in situ hybridisation revealed that CRT mRNA is restricted to the colon epithelial cells. The immunohistochemistry revealed that CRT protein was at the apical membrane of colon epithelia. Maturation decreased colonic CRT activity to undetectable levels and increased CRT mRNA abundance. Western assays revealed 57-, 65-, 80- and 116-kDa polypeptides at the intestinal apical membrane. The abundance of the 65-, 80- and 116-kDa polypeptides decreased with age, and that of 57-kDa was only observed in adult rats. The small and large intestine express AGAT and GAMT mRNAs. Maturation decreased AGAT mRNA abundance without affecting that of GAMT. For comparison, renal AGAT mRNA levels were measured and they were increased with age. The study reports for the first time that: i) the apical membrane of rat colon have an active CRT, ii) development down-regulates CRT activity via post-transcriptional mechanism(s), iii) the intestine might synthesize creatine and iv) intestinal and renal creatine synthesis is ontogenically regulated at the level of AGAT gene expression.

17

An endogenous defensive concept, renewed cytoprotection/adaptive cytoprotection: intra(per)-oral/intragastric administration of strong alcohol in rat. Involvement of pentadecapeptide BPC 157 and nitric oxide system

84%

Becejac T., Cesarec V., Drmic D., Hirsl D., Madzarac G., Djakovic Z., Bunjevac I., Zenko Sever A., Sepac A., Batelja Vuletic L., Stancic Rokotov D., Seiwerth S., Sikiric P.

Journal of Physiology and Pharmacology

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2018

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tom 69

|

nr 3

18

Arginine and tetrahydrobiopterin supplementation in rats with salt-induced blood pressure increase: minor hypotensive effect but improvement of renal haemodynamics

84%

Kuczeriszka M., Walkowska A., Olszynski K. H., Rafalowska J., Sadowski J., Kompanowska-Jezierska E.

Journal of Physiology and Pharmacology

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2019

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tom 70

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nr 2

19

Effect of chlorfenvinphos on the liver and plasma arginase activity in rats

84%

Maciejewska-Kozak H., Szczepaniak S.

Acta Poloniae Toxicologica

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1996

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tom 04

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nr 2

20

Effects of nitrosative stress and reactive oxygen-scavenging systems in esophageal physiopathy under streptozotocin-induced experimental hyperglycemia

84%

Zayachkivska O., Gzregotsky M., Ferentc M., Yaschenko A., Urbanovych A.

Journal of Physiology and Pharmacology. Supplement

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2008

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tom 59

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nr 2

Experimental and clinical gastrointestinal data reported that nitrosative stress development involved in impaired barrier function, altered motility and a lowered threshold to noxious stimuli, but its pathogenetic role in diabetic esophagopathy remains unexplored. We tested the hypothesis that an imbalance in nonenzymatic glycation and glycooxidation, enhanced peroxynitrite formation, may play an important role in development esophageal mucosa (EM) lesions during streptozotocin-induced experimental hyperglycemia (EHG). To understand the biological significance of EM resistance in vivo used a glycomic approach to identification of lectin receptors glycosylation pattern. Were enrolled rat groups without/with EHG & modification of NO/NOS activity by L-arginine (L-arg) and indomethacin pre-treatment. Survival rate, destruction occurrence ratio, the size of EM lesions, and the number of EM lesions was investigated. To access the oligosaccharide residues the peroxidaseconjugated lectin (HPA, SNA, WGA, PNA)-diaminobenzidine procedure was performed to EM sections. EHG was monitored daily by glucometer. Content of NO (NOn) was determinated by Griess reagent and reactive oxygen-scavenging systems (ROSS) activity - generally accepted biochemical methods. In EHG and L-arg pretreatment group reduced NOn and EM injury with markedly rise ROSS activity significantly vs to control; in the group with indomethacin pretreatment existed different ROSS activity. Presence of heterogeneous glycosylation pattern in different layers of EM was shown. In EHG staining with PNA and SNA were strongly positive. NS and ROSS play a critical role in esophagoprotection induced by EHG, because both involved increases in iNOS expression. These results indicate the usefulness of glycomic approach as multifunctional substrate of early evaluation of NS in esophageal physiopathy.

Ograniczanie wyników

Immunohistochemical evaluation of caspase 3 expression in rats' hepatocytes after L-arginine therapy

Duodenocutaneous fistula in rats as a model for "wound healing-therapy" in ulcer healing: the effect of pentadecapeptide BPC 157, L-nitro-arginine methyl ester and L-arginine

Enhanced expression of endothelial nitric oxide synthase in the myocardium ameliorates the progression of left ventricular hypertrophy in L-arginine treated Wistar-Kyoto rats

Nitric oxide mediates antinociceptive effect of leucopyrokinin active analog [2-8]-leucopyrokinin [[2-8]-LPK]

Effect of L-arginine on lead induced oxidative stress in the blood of rats with different resistance to hypoxia

Dietary vitamin E and selenium yeast supplemented with L-arginine enhanced laying performance and egg quality attributes of guinea fowl (Numida meleagris)