15,819 research outputs found

    L-citrulline Sebagai Inhibitor Korosi Pada Tinplate Dalam Media Nacl

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    L-citrulline sebagai inhibitor korosi pada tinplate dalam media NaCl telah diteliti menggunakan metode polarisasi potensiodinamik dan pengurangan berat. Pada penelitian ini dilakukan variasi konsentrasi L-citrulline dan media korosi NaCl. Hasil penelitian menunjukkan bahwa dalam media 2% NaCl, L-citrulline dapat meningkatkan efisiensi inhibisi korosi seiring dengan meningkatnya konsentrasi L-citrulline berturut-turut yaitu sebesar 36% dan 74,59 % pada metode pengurangan berat dan polarisasi potensiodinamik. Pengaruh konsentrasi NaCl terhadap efisiensi inhibisi L-citrulline pada tinplate yaitu dapat meningkatkan densitas arus korosi tinplate dan menurunkan efisiensi inhibisi L-citrulline dalam media 3% NaCl daripada dalam media 2% NaCl. Prosentase efisiensi inhibisi L-Citrulline pada tinplate dalam media 2% NaCl sebesar 74,59% dan dalam media 3% NaCl sebesar 68,96%. Adsorpsi L-citrulline pada permukaan tinplate mengikuti mekanisme adsorpsi isoterm Freundlich dengan nilai Kads dan Gads berturut-turut sebesar 0,9835 dan -23,31 kJmol-1. L-citrulline menunjukkan mekanisme adsorpsi secara kimia (kemisorpsi) dengan tinplate

    Evaluation of anti-diarrhoeal activity of L-citrulline in mice

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    Background: L-citrulline is a naturally occurring physiological non-essential amino acid that plays an important role in the metabolism and regulation of nitric oxide. Nitric oxide is important for physiologic processes of gastrointestinal tract, like motility and absorption. L citrulline is majorly synthesized in the small intestine and considered safe for consumption. However, there is paucity of literature on its anti-diarrhoeal effects. Hence, this study investigated the anti-diarrhoeal activity of L-citrulline in mice.Methods: Anti-diarrhoeal and anti-enteropooling effects of L-citrulline were evaluated by inducing diarrhoea and enteropooling with castor oil. The effect of L-citrulline on normal intestinal motility was also evaluated using charcoal maker. L-citrulline (300 and 600 mg/kg) was administered to test groups, Loperamide (5 mg/kg) was administered to the positive control groups and Normal saline (2ml/kg) was administered to negative control groups. All administrations were via oral route. The results were analyzed using one-way Analysis of variance and Dunnett's post-hoc test.Results: The control groups in all parameters evaluated showed typical diarrhoeal signs. Diarrhoea protections of 93.33% and 55.49% were observed at 300 and 600 mg/kg of L-Citrulline, respectively. L-Citrulline inhibited fluid accumulation by 35.88% and 28.27% at 300 and 600 mg/kg, respectively. The mean percentage distance travelled by the charcoal maker was inhibited by 13.76% and 2.62% at 300 and 600 mg/kg, of L-citrulline, respectively. The observed antidiarrhoeal effects of L-citrulline could be attributed to its ability to inhibit both intestinal motility and fluid accumulation in the mice.Conclusion: This study has shown that L-citrulline possess some anti-diarrhoeal potentials. However, there is need for further anti-diarrhoeal studies using other models and lower graded doses of L-Citrulline to further elucidate L-Citrulline anti-diarrhoeal mechanism of action.Keywords: L-citrulline, anti-diarrhoeal activity, Loperamide, castor oi

    Nitric oxide precursors and congenital heart surgery: A randomized controlled trial of oral citrulline

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    ObjectiveThe study sought to determine whether citrulline supplementation, a precursor to nitric oxide synthesis, is safe and efficacious in increasing plasma citrulline concentrations and decreasing the risk of postoperative pulmonary hypertension.Study DesignForty children, undergoing cardiopulmonary bypass and at risk for pulmonary hypertension, were randomized to receive 5 perioperative doses (1.9 g/m2 per dose) of either oral citrulline or placebo. Plasma citrulline and arginine concentrations were measured at 5 time points. Measurements of systemic blood pressure and presence of pulmonary hypertension were collected.ResultsMedian citrulline concentrations were significantly higher in the citrulline group versus the placebo group immediately postoperatively (36 Ī¼mol/L vs 26 Ī¼mol/L, P = .012) and at 12 hours postoperatively (37 Ī¼mol/L vs 20 Ī¼mol/L, P = .015). Mean plasma arginine concentrations were significantly higher in the citrulline group versus the placebo group by 12 hours postoperatively (36 Ī¼mol/L vs 23 Ī¼mol/L, P = .037). Mean systemic blood pressure did not differ between groups (P = .53). Postoperative pulmonary hypertension developed in 9 patients, 6 of 20 (30%) in the placebo group and 3 of 20 (15%) in the citrulline group (P = .451), all of whom had plasma citrulline concentrations less than age-specific norms. Postoperative pulmonary hypertension did not develop in patients who demonstrated plasma citrulline concentrations in excess of 37 Ī¼mol/L (P = .036).ConclusionsOral citrulline supplementation safely increased plasma citrulline and arginine concentrations compared with placebo after cardiopulmonary bypass. Postoperative pulmonary hypertension did not occur in children with naturally elevated citrulline levels or elevations through supplementation. Oral citrulline supplementation may be effective in reducing postoperative pulmonary hypertension

    COMBINED GRAPE SEED EXTRACT AND L-CITRULLINE SUPPLEMENTATION IMPROVES CYCLING TIME TRIAL PERFORMANCE

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    Studies have shown that L-Citrulline alone improves nitric oxide (NO) production which is beneficial for vasodilation or increasing skeletal blood flow. Grape seed extract (GSE) also has been shown to increase the production of NO via activation of NO synthase, reducing peripheral resistance during exercise. PURPOSE: The aim of this study was to determine if acute administration of the combined GSE and L-Citrulline supplements had a greater effect on exercise performance compared to taking either supplement alone. METHODS: In a randomized cross-over design, 12 healthy male subjects aged between 18 to 30 years were divided into four groups: Placebo (starch), L-Citrulline, GSE, and GSE and L-Citrulline combined. They performed a timed trial (8 km) using a cycle ergometer to evaluate exercise performance after taking each supplement. RESULTS: There was no significant difference in heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), and ratings of perceived exertion (RPE) across supplementations. Combined GSE and L-Citrulline supplementation significantly lowered a time trial compared to other supplements (placebo: 19.9Ā±1.0 min; GSE: 19.3Ā±1.0 min; L-Citrulline:19.6Ā±0.9 min; GSE+L-Citrulline; 18.9Ā±1.0 min. CONCLUSION: our results suggest that acute supplementation with combined GSE and L-citrulline appears to be an ergogenic aid that can improve exercise performance

    Watermelon Juice: Potential Functional Drink for Sore Muscle Relief in Athletes

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    L-Citrulline is an excellent candidate to reduce muscle soreness, and watermelon is a fruit rich in this amino acid. This study investigated the potential of watermelon juice as a functional drink for athletes. An in vitro study of intestinal absorption of l-citrulline in Caco-2 cells was performed using unpasteurized (NW), pasteurized (80 Ā°C for 40 s) watermelon juice (PW) and, as control, a standard of l-citrulline. l-citrulline bioavailability was greater when it was contained in a matrix of watermelon and when no heat treatment was applied. In the in vivo experiment (maximum effort test in a cycloergometer), seven athletes were supplied with 500 mL of natural watermelon juice (1.17 g of l-citrulline), enriched watermelon juice (4.83 g of l-citrulline plus 1.17 g from watermelon), and placebo. Both watermelon juices helped to reduce the recovery heart rate and muscle soreness after 24 h.Actividad FĆ­sica y Deport

    Citrulline a More Suitable Substrate than Arginine to Restore NO Production and the Microcirculation during Endotoxemia

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    BACKGROUND: Impaired microcirculation during endotoxemia correlates with a disturbed arginine-nitric oxide (NO) metabolism and is associated with deteriorating organ function. Improving the organ perfusion in endotoxemia, as often seen in patients with severe infection or systemic inflammatory response syndrome (SIRS) is, therefore, an important therapeutic target. We hypothesized that supplementation of the arginine precursor citrulline rather than arginine would specifically increase eNOS-induced intracellular NO production and thereby improve the microcirculation during endotoxemia. METHODOLOGY/PRINCIPAL FINDINGS: To study the effects of L-Citrulline and L-Arginine supplementation on jejunal microcirculation, intracellular arginine availability and NO production in a non-lethal prolonged endotoxemia model in mice. C57/Bl6 mice received an 18 hrs intravenous infusion of endotoxin (LPS, 0.4 Āµg ā€¢ g bodyweight(-1) ā€¢ h(-1)), combined with either L-Citrulline (6.25 mg ā€¢ h-1), L-Arginine (6.25 mg ā€¢ h(-1)), or L-Alanine (isonitrogenous control; 12.5 mg ā€¢ h(-1)) during the last 6 hrs. The control group received an 18 hrs sterile saline infusion combined with L-Alanine or L-Citrulline during the last 6 hrs. The microcirculation was evaluated at the end of the infusion period using sidestream dark-field imaging of jejunal villi. Plasma and jejunal tissue amino-acid concentrations were measured by HPLC, NO tissue concentrations by electron-spin resonance spectroscopy and NOS protein concentrations using Western blot. CONCLUSION/SIGNIFICANCE: L-Citrulline supplementation during endotoxemia positively influenced the intestinal microvascular perfusion compared to L-Arginine-supplemented and control endotoxemic mice. L-Citrulline supplementation increased plasma and tissue concentrations of arginine and citrulline, and restored intracellular NO production in the intestine. L-Arginine supplementation did not increase the intracellular arginine availability. Jejunal tissues in the L-Citrulline-supplemented group showed, compared to the endotoxemic and L-Arginine-supplemented endotoxemic group, an increase in degree of phosphorylation of eNOS (Ser 1177) and a decrease in iNOS protein level. In conclusion, L-Citrulline supplementation during endotoxemia and not L-Arginine reduced intestinal microcirculatory dysfunction and increased intracellular NO production, likely via increased intracellular citrulline and arginine availability

    l-Citrulline Supplementation-Increased Skeletal Muscle PGC-1Ī± Expression Is Associated with Exercise Performance and Increased Skeletal Muscle Weight

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    1 Scopelā€citrulline has recently been reported as a more effective supplement for promoting intracellular nitric oxide (NO) production compared to lā€arginine. Here, the effect of lā€citrulline on skeletal muscle and its influence on exercise performance were investigated. The underlying mechanism of its effect, specifically on the expression of skeletal muscle peroxisome proliferatorā€activated receptorā€gamma coactivatorā€1Ī± (PGCā€1Ī±), was also elucidated.2 Methods and resultsSixā€weekā€old ICR mice were orally supplemented with lā€citrulline (250 mg kgāˆ’1) daily, and their performance in weightā€loaded swimming exercise every other day for 15 days, was evaluated. In addition, mice muscles were weighed and evaluated for the expression of PGCā€1Ī± and PGCā€1Ī±ā€regulated genes. Mice orally supplemented with lā€citrulline had significantly higher gastrocnemius and biceps femoris muscle mass. Although not statistically significant, lā€citrulline prolonged the swimming time to exhaustion. PGCā€1Ī± upregulation was associated with vascular endothelial growth factor Ī± (VEGFĪ±) and insulinā€like growth factor 1 (IGFā€1) upregulation. VEGFĪ± and IGFā€1 are important for angiogenesis and muscle growth, respectively, and are regulated by PGCā€1Ī±. Treatment with NGā€nitroā€lā€arginine methyl ester hydrochloride (lā€NAME), a nitric oxide synthesis inhibitor, suppressed the lā€citrullineā€induced PGCā€1Ī± upregulation in vitro.3 ConclusionSupplementation with lā€citrulline upregulates skeletal muscle PGCā€1Ī± levels resulting in higher skeletal muscle weight that improves time to exhaustion during exercise

    Sodium-coupled neutral amino acid transporter 1 (SNAT1) modulates L-citrulline transport and nitric oxide (NO) signaling in piglet pulmonary arterial endothelial cells

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    Rationale There is evidence that impairments in nitric oxide (NO) signaling contribute to chronic hypoxia-induced pulmonary hypertension. The L-arginine-NO precursor, L-citrulline, has been shown to ameliorate pulmonary hypertension. Sodium-coupled neutral amino acid transporters (SNATs) are involved in the transport of L-citrulline into pulmonary arterial endothelial cells (PAECs). The functional link between the SNATs, L-citrulline, and NO signaling has not yet been explored. Objective We tested the hypothesis that changes in SNAT1 expression and transport function regulate NO production by modulating eNOS coupling in newborn piglet PAECs. Methods and Results A silencing RNA (siRNA) technique was used to assess the contribution of SNAT1 to NO production and eNOS coupling (eNOS dimer-to-monomer ratios) in PAECs from newborn piglets cultured under normoxic and hypoxic conditions in the presence and absence of L-citrulline. SNAT1 siRNA reduced basal NO production in normoxic PAECs and prevented L-citrulline-induced elevations in NO production in both normoxic and hypoxic PAECs. SNAT1 siRNA reduced basal eNOS dimer-to-monomer ratios in normoxic PAECs and prevented L-citrulline-induced increases in eNOS dimer-to-monomer ratios in hypoxic PAECs. Conclusions SNAT1 mediated L-citrulline transport modulates eNOS coupling and thus regulates NO production in hypoxic PAECs from newborn piglets. Strategies that increase SNAT1-mediated transport and supply of L-citrulline may serve as novel therapeutic approaches to enhance NO production in patients with pulmonary vascular disease

    Citrulline supplementation improves organ perfusion and arginine availability under conditions with enhanced arginase activity

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    Enhanced arginase-induced arginine consumption is believed to play a key role in the pathogenesis of sickle cell disease-induced end organ failure. Enhancement of arginine availability with l-arginine supplementation exhibited less consistent results; however, l-citrulline, the precursor of l-arginine, may be a promising alternative. In this study, we determined the effects of l-citrulline compared to l-arginine supplementation on arginine-nitric oxide (NO) metabolism, arginine availability and microcirculation in a murine model with acutely-enhanced arginase activity. The effects were measured in six groups of mice (n = 8 each) injected intraperitoneally with sterile saline or arginase (1000 IE/mouse) with or without being separately injected with l-citrulline or l-arginine 1 h prior to assessment of the microcirculation with side stream dark-field (SDF)-imaging or in vivo NO-production with electron spin resonance (ESR) spectroscopy. Arginase injection caused a decrease in plasma and tissue arginine concentrations. l-arginine and l-citrulline supplementation both enhanced plasma and tissue arginine concentrations in arginase-injected mice. However, only the citrulline supplementation increased NO production and improved microcirculatory flow in arginase-injected mice. In conclusion, the present study provides for the first time in vivo experimental evidence that l-citrulline, and not l-arginine supplementation, improves the end organ microcirculation during conditions with acute arginase-induced arginine deficiency by increasing the NO concentration in tissues

    Potential Deleterious Effects of L-Citrulline Supplementation in Isoproterenol-Induced Myocardial Infarction: Focus on Nitrosative Stress

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    L-Citrulline shows potential activity as a supplement to prevent myocardial infarction through vasodilative and possible antioxidative effects but may be deleterious by causing nitrosative stress. This study determined the potentially deleterious effects of L-citrulline supplementation in isoproterenol-induced myocardial infarction with a focus on nitrosative stress. L-Citrulline supplementation was given orally at dosages of 300 or 600mg/kg body weight daily for 6 days. Myocardial infarction was induced in Wistar rats via subcutaneous injection of isoproterenol (85 mg/kg body weight (BW)) on day 4 and 5. Blood pressure was measured at the end of the study (day 6) and rats were sacrificed to collect heart tissue samples for a histopathological evaluation. The histopathological evaluation was done using hematoxylin and eosin staining for the myocardial damage evaluation and immunohistochemical (IHC) staining of arginase-2, inducible nitric oxide synthase (iNOS), and 3-nitrotyrosine to evaluate nitrosative stress. L-Citrulline supplementation failed to show a significant protective effect on blood pressure and exacerbated the decrease of diastolic blood pressure. Both low and high dose L-citrulline supplementation had a significant protective effect on myocardial damage compared to the isoproterenol group (p<0.01). L-Citrulline also caused increased nitrosative stress as shown by increased expression of arginase-2 and 3-nitrotyrosine on IHC staining but tended to show an ameliorative effect on iNOS expression. A significant increase in arginase-2 expression was detected between the high dose group and the other groups (p<0.01 vs. normal and isoproterenol groups; p<0.05 vs. low dose group). L-Citrulline supplementation increased 3-nitrotyrosine expression in a dose-dependent manner, which was significantly different compared to the normal group (low dose: p<0.013; high dose: p<0.003). L-Citrulline increased the production of nitrosative stress but resulted in less myocardial damage through its other effects
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