Relevant bibliographies by topics / L-arginine aspartate

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Academic literature on the topic 'L-arginine aspartate'

Author: Grafiati
Published: 4 June 2025
Last updated: 23 June 2025

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Journal articles on the topic "L-arginine aspartate"

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Frame, Mary D. S. "Conducted signals within arteriolar networks initiated by bioactive amino acids." American Journal of Physiology-Heart and Circulatory Physiology 276, no. 3 (1999): H1012—H1021. http://dx.doi.org/10.1152/ajpheart.1999.276.3.h1012.

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Our purpose was to determine the specificity of l-arginine (l-Arg)-induced conducted signals for intra- vs. extracellular actions ofl-Arg. Diameter and red blood cell velocities were measured for arterioles [18 ± 1.6 (SE) μm] in the cremaster muscle of pentobarbital sodium-anesthetized (Nembutal, 70 mg/kg) hamsters ( n = 53). Remote (conducted) responses were viewed ∼1,000 μm upstream from the local (micropipette) application. Six amino acids were tested:l-arginine,l-cystine,l-leucine,l-lysine,l-histidine, andl-aspartate (100 μM each). Only l-Arg induced a remote dilation; l-lysine andl-aspartate had no effect, and the others each induced a significant remote constriction. There is a second conducted signal initiated byl-arginine that preconditions the arteriolar network and upregulates a direct response ofl-arginine to dilate the remote site. This was blocked by inhibition ofl-arginine uptake at the local (preconditioning) site (100 μMl-histidine or 1 mM phenformin). Arginine-glycine-aspartate (100 μM)-induced remote dilations (+3.2 ± 0.3 μm) were not mimicked by a peptide control and were prevented by anti- integrin αv monoclonal antibody. Remote dilations were greater in animals with a higher wall shear stress for arginine-glycine-aspartate ( r 2 = 0.92) but not for l-arginine ( r 2 = 0.12). Thusl-arginine initiates separate conducted signals related to system y+ transport, integrins, and baseline flow.
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2

Kuvaeva, Z. I., D. V. Lopatik, M. M. Markovich, L. G. Vinokurova, and O. P. Popova. "Synthesis of L-ornithine L-aspartate from L-arginine." Pharmaceutical Chemistry Journal 46, no. 8 (2012): 495–97. http://dx.doi.org/10.1007/s11094-012-0833-x.

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Yamamoto, Tatsuo, and Naohito Shimoyama. "Role of Nitric Oxide in the Development of Thermal Hyperesthesia Induced by Sciatic Nerve Constriction Injury in the Rat." Anesthesiology 82, no. 5 (1995): 1266–73. http://dx.doi.org/10.1097/00000542-199505000-00022.

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Background Nitric oxide (NO) has been shown to be involved in mediating nociceptive information transmission in the spinal cord. It is known that the N-methyl-D-aspartate receptor plays an important role in the development of the spinal facilitation evoked by a protracted small afferent input and that this effect is mediated at least in part by NO. Recently, it has been found that N-methyl-D-aspartate receptor-mediated spinal facilitation is crucial in the development of thermal hyperesthesia evoked by a nerve constriction injury. In the current study, we investigated the role of NO in the development of thermal hyperesthesia after a nerve constriction injury. Methods The Bennett and Xie model (four loose chromic gut ligations around the rat sciatic nerve) was used to examine the development of thermal hyperesthesia. An NO synthase inhibitor (N omega-nitro-L-arginine or N omega-nitro-L-arginine methyl ester hydrochloride), rat hemoglobin, or L-arginine was administered intrathecally 10 min before the nerve injury (pretreatment study) or 15 min after the nerve injury (posttreatment study). Results Pretreatment but not posttreatment administration of NO synthase inhibitor significantly delayed the development of thermal hyperesthesia. The effect of NO synthase inhibitor was reversed by the coadministration of L-arginine but not by the coadministration of D-arginine. Pretreatment with rat hemoglobin also delayed the development of thermal hyperesthesia. L-Arginine itself had no effect on the development of thermal hyperesthesia. Conclusions NO may play an important role in the development of N-methyl-D-aspartate receptor-mediated spinal facilitation after a nerve constriction injury.
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Joung, Seung-Sam, and Sung-Keun Choi. "The effects of administration of L-arginine and L-aspartate on energy substrate utilization and endurance performance during exercise." Korean Journal of Sports Science 27, no. 5 (2018): 1591–604. http://dx.doi.org/10.35159/kjss.2018.10.27.5.1591.

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5

Bentsa, T. M., and O. A. Pastukhova. "Clinical efficacy of L-arginin aspartate in complex treatment of patients with essential arterial hypertension with concomitant type 2 diabetes mellitus." Infusion & Chemotherapy, no. 3.1 (October 11, 2020): 10–11. http://dx.doi.org/10.32902/2663-0338-2020-3.1-06.

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Objective. Investigate directly the clinical efficacy of L-arginine aspartate in the treatment of patients with essential arterial hypertension (EAG) and type 2 diabetes mellitus (DM).
 Materials and methods. The study included 43 patients with EAG II in combination with type 2 DM. The mean age of patients was 55,7±0,6 years, of which 20 (46,5 %) were men and 23 (53,5 %) were women. The duration of the disease on the EAG averaged 8,4±0,4 years, on type 2 DM – 6,5±0,5 years. A comprehensive clinical, laboratory and instrumental examination was carried out. All patients were divided into two groups. Patients in both groups received ramipril 5-10 mg a day in combination with amlodipine 5-10 mg a day and antidiabetic drugs (metformin, gliclazide or a combination thereof) as basic therapy. Patients in group 2 (n=22) were additionally prescribed the drug L-arginine aspartate orally 3 g 3 times a day for 4 weeks. The course of treatment was repeated after 2 months.
 Results and discussion. In group 2 there was a more pronounced tendency to decrease the average daily and night blood pressure levels, in particular diastolic (3,2 and 2,9 mm Hg; p>0,05) and heart rate (by 17,3 %; p<0,05). The use of L-arginine aspartate significantly improved systolic (ejection fraction increased by 7,1 % vs 4,4 % in group 1; p<0,05) and left ventricular (LV) diastolic function (Em/Am increased by 48,8 % vs 34,7 % in group 1; p<0,05), a decrease in the size of the left atrium (10,2 % vs 8,3 % in group 1; p<0,05) and the reversal of LV hypertrophy (index LV myocardial mass decreased by 20,1 % against 15,9 % in group 1; p<0,05). Additional administration of L-arginine aspartate also led to a decrease in fasting and postprandial plasma glucose (4,9 % and 7,0 %; p<0,05, respectively) than the use of basic therapy alone. At the same time in group 2 there was a decrease in microalbuminuria by 27,6 % (p<0,05) and an increase in glomerular filtration rate by 11,4 % (p>0,05).
 Conclusions. L-arginine aspartate should be used in patients with EAG in combination with type 2 DM and microalbuminuria to increase the cardio- and nephroprotective efficacy of basic therapy.
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Cole, S. C., P. A. Yaghmaie, P. J. Butterworth, and R. J. Yon. "Inactivation of wheat-germ aspartate transcarbamoylase by the arginine-specific reagent phenylglyoxal." Biochemical Journal 233, no. 1 (1986): 303–6. http://dx.doi.org/10.1042/bj2330303.

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Wheat-germ aspartate transcarbamoylase (EC 2.1.3.2) was inactivated by phenylglyoxal in a first-order process, provided that the inactivation time did not exceed 10 min. Apparent first-order rate constants were linearly dependent on phenylglyoxal concentration, indicating a bimolecular reaction between a single active-centre residue and phenylglyoxal, with second-order constant of 0.023 mM-1 X min-1. A plot of apparent first-order rate constant versus pH showed a steep rise above pH 9.5, indicating that the essential residue has a pKa value of 10.5 or higher, consistent with an arginine residue. Saturating concentrations of the following ligands provided a degree of protection (percentages in parentheses) against 1 mM-phenylglyoxal: N-phosphonoacetyl-L-aspartate, a bisubstrate analogue (94%); carbamoyl phosphate (75%); UMP, an end-product inhibitor (53%). Succinate (an analogue of L-aspartate) alone gave no protection, but in combination with carbamoyl phosphate raised the protection to 92%, in agreement with the known binding order of the two substrates. These results indicate that the essential arginine residue is close to the carbamoyl phosphate site, probably oriented towards the aspartate site. Attempts to desensitize the UMP-binding site by reaction with phenylglyoxal, while protecting the active centre, were unsuccessful. The essential active-centre arginine residue is compared with a similar residue in the Escherichia coli enzyme.
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Kohan, D. E., and G. F. Schreiner. "Interleukin 1 modulation of renal epithelial glucose and amino acid transport." American Journal of Physiology-Renal Physiology 254, no. 6 (1988): F879—F886. http://dx.doi.org/10.1152/ajprenal.1988.254.6.f879.

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We have investigated the effect of immune factors on glucose and amino acid transport by proximal tubular epithelium. Proximal tubular cells were obtained by enzymatic digestion of mouse renal cortex and grown to confluent monolayers. alpha-[14C]methylglucoside (AMG), D-[3H]-aspartate, L-[3H]leucine, and L-[3H]arginine uptake were assayed. Proximal tubular epithelium coincubated with supernatants derived from lipopolysaccharide (LPS)-stimulated mouse peritoneal macrophages had a twofold increase in AMG and aspartate uptake that was sodium dependent, was prevented by cycloheximide or actinomycin D, and was not associated with changes in cell growth or differentiation. Chromatographic separation of the macrophage supernatant yielded one fraction, mol wt 16,000-20,000, that enhanced AMG and aspartate uptake and contained interleukin 1 (IL 1) determined by bioassay. Recombinant IL 1 (mol wt 17,500) reproduced changes in AMG and aspartate uptake seen with macrophage supernatants. In contrast, neither macrophage supernatants nor IL 1 affected sodium-independent leucine or arginine transport. IL 1 directly increased 22Na transport into proximal tubular cells. These data indicate that macrophages, via IL 1 secretion, are capable of modulation of sodium-linked solute transport in proximal tubular epithelium.
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8

Burnat, Mireia, Antonia Herrero, and Enrique Flores. "Compartmentalized cyanophycin metabolism in the diazotrophic filaments of a heterocyst-forming cyanobacterium." Proceedings of the National Academy of Sciences 111, no. 10 (2014): 3823–28. http://dx.doi.org/10.1073/pnas.1318564111.

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Heterocyst-forming cyanobacteria are multicellular organisms in which growth requires the activity of two metabolically interdependent cell types, the vegetative cells that perform oxygenic photosynthesis and the dinitrogen-fixing heterocysts. Vegetative cells provide the heterocysts with reduced carbon, and heterocysts provide the vegetative cells with fixed nitrogen. Heterocysts conspicuously accumulate polar granules made of cyanophycin [multi-L-arginyl-poly (L-aspartic acid)], which is synthesized by cyanophycin synthetase and degraded by the concerted action of cyanophycinase (that releases β-aspartyl-arginine) and isoaspartyl dipeptidase (that produces aspartate and arginine). Cyanophycin synthetase and cyanophycinase are present at high levels in the heterocysts. Here we created a deletion mutant of geneall3922encoding isoaspartyl dipeptidase in the model heterocyst-forming cyanobacteriumAnabaenasp. strain PCC 7120. The mutant accumulated cyanophycin and β-aspartyl-arginine, and was impaired specifically in diazotrophic growth. Analysis of anAnabaenastrain bearing an All3922-GFP (green fluorescent protein) fusion and determination of the enzyme activity in specific cell types showed that isoaspartyl dipeptidase is present at significantly lower levels in heterocysts than in vegetative cells. Consistently, isolated heterocysts released substantial amounts of β-aspartyl-arginine. These observations imply that β-aspartyl-arginine produced from cyanophycin in the heterocysts is transferred intercellularly to be hydrolyzed, producing aspartate and arginine in the vegetative cells. Our results showing compartmentalized metabolism of cyanophycin identify the nitrogen-rich molecule β-aspartyl-arginine as a nitrogen vehicle in the unique multicellular system represented by the heterocyst-forming cyanobacteria.
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Lyalyukova, E. A., M. A. Livzan, A. V. Lyalyukov, and A. N. Sudakova. "L-ornithine-L-aspartate in patients with non-alcoholic fatty liver disease." RMJ, no. 10 (2024): 27–31. https://doi.org/10.32364/2225-2282-2024-10-5.

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Non-alcoholic fatty liver disease (NAFLD) is a prevalent chronic hepatic disorder marked by excessive lipid accumulation in hepatocytes. Current evidence underscores the multifactorial etiology of NAFLD, involving insulin resistance, lipotoxicity, neurohumoral alterations accompanied by elevated proinflammatory cytokine and adipokine release, activation of innate immunity, dysbiosis of the gut microbiota, increased intestinal permeability, and genetic susceptibility. Recent studies have identified hyperammonemia as a pivotal factor in NAFLD pathogenesis. Ammonia accumulation in the liver maintains inflammatory processes, stellate cell activation, and initiates fibrogenesis, heightening the risk of progression to cirrhosis and hepatocellular carcinoma. Furthermore, systemic hyperammonemia detrimentally impacts other organ systems, notably contributing to cognitive deficits and sarcopenia. Hence, it is pathophysiologically rational to administer L-ornithine-L-aspartate to individuals with NAFLD. This compound not only possesses hypoammonemic effects but also exhibits hepatoprotective, hypoazotemic, and detoxifying actions. The beneficial effects of L-ornithine-L-aspartate are also attributed to the metabolic conversion of L-ornithine and L-aspartate into L-glutamine, L-arginine, and glutathione, which are potent antioxidants safeguarding hepatocytes against lipid peroxidation and enhancing hepatic microcirculation. Collectively, these mechanisms contribute to the efficacy of L-ornithine-L-aspartate in mitigating the extent of steatosis, inflammation, and even hepatic fibrosis in NAFLD patients. Keywords: non-alcoholic fatty liver disease, L-ornithine-L-aspartate, hyperammonemia, metabolic syndrome, oxidative stress. For citation: Lyalyukova E.A., Livzan M.A., Lyalyukov A.V., Sudakova A.N. L-ornithine-L-aspartate in patients with non-alcoholic fatty liver disease. RMJ. 2024;10:27–31. DOI: 10.32364/2225-2282-2024-10-5
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Lefin, Nicolás, Javiera Miranda, Iris Munhoz Costa, et al. "Optimized Amino Acid-Enhanced Medium for Efficient L-Asparaginase II Production in E. coli: From Shake Flask to Bioreactor." Fermentation 11, no. 5 (2025): 239. https://doi.org/10.3390/fermentation11050239.

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L-asparaginase (L-ASNase) is a key enzyme in the treatment of leukemia and lymphoma, with high demand in cancer therapies. Advances in recombinant protein production have improved yields and reduced costs, enabling large-scale production. However, optimizing culture conditions remains crucial for maximizing production. This study focused on optimizing the production of double mutant L-ASNase expressed in Escherichia coli BL21 (DE3) by supplementing media with amino acids. Five amino acids were evaluated at a shake flask scale using the design of experiments, with arginine and aspartate showing the most positive effects. Under optimized conditions (14.5 mM arginine, 12.7 mM aspartate, and 0 mM cysteine), the activity model reached 12,513 U L−1, experimentally validated at 10,089 U L−1. The maximum specific cell growth rate was µx,max = 0.74 h−1, with substrate–biomass conversion factor Yx/s = 1.16 g/g and cell–product conversion factor Yp/x = 13,891 U/gcell. Amino acid supplementation resulted in a ten-fold increase in L-ASNase activity. Finally, at the bioreactor scale, adding amino acids and the inducer at the end of the exponential phase increased activity by 135% compared to conventional MD, demonstrating its potential for industrial-scale production.
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Dissertations / Theses on the topic "L-arginine aspartate"

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Desmurs, Silvia. "Intérêt de L-aspartate de L-arginine dans les traitementsde stimulation ovarienne : rédaction du protocole de l'essai clinique." Poitiers, 1994. http://www.theses.fr/1994POIT1514.

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Prysiazhniuk, I. V. "Effect of L-arginine aspartate in complex treatment of patients with chronic cholecystitis and hypothyroidism." Thesis, БДМУ, 2021. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/18598.

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Conference papers on the topic "L-arginine aspartate"

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Shtefiuk, O., and R. Yatsyshyn. "AB0433 Correction of lipid and endothelial dysfunction by using no donators (4,2% solution of arginine hydrochloride and l-arginine aspartate) in patient with rheumatoid arthritis in combination with the raynaud's syndrome." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.1132.

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Silva, Karolaine Moura da, Allyson de Andrade Mendonça, and Marcos Antônio de Morais Junior. "ANÁLISE DO EFEITO DA SUPLEMENTAÇÃO DE AMINOÁCIDOS NA CIM DA BACTÉRIA LACTOBACILLUS HALOTOLERANS." In XXVII Semana de Biomedicina Inovação e Ciência. Editora IME, 2021. http://dx.doi.org/10.51161/9786588884119/30.

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Introdução: A microbiota humana é composta por vários gêneros bacterianos, dentre eles estão os Lactobacillus(1). Além do corpo humano, estas bactérias podem estar presentes nos processos fermentativos para produção de etanol, sendo responsáveis por boa parte da contaminação do mosto fermentativo(4). A utilização de tratamentos físicos e químicos, como administração de antimicrobianos, é realizada para o controle bacteriano. Entretanto, nas últimas décadas, resistência a diversos antibióticos utilizados na indústria foram surgindo(2). Em estudos anteriores foi identificado que cepas de Lactobacillus vini cultivadas em meio MRS suplementado com o aminoácido cisteína mostram-se mais resistentes ao antibiótico eritromicina(³). Objetivos: Assim, este trabalho teve como objetivo analisar o efeito dos vinte aminoácidos sobre a CIM, para o antibiótico tetraciclina, da espécie bacteriana Lactobacillus halotolerans, pertencente do gênero Lactobacillus. Métodos: Foi determinada a concentração inibitória mínima (CIM) da espécie L. halotolerans utilizando a metodologia de microdiluição em caldo para o antibiótico tetraciclina, na ausência ou na presença de cada um dos 20 aminoácidos na concentração de 40mM. Resultados: Foi observado que na maioria dos casos, a suplementação com os aminoácidos teve efeito neutro ou induziu um leve aumento da tolerância à droga. Os aminoácidos alanina, arginina, histidina, isoleucina, leucina, fenilalanina, triptofano e valina aumentaram o CIM da droga em 2x. Enquanto que os aminoácidos aspartato, cisteína, glutamato, glutamina, glicina, metionina, prolina, serina, treonina e tirosina não modificaram o CIM para tetraciclina. O aminoácido lisina foi o único que teve efeito de diminuição da tolerância, reduzindo-a em 2x. Já a asparagina foi responsável por um aumento de 8x em comparação ao CIM original, sendo o aminoácido que mais aumentou a tolerância do microrganismo à tetraciclina. Conclusões: Com isso, concluímos que os aminoácidos podem vir a causar uma modificação na CIM da espécie de Lactobacillus halotolerans, tanto aumentando ou diminuindo a sua tolerância, sendo válido estudar mais a fundo em demais microrganismos e qual mecanismo por trás de tais efeitos. ISBN: 978-
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