Disease relevance of N-carbamimidoyl-L-aspartic acid

• We then determined whether calcitriol production was suppressed by preincubation with either dexamethasone or the putative uremia toxin guanidinosuccinic acid (GSA) [1].
• Accumulation of guanidinosuccinic acid increased with increasing degree of renal failure with levels up to 65 nmol/g tissue in the hypophysis [2].
• Behavioral toxicity of guanidinosuccinic acid in adult and young mice [3].
• Effect of low protein diet and surplus of essential amino acids on the serum concentration and the urinary excretion of methylguanidine and guanidinosuccinic acid in chronic renal failure [4].
• Within each subgroup, serum and urinary GSA levels were significantly lower in patients with alcohol-induced cirrhosis than in nonalcoholic cirrhotic patients [5].

Psychiatry related information on N-carbamimidoyl-L-aspartic acid

• A significant dose-dependent effect of i.h. injection of GSA on cognitive performance, activity and social exploratory behavior was observed [6].

High impact information on N-carbamimidoyl-L-aspartic acid

• Addition of urea, creatinine, and guanidinosuccinic acid to normal serum did not impair its ability to support erythropoiesis in this system [7].
• Guanidinosuccinic acid inhibits excitatory synaptic transmission in CA1 region of rat hippocampal slices [8].
• Methylguanidine and guanidine stimulated the proliferation of undifferentiated HL-60 cells and the antiproliferative effect of calcitriol (P < 0.05) was neutralized in the presence of methylguanidine (P < 0.05) and guanidinosuccinic acid (P < 0.05) [9].
• Aminoguanidine, NG-monomethyl-L-arginine (L-NMMA), NGNGdimethyl-L-arginine (asymmetric dimethylarginine; ADMA), creatinine, guanidinosuccinic acid, guanidinoproprionic acid and methylguanidine were added to cultures of activated murine macrophages [10].
• Incubation of normal 51-Cr-labeled human and guinea pig lymphocytes with uremic serum or guanidinosuccinic acid did not cause an increase in 51-Cr release [11].

Chemical compound and disease context of N-carbamimidoyl-L-aspartic acid

• (4) Guanidinosuccinic acid and methylguanidine appear to provide alternative pathways for the excretion of nitrogen in patients with renal failure [12].
• The best correlation between serum guanidino compound levels and the degree of renal insufficiency is found for GSA, SDMA, methylguanidine, and guanidine [13].
• Creatinine inhibited glucose utilization only at a concentration of 30 mg/dl; no effect of urea was found. o-Hydroxyphenolic acid and guanidinosuccinic acid, which were supposed to interfere with platelet function, inhibited glucose utilization at concentrations found in plasma of patients with chronic renal failure (CRF) [14].
• Blood and tissue guanidinosuccinic acid levels were not elevated during urease induced hyperammonemia, supporting the hypothesis that urea is a precursor for the synthesis of guanidinosuccinic acid [15].

Biological context of N-carbamimidoyl-L-aspartic acid

• Guanidinosuccinic acid (GSA) is noted for its nitric oxide (NO) mimicking actions such as vasodilatation and activation of the N-methyl-D-aspartate (NMDA) receptor [16].
• Two suspected uremic 'toxins', urea and guanidinosuccinic acid, were then administered in order to determine if either of these substances would independently alter the kinetics under study [17].
• Other known uremic compounds, guanidine, methylguanidine, and guanidinosuccinic acid, do not displace phenytoin from the protein-binding sites [18].
• Pretreatment with creatinine and guanidinosuccinic acid did not alter the effect of norepinephrine on mechanical activity and oxygen consumption when compared with the effects of norepinephrine (1 X 10(-8) g/ml and 1 X 10(-7) g/ml) given alone [19].

Anatomical context of N-carbamimidoyl-L-aspartic acid

• Guanidinosuccinic acid (GSA) is a guanidino compound found in mammalian central nervous system and physiological fluids [20].
• Using rat hepatocytes and microsomes as model proof of concept systems, we examined six uremic toxins, 3-carboxy-4-methyl-5-propyl-2-furan-propanoic acid (CMPF), indoxyl sulfate (IS), hippuric acid (HA), indole acetic acid (IA), guanidinosuccinic acid (GSA), and indoxyl-beta-D-glucuronide (IG), for their effects on Ery uptake and metabolism [21].
• Systemic GSA injection increased cGMP concentration in hippocampal formation [6].
• The concentrations of guanidinosuccinic acid are decreased in urine, plasma and cerebrospinal fluid [22].
• Pepsinogen release by isolated gastric glands of guinea pigs was suppressed by guanidinosuccinic acid and was facilitated by calcium [23].

Associations of N-carbamimidoyl-L-aspartic acid with other chemical compounds

• Creatinine, guanidine hydrochloride, guanidinosuccinic acid, and guanidinobutyric acid did not affect the number of CFU-E in normal rabbit bone marrow cultures [24].

Gene context of N-carbamimidoyl-L-aspartic acid

• The uremic guanidino compound guanidinosuccinic acid induces behavioral convulsions and concomitant epileptiform electrocorticographic discharges in mice [25].
• Guanidinosuccinic acid (GSA), a guanidino compound found to be greatly increased in uremia, was administered by intraperitoneal (i.p.) injection to adult albino mice and to young mice 7, 14 and 21 days old [3].
• The effect of co-application of NMDA-receptor antagonist CGP37849 with GSA was tested, in vivo, after hippocampal GSA injection and, in vitro, on GSA evoked currents in spinal cord neurons [6].
• Role of nitric oxide in the synthesis of guanidinosuccinic acid, an activator of the N-methyl-D-aspartate receptor [26].
• Because of the marked increase in guanidinosuccinic acid, a known uremic toxin, we speculate that guanidinosuccinic acid may be important in the pathophysiology of endotoxemia [27].

Analytical, diagnostic and therapeutic context of N-carbamimidoyl-L-aspartic acid

• Removal of guanidinosuccinic acid by hemodialysis [28].
• Animal models like the 'GSA mouse model' are useful tools for research in this context [6].

References