Chemical Formula: C5H9N3O4

Chemical Formula C5H9N3O4

Found 10 metabolite its formula value is C5H9N3O4

Guanidinosuccinic acid

(2S)-2-(diaminomethylideneamino)butanedioic acid

C5H9N3O4 (175.0593034)


Guanidinosuccinic acid (GSA) has been identified as a uremic toxin according to the European Uremic Toxin Working Group (PMID:22626821). It is one of the earliest uremic toxins isolated and its toxicity identified. Its metabolic origins show that it arose from the oxidation of argininosuccinic acid (ASA) by free radicals. The stimulus for this oxidation, occurring optimally in the presence of the failed kidney, is the rising level of urea which, through enzyme inhibition, results in a decline in hepatic levels of the semi-essential amino acid, arginine. It is further noted that concentrations of GSA in both serum and urine decline sharply in animals and humans exposed to the essential amino acid, methionine. Uremic patients suffer from a defective ability to generate methyl groups due to anorexia, dietary restrictions and renal protein leakage. This leads to the accumulation of homocysteine, a substance known to produce vascular damage. Even in healthy subjects intake of choline together with methionine is insufficient to satisfy total metabolic requirements for methyl groups. In end-stage renal disease, therefore, protein restriction contributes to the build-up of toxins in uremia. Replacement using specific amino acid mixtures should be directed toward identified deficiencies and adequacy monitored by following serum levels of the related toxins, in this case GSA and homocysteine. (PMID 12701806). Guanidinosuccinic acid (GSA) is one of the earliest uremic toxins isolated and its toxicity identified. Its metabolic origins show that it arose from the oxidation of argininosuccinic acid (ASA) by free radicals. The stimulus for this oxidation, occurring optimally in the presence of the failed kidney, is the rising level of urea which, through enzyme inhibition, results in a decline in hepatic levels of the semi-essential amino acid, arginine. It is further noted that concentrations of GSA in both serum and urine decline sharply in animals and humans exposed to the essential amino acid, methionine. Uremic patients suffer from a defective ability to generate methyl groups due to anorexia, dietary restrictions and renal protein leakage. This leads to the accumulation of homocysteine, a substance known to produce vascular damage. Even in healthy subjects intake of choline together with methionine is insufficient to satisfy total metabolic requirements for methyl groups. In end-stage renal disease, therefore, protein restriction contributes to the build-up of toxins in uremia. Replacement using specific amino acid mixtures should be directed toward identified deficiencies and adequacy monitored by following serum levels of the related toxins, in this case GSA and homocysteine. (PMID 12701806) [HMDB] Guanidinosuccinic acid is a nitrogenous metabolite.

   

Guanidinosuccinic acid

Guanidinosuccinic acid

C5H9N3O4 (175.0593034)


Guanidinosuccinic acid is a nitrogenous metabolite.

   

N-AMIDINO-ASPARTATE

N-AMIDINO-ASPARTATE

C5H9N3O4 (175.0593034)


   

Guanidinosuccinate

Guanidinosuccinic acid

C5H9N3O4 (175.0593034)


Guanidinosuccinic acid is a nitrogenous metabolite.

   

N-Amidino-L-aspartate

N-Amidino-L-aspartate

C5H9N3O4 (175.0593034)


   

N-AMIDINO-ASPARTIC ACID

N-AMIDINO-ASPARTIC ACID

C5H9N3O4 (175.0593034)


   

PROLI NONOate

1-(hydroxy-NNO-azoxy)-L-proline, disodium salt

C5H9N3O4 (175.0593034)


   

beta-Xylopyranosyl azide

beta-Xylopyranosyl azide

C5H9N3O4 (175.0593034)


   

N-amidinoaspartic acid

N-amidinoaspartic acid

C5H9N3O4 (175.0593034)


   

N-Amidino-L-aspartic acid

N-Amidino-L-aspartic acid

C5H9N3O4 (175.0593034)


An aspartic acid derivative comprising L-aspartic acid carrying an N-amidino substituent.