Natural Guanidino Compounds

Robin, Y; Marescau, B.

doi:10.1007/978-1-4757-0752-6_38

Cited by 34 publications

(16 citation statements)

References 229 publications

(221 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This is essentially the same result as in earlier reports [18,20,22] except for the possibility that GAA and arginine serve as a precursor of G in organs beside the liver as previously reported [18,19]. Regarding the origin of cana vanine, there are two possibilities: one is dietary because canavanine is identified in the seeds of a great number of leguminous plants [23] and the other is an endogenous synthesis via the 'guanidine cycle' as advocated by Natelson and Shirwin [24], However, the origin of canavanine re mains to be explored.…”

Section: Discussionsupporting

confidence: 77%

Biosynthesis of Guanidine in Isolated Rat Hepatocytes, Perfused Rat Liver and Intact Animals

Takemura

Nagase

Aoyagi

et al. 1994

Nephron

View full text Add to dashboard Cite

Plasma levels of guanidine (G) are reported to be increased in uremic patients and are synthesized from various guanidino compounds via a chemical reaction involving the hydroxyl radical in vitro. To identify both the metabolic precursor and the synthesizing organ of G, we investigated the concentrations of G in various organs of rats administered several guanidino compounds and we attempted to synthesize G biologically using isolated rat hepatocytes or perfused rat liver. In addition, we investigated the effect of the peroxidative state on the G synthesis in isolated hepatocytes using various reagents which alter this condition. Results show that the concentration of G increased in the kidney, liver and muscle following the administration of L-canavanine. In addition, G increased in the kidney at 90 min after the administration of guanidinoacetic acid (GAA). Moreover, G is synthesized from L-canavanine in isolated rat hepatocytes and perfused rat liver, and G synthesis in hepatocytes is partially inhibited by the addition of superoxide dismutase, catalase, glutathione or ethylenediaminetetraacetic acid. These results suggest that L-canavanine is possibly a biological precursor and GAA is an endogenous precursor of G. Furthermore, it is suggested that these reactions are closely related to the peroxidative state.

show abstract

Section: Discussionsupporting

confidence: 77%

Biosynthesis of Guanidine in Isolated Rat Hepatocytes, Perfused Rat Liver and Intact Animals

Takemura

Nagase

Aoyagi

et al. 1994

Nephron

View full text Add to dashboard Cite

show abstract

“…An amidine group of Arg and canavanine could be transferred to Gly by GAT action and result in the Renal GAT activity, ggig ■ wet tissue/h production of GAA and ornithine, and GAA and canaiine, respectively. Robin et al [24] reported that canavanine and canavaninosuccinic acid in the guanidine cycle have never been detected in animal tissues but only in some plant seeds. Also, canaiine has never been detected in vertebrates.…”

Section: Discussionmentioning

confidence: 99%

Study on Impaired Metabolism of Guanidinoacetic Acid in Chronic Renal Failure Rabbits with Special Reference to Impaired Conversion of Arginine to Guanidinoacetic Acid

Kuroda

1993

Nephron

View full text Add to dashboard Cite

Most chronic renal failure (CRF) patients show low serum concentrations of guanidinoacetic acid (GAA). In this study, the author investigated the impaired metabolism of GAA in CRF focusing on the transformation of arginine (Arg) to GAA by analyzing CRF rabbits using ¹⁴C-Arg. The CRF group which consisted of 6 CRF rabbits, was compared with 6 normal rabbits (normal group). Blood samples were obtained from each abdominal aorta after a bolus injection of 30 μCi of ¹⁴C-Arg into an ear vein of each rabbit. After the last sampling, the left kidney was obtained for measurement of renal glycine amidinotransferase (GAT) activity. In each blood sample, the concentrations of blood urea nitrogen (BUN), serum creatinine (Cr), GAA and Arg were measured. The radioactivity of serum ¹⁴C-GAA was measured with a liquid scintillation system. Δ¹⁴C-GAA was calculated as the difference between the ¹⁴C-GAA count and the Δ¹⁴C -background count. Serum concentrations of GAA and renal GAT activity were significantly lower in the CRF group as compared with the normal group. Significant negative correlations were found between the two groups for the following comparisons: serum concentrations of Cr and GAA, concentrations of BUN and renal GAT activity, and serum concentrations of Cr and renal GAT activity. There was a significant positive correlation in the two groups, between renal GAT activity and serum concentrations of GAA. The fact that the concentrations of neither GAA nor Arg changed significantly after the injection of ¹⁴C-Arg in either group suggested that the dosage of injected Arg is not sufficient to affect the transformation of Arg to GAA. After 5 min and at the following 5-min intervals, Δ¹⁴C-GAA was significantly lower in the CRF group than in the normal group. There was a positive correlation between Δ¹⁴C-GAA after 5 min and renal GAT activity. These results clearly show that renal GAT activity decreases with the progression of renal dysfunction, which directly causes a reduced transformation of Arg to GAA in the kidney, resulting in lower serum concentrations of GAA.

show abstract

“…More than one hundred naturally occuring guanidino compounds, substances that have guanidino group(s), H2N-C(=NH)-NH-, have been identified in plants and animals (1). Guanidino…”

Section: Introductionmentioning

confidence: 99%

Guanidino compounds generate reactive oxygen species

et al. 1996

View full text Add to dashboard Cite

SUMMARYMethylguanidine, guanidinoacetic acid and guanidinosuccinic acid are endogenous substances in body tissues. Extremely high levels of these substances are known to be related to the pathogenesis of epilepsy and renal failure such as uremia. In this study it was demonstrated that methylguanidine, guanidinoacetic acid and guanidinosuccinic acid, and arginine generate hydroxyl radicals in aqueous solution. These findings suggest that a high level of guanidino compounds accumulating near or within cells such as neurons (in an epileptogenic focus) or nephrons (in uremic patients) may cause free radical damage leading to these clinical disorders. Arginine may have a similar role in the pathogenesis of hyperarginemia.

show abstract

Natural Guanidino Compounds

Cited by 34 publications

References 229 publications

Biosynthesis of Guanidine in Isolated Rat Hepatocytes, Perfused Rat Liver and Intact Animals

Biosynthesis of Guanidine in Isolated Rat Hepatocytes, Perfused Rat Liver and Intact Animals

Study on Impaired Metabolism of Guanidinoacetic Acid in Chronic Renal Failure Rabbits with Special Reference to Impaired Conversion of Arginine to Guanidinoacetic Acid

Guanidino compounds generate reactive oxygen species

Contact Info

Product

Resources

About