Separation and estimation of certain guanidino compounds. Application to human urine

Bonas, John E.; Cohen, Bertram I.; Natelson, Samuel

doi:10.1016/0026-265x(63)90012-2

Cited by 71 publications

(27 citation statements)

References 13 publications

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“…The lack of correlation between PF3-A and serum urea, creatinine, calcium, and phosphorus also indicates that these substances are not responsible for the abnormality. In addition GAA, a substance found to be increased in urine of uremic patients (17), had no effect on PF3-A time.…”

Section: Discussionmentioning

confidence: 81%

“…There was no demonstrable effect of increased calcium on PF3-A time. The effect of GSA on PF3-A time was also investigated, since this substance, which is increased in urine of uremic patients (17,18), has been reported to interfere with PF3-A (19). Varying concentrations of GSA dissolved in buffered saline were added to the mixture of PRP and PPP, before the addition of Celite, to obtain a final concentration of 0.03-1.6 mmole/liter.…”

Section: Day-to-day Variation and Reproducibilitymentioning

confidence: 99%

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Platelet factor 3 in normal subjects and patients with renal failure

Rabiner¹,

Hrodek²

1968

J. Clin. Invest.

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Two tests were used to differentiate abnormalities in release of platelet factor 3 (PF3) from quantitative deficiencies of this factor in normal subjects and in patients with renal failure. The first test was an assay which determined availability of PF3 (PF3-A time) and involved the use of a mixture of patient's plateletrich plasma (PRP) and normal platelet-poor plasma (PPP) in a fixed ratio (1: 8). The second test was similar but used "frozen and thawed" platelets to obtain a quantitative estimate of PF3 (PF3-F time). An abnormal PF3-A time was found in approximately three-quarters of 55 patients with renal insufficiency; 43 of these had chronic and 12 had acute renal failure. This abnormality was present both in patients with and without hemorrhagic manifestations, although it was slightly more common in bleeders. The PF3-F test was abnormal in approximately one-third of the bleeding patients and one-quarter of the nonbleeders. The PF3-A time returned to normal or was significantly shortened 24-48 hr after peritoneal or hemodialysis. Studies on patients who were not dialyzed showed no statistically significant correlations between the PF3-A time and either the serum urea nitrogen, creatinine, calcium, or phosphorus. Furthermore, the PF3-A time was not affected by guanidinosuccinic or guanidinoacetic acids. We therefore conclude that the demonstrable platelet abnormality in patients with uremia is produced by an unknown dialyzable material.Dr. Hrodek's present address is 2nd Pediatric

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Section: Discussionmentioning

confidence: 81%

Section: Day-to-day Variation and Reproducibilitymentioning

confidence: 99%

Platelet factor 3 in normal subjects and patients with renal failure

Rabiner¹,

Hrodek²

1968

J. Clin. Invest.

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“…MG [15][16][17][18] and GSA [19][20][21] have been known to be highly concentrated in the serum of uremic patients. Re cently, MG [16,[22][23][24][25][26] and GSA [16.27-31] have been found to have many toxic effects in vitro, especially MG, bringing about the same symptoms as those of uremia in normal dogs subjected to repeated injections up to the serum level of the uremic state [32], These experimental findings suggest that MG and GSA play an important role in the uremic state.…”

Section: Introductionmentioning

confidence: 99%

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

Ando¹,

Orita²,

Nakata³

et al. 1979

Nephron

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20 patients with moderate renal failure (serum creatinine 4.5–12.0 mg/dl) and some uremic symptoms on a diet ad libitum were treated with a high caloric diet containing 0.5–0.7 g/kg/day protein, supplemented with eight essential amino acids and histidine in the form of solution and/or granules. During the treatment uremic symptoms subsided or diminished without the signs of malnutrition, SUN and the ratio SUN/S-creatinine fell and the nitrogen balance and the ratio N-balance/intake N improved. The serum concentration and the urinary excretion of MG and GSA of the 12 patients were determined by Stein’s method using the modified Sakaguchi reaction. In all patients, the serum, concentration and the urinary excretion of MG and GSA diminished remarkably during the treatment with a low protein diet alone and furthermore with a low protein diet and essential amino acid supply. We concluded that conservative treatment – low nitrogen diet supplemented with sufficient calories and essential amino acids – improved the nutritional state of uremic subjects, and decreased the metabolic production of MG and GSA. The results show that the supplementation of essential amino acids to uremic patients may be a useful treatment.

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“…After washing the resin with 3 M ammonia, a solution able to elute all hydroxyguanidine and substances as basic as arginine, guanidine was obtained by developing the column with 5 M ammonia. The eluted guanidine was identified by colorimetric analysis using the diacetyl reaction and guanidine⅐HCl as a standard (23).…”

Section: Methodsmentioning

confidence: 99%

The biochemical basis for l -canavanine tolerance by the tobacco budworm Heliothis virescens (Noctuidae)

Melangeli

Rosenthal

Dalman

1997

Proc. Natl. Acad. Sci. U.S.A.

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The tobacco budworm, Heliothis virescens (Noctuidae), a destructive insect pest, is remarkably resistant to L-canavanine, L-2-amino-4-(guanidinooxy)butyric acid, an arginine antimetabolite that is a potent insecticide for nonadapted species. H. virescens employs a constitutive enzyme of the larval gut, known trivially as canavanine hydrolase (CH), to catalyze an irreversible hydrolysis of L-canavanine to L-homoserine and hydroxyguanidine. As such, it represents a new type of hydrolase, one acting on oxygen-nitrogen bonds (EC 3.13.1.1). This enzyme has been isolated from the excised gut of H. virescens and purified to homogeneity; it exhibits an apparent K m value for L-canavanine of 1.1 mM and a turnover number of 21.1 mol⅐min ؊1 ⅐mol ؊1 . This enzyme has a mass of 285 kDa and is composed of two subunits with a mass of 50 kDa or 47.5 kDa. CH has a high degree of specificity for L-canavanine as it cannot function effectively with either L-2-amino-5-(guanidinooxy)pentanoate or L-2-amino-3-(guanidinooxy)propionate, the higher or lower homolog of L-canavanine, respectively. L-Canavanine derivatives such as methyl-L-canavanine, or L-canaline and O-ureido-L-homoserine, are not metabolized significantly by CH.

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Separation and estimation of certain guanidino compounds. Application to human urine

Cited by 71 publications

References 13 publications

Platelet factor 3 in normal subjects and patients with renal failure

Platelet factor 3 in normal subjects and patients with renal failure

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

The biochemical basis for l -canavanine tolerance by the tobacco budworm Heliothis virescens (Noctuidae)

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