F S Russo | PubMed Health

PubMed1978

A fluorogenic substrate for angiotensin-converting enzyme in plasma.

A simple, sensitive, and reproducible assay for angiotensin-converting enzyme is described. It is based on the hydrolysis of the minimally fluorescent substrate p-nitrobenzyloxycarbonylglycyl-L-tryptophylglycine to the products p-nitrobenzyloxycarbonylglycine and the highly fluorescent L-tryptophylglycine. The L-tryptophylglycine was analyzed by fluorometry (lambda excitation = 285 nm; lambda emission = 350 nm). The mean value for human plasma (serum) is 16.5 nmol of substrate hydrolyzed per minute per milliter of plasma under the described assay conditions.

Dipeptides↗

PubMedDate not supplied

L-alanine plasma levels after oral loads in non-alcoholic liver cirrhosis: relationship with urea extraformation and ammoniogenesis.

In the post-absorptive stage L-alanine is the main source of alpha-amino-nitrogen reaching the liver as glucose precursor. This aminoacid has been used as a measure of urea synthesis capacity in several pathologic conditions, but it has not been employed sistematically in patients with liver cirrhosis. We tried to address this issue by evaluating: a) L-alanine plasma levels, b) urea extraformation (UE), and c) ammoniogenesis after oral L-alanine (0.25 and 0.50 g/kg b wt) in healthy control subjects and in patients with nonalcoholic compensated (Child-Pugh's A class) and decompensated (Child-Pugh's B and C) liver cirrhosis. L-alanine plasma levels after oral load were higher and lasted longer in cirrhotics as compared to controls. Furthermore, after L-alanine oral load, significantly higher ammonia plasma levels were observed in cirrhotics than in controls. Changes in the urea extraformation were comparable in cirrhotics and controls. Both delayed L-alanine elimination from plasma and L-alanine-induced hyperammoniemia were more evident in decompensated cirrhotics and related to L-alanine dose.

Administration, Oral↗