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Titolo:
Role of nitric oxide in the synthesis of guanidinosuccinic acid, an activator of the N-methyl-D-aspartate receptor
Autore:
Aoyagi, K; Shahrzad, S; Iida, S; Tomida, C; Hirayama, A; Nagase, S; Takemura, K; Koyama, A; Ohba, S; Narita, M; Cohen, BD;
Indirizzi:
Univ Tsukuba, Inst Clin Med, Dept Internal Med, Tsukuba, Ibaraki 3058575, Japan Univ Tsukuba Tsukuba Ibaraki Japan 3058575 sukuba, Ibaraki 3058575, Japan Mito Cent Hosp, Ibaraki, Osaka, Japan Mito Cent Hosp Ibaraki Osaka JapanMito Cent Hosp, Ibaraki, Osaka, Japan Albert Einstein Coll Med, New York, NY USA Albert Einstein Coll Med New York NY USA tein Coll Med, New York, NY USA
Titolo Testata:
KIDNEY INTERNATIONAL
, volume: 59, anno: 2001, supplemento:, 78
pagine: S93 - S96
SICI:
0085-2538(200102)59:<S93:RONOIT>2.0.ZU;2-1
Fonte:
ISI
Lingua:
ENG
Soggetto:
ARGININOSUCCINATE;
Keywords:
argininosuccinate; reactive oxygen; uremic toxin; urea cycle enzyme; hydroxyl radical;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
17
Recensione:
Indirizzi per estratti:
Indirizzo: Aoyagi, K Univ Tsukuba, Inst Clin Med, Dept Internal Med, Tsukuba, Ibaraki3058575, Japan Univ Tsukuba Tsukuba Ibaraki Japan 3058575 araki 3058575, Japan
Citazione:
K. Aoyagi et al., "Role of nitric oxide in the synthesis of guanidinosuccinic acid, an activator of the N-methyl-D-aspartate receptor", KIDNEY INT, 59, 2001, pp. S93-S96

Abstract

Background. We propose that reactive oxygen and argininosuccinic acid (ASA) form guanidinosuccinic acid (GSA). An alternative to this hypothesis is the so-called guanidine cycle, which consists of a series of hydroxyurea derivatives that serve as intermediates in a pathway leading from urea to GSA. We compare the role of the guanidine cycle to that of nitric oxide (NO) inthe synthesis of GSA. Methods, The members of the guanidine cycle (hydroxyurea, hydroxylamine plus homoserine, L-canaline, and L-cana-vanine) were incubated with isolated rat hepatocytes. The known NO donors, NOR-2, NOC-7, and SIN-1, were incubated with ASA in vitro. Ornithine, arginine, or citrulline, which increase arginine, a precursor of NO, were incubated with isolated rat hepatocytes. GSA was determined by high-performance liquid chromatography. Results. None of guanidine cycle members except for urea formed GSA. SIN-1, which generates superoxide and NO formed GSA, but other simple NO donors,did not. Both carboxy-PTIO, a scavenger of NO, and dimethyl sulfoxide, a hydroxyl radical scavenger, completely inhibited GSA synthesis by SIN-1. GSAformation by SIN-1 reached a maximum at 0.5 mmol/L and decreased at higherconcentrations. GSA synthesis, stimulated by urea in isolated hepatocytes,was inhibited by ornithine, arginine, or citrulline with ammonia, but not by ornithine without ammonia, where arginine production is limited. Conclusion. GSA is formed from ASA and the hydroxyl radical. When arginineincreased in hepatocytes, OSA synthesis decreased. These data suggest thatincreased NO, which results from high concentrations of arginine, or SIN-Iscavenges the hydroxyl radical. This may explain the decreased GSA synthesis in inborn errors of the urea cycle where ASA is decreased, and also the diminished GSA excretion in arginemia.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 24/09/20 alle ore 21:23:46