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K Ienaga

Publications and source records attributed to K Ienaga.

36 records · Page 2Linked to original sources
PubMed1993

L-gulono-gamma-lactone oxidase is the enzyme responsible for the production of methylguanidine in the rat liver.

A methylguanidine-synthesizing enzyme localized in rat liver microsomes produces methylguanidine via the intermediates creatone A and creatone B from the substrate, creatol, a substance produced from creatinine mainly by reaction with hydroxyl radicals. This enzyme has been identified as L-gulono-gamma-lactone oxidase (EC 1.1.3.8). However, no corresponding activity was found in extracts from human livers.

Amino Acid Sequence↗
PubMed1993

Purification of methylguanidine synthase from the rat kidney.

Methylguanidine (MG)-synthesizing enzyme was purified from rat kidney lysosomes and peroxisomes. The enzyme was a flavoprotein with a molecular weight of about 37,000 and oxidized creatol to produce MG. The present results suggest that the reaction mechanism of this enzyme is different from that of L-gulono-gamma-lactone oxidase (EC 1.1.3.8) isolated from rat liver microsomes.

Amino Acid Sequence↗
PubMed1993

Comparison of renal effects of creatinine, creatol and methylguanidine in rats with adenine-induced chronic renal failure.

Creatinine (Cr), creatol and methylguanidine (MG), which accumulate in the body with the progress of renal failure after adenine administration, were given separately to rats in order to compare their toxicities. Food containing adenine was given to rats for 20 days to induce renal failure. Then each of the test substances was administered intraperitoneally, and renal function of the rats was determined. The changes in glomerular filtration rate, renal plasma flow and renal blood flow after administration of Cr were only slight in comparison with those of the control group. Creatol or MG administration induced a significant decrease in renal function. In addition, the level of MG in serum, liver and kidney was extraordinarily high in rats given creatol or MG. The toxic effects are discussed on the basis of these results.

Adenine↗
PubMed1992

Gamma-glutamyltaurine has potent and long-lasting antiepileptic action as demonstrated by intra-amygdaloid injection in amygdala-kindled rats.

Intra-amygdaloid injections of gamma-glutamyltaurine, a recently identified brain dipeptide, strongly suppressed seizures in amygdala-kindled rats stimulated with intensities 10 or 50 microA above the generalized seizure triggering threshold (mean 82 microA). The suppressive effect persisted as long as 3 days. Taurine had relatively weak suppressive effects. Thus gamma-glutamyltaurine seems much more potent than taurine in the suppression of epileptic seizures when injected directly into the kindling site.

Amygdala↗
PubMed1992

First isolation of gamma-L-glutamyl-gamma-aminobutyric acid from bovine brains.

We had obtained some immunohistochemical indications which suggested that peptide(s) containing GABA at the C-terminal could exist in specific neurons in brains. We therefore sought such GABA conjugate(s) by isolating an acidic GABA-dipeptide from bovine brains and determined its structure as gamma-L-glutamyl-gamma-aminobutyric acid (gamma-L-Glu-gamma Abu:GluGABA). Its gamma-linkage was determined by a mass-spectrometric (B/E linked scan SIMS) analysis; its chirality was established by a chiral column HPLC technique. This peptide is the first acidic GABA-peptide recognized in brain and the first brain peptide containing GABA at the C-terminal.

Animals↗
PubMed1992

Effects of creatinine, creatol and methylguanidine on renal function.

Creatinine (Cr), creatol or methylguanidine (MG) was administered intraperitoneally to normal rats, and several renal function parameters were examined in an attempt to clarify the pathology under the various conditions. The glomerular filtration rate, renal plasma flow and renal blood flow after administration of Cr remained virtually unchanged when compared to those in the control group. In contrast, administration of creatol induced a significant decrease in these renal functions. Further decreases in the renal functions were observed in the rats given MG. However, the level of serum MG was extraordinarily high in the rats given creatol or MG. The toxic effects are discussed on the basis of the above results.

Animals↗
PubMed1991

Possible role of tumor necrosis factor and interleukin-1 in the development of diabetic nephropathy.

The possibility that tumor necrosis factor (TNF) and interleukin-1 (IL-1) could participate in the development of diabetic nephropathy was evaluated in streptozocin (STZ)-treated diabetic rats. Diabetic rats were divided into two groups: aminoguanidine treated group (25 mg/kg body wt, daily i.p. injection; DM-AG group) and untreated group (DM group). Non-diabetic age-matched rats were also divided into two groups with the same manner and used as controls. After twelve weeks of treatment, glomerular basement membranes (GBM) were isolated from rats of each experimental group. When thioglycollate-elicited peritoneal macrophages (M phi) from normal rats were incubated with these GBM materials, GBM from DM group induced significantly greater levels of TNF and IL-1 production than did GBM from other three groups with at doses of 2.5 to 10 mg. The TNF and IL-1 production by stimulation of GBM from the DM-AG group were similar to those from each control group. Aminoguanidine treatment significantly decreased the accumulation of advanced glycation end-products (AGEs) in GBM of diabetic rats. These findings suggest that AGE-proteins may be involved in the production of TNF and IL-1 from M phi. AGE-induced cytokines may be implicated in the development of diabetic nephropathy.

Albuminuria↗
PubMed1991

Effects of intraamygdaloid injection of taurine and valyltaurine on amygdaloid kindled seizure in rats.

Antiepileptic effects of intracerebral injections of taurine and valyltaurine were examined in amygdaloid kindled rats. The effects were assessed whether the animals can evoke generalized seizures by a 10 microA higher stimulation intensity than triggering thresholds. In all fully-kindled animals that have received intraamygdaloid injection of 500 nmol taurine, the kindled seizure was completely abolished. Such a significant seizure suppression (p less than 0.05) was observed 12-24 h after the taurine injection. Valyltaurine (500 nmol) also suppressed the seizure in 60% of animals tested, but the effect was not statistically significant. The results indicate that taurine may effectively suppress epileptic seizures when it acts directly at the stimulation site amygdala.

Amygdala↗
PubMed1991

Production of methylguanidine from creatinine via creatol by active oxygen species: analyses of the catabolism in vitro.

The chemical oxidative conversion of creatinine (Cr) into methylguanidine (MG) has been followed by 1H-NMR and HPLC. By using active oxygen species generated by Fenton's reagent (Fe2+ and H2O2) or the similar reagent (Fe3+ and H2O2), creatol (CTL), a metabolite newly isolated from the urine of uremic patients, and creatones A and B were experimentally detected in the reaction mixture and implicated as successive intermediates in the pathway from CR to MG. An alternative oxidation of Cr to demethylcreatinine (glycocyamidine) was also observed. The importance of CTL in this in vitro oxidation mechanism is discussed.

Chromatography, High Pressure Liquid↗
PubMed1990

Creatol (5-hydroxycreatinine), a new toxin candidate in uremic patients.

Both 5-hydroxy-1-methylhydantoin (3) and the hitherto unrecognized 5-hydroxycreatinine (2-amino-5-hydroxy-1-methyl-imidazol-4(5H)-one or creatol) (6) can be isolated from the urine of uremic patients, in whom these compounds probably arise as oxidative metabolites of creatinine (1). The enhanced production of the well-known uremic toxin, methylguanidine (8), from creatinine (1) in such patients, almost certainly occurs via the newly recognized metabolite.

Chemical Phenomena↗
PubMed1990

Isolation of glutamyltaurine from bovine brains and proof of its gamma-linkage by the B/E linked scan SIMS technique.

We isolated a glutamyltaurine from bovine brains and determined its structure as gamma-glutamyltaurine (gamma-Glu-Tau; glutaurine) by use of a new mass spectrometric technique [B/E linked scan sputtered ion mass spectrometry (SIMS)], which we have recently shown to be useful for distinguishing the gamma- from the alpha-isomer of glutamyl-dipeptides. Neither the alpha-isomer of glutamyltaurine nor any aspartyltaurines could be detected in bovine brain.

Animals↗
PubMed1989

Simple method for determination of A1c-type glycated hemoglobin(s) in rats using high performance liquid chromatography.

We have developed a new chromatographic method for the determination of rat glycated hemoglobins by cation exchange high-performance liquid chromatography. The hemoglobins were eluted by a two-step gradient, and the total assay time, including re-equilibration of the column, was 27 min. Two A1c type and one pre-A1c type rat glycated hemoglobins were separated and measured. The change in major HbA1c of rats, in which diabetes was induced by streptozotocin and which were subsequently treated with insulin, was monitored. In diabetic rats (n = 10, average blood glucose greater than 300 mg/dL), major HbA1c rose to 3.39 +/- 0.06% compared with controls (n = 10, 1.20 +/- 0.03%) during 5 wk. Insulin treatment decreased the HbA1c from 3.48 +/- 0.16% to 2.74 +/- 0.15% (p less than 0.01) in 6 wk. This method was also effective for the determination of mouse HbA1c.

Animals↗
PubMed1988

The metabolism of 1-methylhydantoin via 5-hydroxy-1-methylhydantoin in mammals.

The metabolic pathway of 1-methylhydantoin (2) via 5-hydroxy-1-methylhydantoin (3), methylparabanic acid (4) and N5-methyloxaluric acid (5) proved to be a major and general one in mammals. Hence the formation of (3), which has not been detected in normal tissue, is likely to be indirect in inflamed tissue, probably depending on the arising formation of (2) from creatinine (1).

Animals↗