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At least 19 recordsLinked to original sources
PubMed1976

Importance of sarcosine formation in methionine methyl carbon oxidation in the rat.

Experiments in vitro using rat liver slices indicated that the incorporation of the methionine methyl carbon into sarcosine and serine was dependent upon available glycine and most probably involves glycine methyltransferase. Although the sarcosine methyl carbon was rapidly oxidized to CO2, its formation accounted for only a small proportion of the oxidation of the methionine methyl carbon to CO2 under these conditions. In vivo experiments using a sarcosine trapping pool with 0.3% to 3.0% L-[methyl-14C]methionine in the diet indicated that from 5% to 14% of the absorbed methionine methyl carbon was metabolized via sarcosine, and that this accounted for only 10% to 20% of the observed oxidation of the methyl carbon to CO2. The adaptive response of the rat to high levels of dietary methionine, as indicated by greater oxidation of the methyl carbon to CO2, is in part due to increased sarcosine synthesis. The failure of supplemental glycine to stimulate oxidation of the methionine methyl carbon to CO2 in rats receiving 3% methionine plus 10% sarcosine may be due to sufficient glycine being produced from sarcosine metabolism.

Acetates↗
PubMed1977

Synthesis of [1-sarcosine, 8-O-methylserine]angiotensin II and 1-substituted analogues of [8-threonine]angiotensin II as antagonists of angiotensin II.

[1-N-methylisoleucine,8-threonine]-(I), [1-dimethylglycine,8-threonine]-(II), [1-guanidineacetic acid,8-threonine]-(III), des-1-aspartic acid-[8-threonine]-(IV), and [1-sarcosine,8-O-methylserine]angiotensin II (V) were synthesized by Merrifield's solid-phase procedure to study the effect of (a) substituents in position 1 on the antagonistic activity of [1-sarcosine,8-threonine]angiotensin II, and (b) a change in size and branching in position 8 of [1-sarcosine,-8-O-methylthreonine]angiotensin II. The analogues I-V caused an initial rise in blood pressure (30 min of infusion, 250 ng/kg/min in vagotomized ganglion-blocked rats) of 8.05, 11.7, 3.50, 4.5, and 11.16 mmHg. The pA2 values (rabbit aortic strips) obtained were 7.68, 7.53, 7.23, 7.53, and 9.66, and the dose ratios (in vagotomized ganglion-blocked rats infused at 250 ng/kg/min) obtained were 2.37, 4.49, 1.02, 1.47, and 24.04, respectively. The results obtained indicate that (a) the nature of the substituent in position 1 has an important influence on the biological activity of these peptides, and (b) the potency of antagonists I-IV (all less potent antagonists than [1-sarcosine,8-threonine]angiotensin II) is very much influenced by the length and branching of the side chain in position 8. The in vivo antagonistic activity of [1-sarcosine,8-O-methylthreonine]angiotensin II is reduced considerably by shortening the chain length by one carbon atom as is in V.

Angiotensin II↗
PubMed1992

Molecular cloning and expression of a Streptomyces sarcosine oxidase gene in Streptomyces lividans.

A genomic library of Streptomyces sp. KB210-8SY, prepared in the plasmid vector pACYC184, was screened to obtain the gene encoding sarcosine oxidase with probes based on the amino acid sequence of the protein. A plasmid pSOXS13, which was isolated from a clone identified by hybridization with the probes, contained a 8.4-kb insert of Streptomyces DNA. When the 2.0-kb MIuI/EcoRV DNA fragment of pSOXS13 was inserted into the Streptomyces vector pIJ680 and introduced into S. lividans, the transformants produced 100-fold more sarcosine oxidase intracellularly than KB210-8SY. The nucleotides of the 1.7-kb fragment containing the sarcosine oxidase gene were sequenced. An open reading frame encoded a mature sarcosine oxidase consisting of 388 amino acids, with a calculated molecular mass of 42,107 daltons.

Amino Acid Sequence↗
PubMed1991

Cloning and expression of the sarcosine oxidase gene from Bacillus sp. NS-129 in Escherichia coli.

The gene coding for a thermostable sarcosine oxidase (EC 1.5.3.1) was isolated from Bacillus sp. NS-129. The primary structure of sarcosine oxidase deduced from the nucleotide sequence was a protein composed of 387 amino acids with molecular weight 42,955. When the sarcosine oxidase was overproduced to about 35% of soluble protein in E. coli under the control of a lac promoter, the sarcosine oxidase activity of the crude extract was increased 3-fold by the addition of FAD. This indicates that most of the enzyme is accumulated in an active form, a flavinless aporotein, in the cell.

Amino Acid Sequence↗
PubMed1975

The identification of dansyl sarcosine and its occurrence in molluscs.

An unknown dansyl derivative was identified as dansyl sarcosine. In molluscs, sarcosine was found to be largely localized to the nervous system. Examination of individual snail neurones, regions of the octopus brain and the squid giant synapse showed dramatic variations in sarcosine levels.

Animals↗
PubMed1976

In vitro and in vivo studies of (1-sarcosine, 8-threonine) angiotensin II.

The capacity of (1-Sarcosine, 8-Threonine) angiotensin II to block the contractile and pressor effects of exogenous and endogenous angiotensin II was examined. In isolated rabbit aorta, the pA2 value (from pA2 plots) for the analog was 8.75 +/- 0.11. Both the maximum response and the slope of the dose-response curve to angiotensin II were unchanged by the analog. In ganglion-blocked vagotomized rats, infusion of the analog produced a dose-dependent blockage of the angiotensin II pressor effect. In these rats, the analog displayed less agonistic activity than that of (1-Sarcosine, 8-Isoleucine) and (1-Sarcosine, 8-Alanine) angiotensin II. In two-kidney hypertensive rats, the angiotensin II antagonist significantly reduced the arterial blood pressure. The results indicate that (1-Sar, 8-Thr) angiotensin II is a potent antagonist of angiotensin II with less inherent agonistic activity than previously reported analogs.

Adrenal Glands↗
PubMed1979

Synthesis of angiotensin II antagonists containing sarcosine in position 7.

Analogues of the type [1-sarcosine,7-sarcosine, 8-X]angiotensin II, where X = isoleucine, leucine, alanine, methionine, O-methylthreonine, or DL-alloisoleucine, were synthesized by the solid-phase method and purified by partition chromatography, cation-exchange chromatography, and high-pressure liquid chromatography. In the isolated rat uterus, these analogues had activities of less than 0.1, less than 0.1, less than 0.1, less than 0.1, less than 0.1, and 0.7%, respectively, of the hyotropic activity of angiotensin II and inhibited the contractile response to angiotensin II with pA2 values of 8.1, 7.2, 6.7, 7.7, 7.4, and 8.4, respectively. In the vagotomized ganglion blocked rat, the analogues had 0.7, 0.21, 0.06, 0.72, 0.13, and 12.5%, respectively, of the pressor activity of angiotensin II.

Angiotensin II↗
PubMed1976

Oxidation of sarcosine and N-alkyl derivatives of glycine by D-amino-acid oxidase.

1. Sarcosine was oxidized by D-amino-acid oxidase (D-amino-acid: O2 oxidoreductase (deaminating), EC 1.4.3.3) to yield methylamine and glyoxylic acid. A seriies of N-alkyl glycines were also oxidized by this enzyme. 2. N-Acetyl- and N-Phenylglycine inhibited the oxidase by competing with the substrate, while N-methyl-N-acetylglycine did not bind to the enzyme. This suggests the requirement of at least one unsubstituted hydrogen atom at the amino group ofglycine for binding. 3. The primary step in the reaction was the release of a proton from the substrate, indicating the formation of a substituted imino acid, which was spontaneously hydrolyzed to glyoxylic acid acid and an amine.

Animals↗
PubMed1978

Solubilization of Spiroplasma citri cell membrane proteins with the anionic detergent sodium lauroyl-sarcosinate (Sarkosyl).

1. Up to 90 per cent of the membrane proteins from Spiroplasma citri could be solubilized with the anionic detergent Sarkosyl (sodium lauroyl-sarcosinate). Maximal solubilization was obtained with 6 to 20 mumoles of of detergent per mg of membrane protein. The insoluble residue, comprising about 10 per cent of the membrane protein, contained mainly the protein spiralin, which is quantitatively the major one of this membrane. 2. Mg2+ ions completely prevented solubilization of the membrane proteins at a molar ratio of MgCl2/Sarkosyl greater than 0.5. 3. The selectivity of Sarkosyl was also tested at low detergent concentrations and in the presence of Mg2+ ions. Spiralin was the least soluble protein also under these conditions. Other proteins were not selectively solubilized. 4. An electrophoretical and immunoelectrophoretical approach was used to study the interaction between Sarkosyl and membrane proteins. The results indicated that Sarkosyl should be considered as a mild detergent which usually solubilizes membrane proteins without gross donformational changes. This hypothesis was supported by experiments with a membrane-bound enzyme in the presence of Sarkosyl.

Bacterial Proteins↗
PubMed1992

A comparison of glycine, sarcosine, N,N-dimethylglycine, glycinebetaine and N-modified betaines as liposome cryoprotectants.

Glycinebetaine has previously been shown to be effective at reducing leakage from liposomes which are frozen then thawed. This study involved the preparation of a series of N-modified betaines and the comparison of their cryoprotective activities with those of glycine, sarcosine, N,N-dimethylglycine and glycinebetaine. All the compounds investigated, with the exception of (dimethyloctylammonio)acetate, reduced the degree of leakage, after freezing and thawing, with additive concentrations up to 0.6 M. Reducing the degree of N-terminal methylation of glycinebetaine appeared to increase the leakage from liposomes at additive concentrations between 0.2 and 0.6 M. (Dimethylethylammonio)acetate, (dimethylisopropylammonio)acetate and (N,N,N',N'-tetramethylethylenediammonio)-N,N'-diacetate appeared to be no more effective than glycinebetaine, whereas improved protection was afforded by (triethylammonio)acetate and (diethylmethylammonio)acetate at most concentrations. This study demonstrates that the cryoprotective activity of glycinebetaine may be improved with modifications to the N-terminal.

Amaranth Dye↗
PubMed1979

Effects of an angiotensin II antagonist; [sarcosine 1, isoleucine 8] angiotensin II, on blood pressure, plasma renin activity and plasma aldosterone concentration in hypertensive and normotensive subjects taking oral contraceptives.

To examine the involvement of renin-angiotensin-aldosterone system in the etiology of oral contraceptive induced hypertension, normal women (Group I), normotensive (Group II) and hypertensive (Group III) women taking Ovulen (R) were infused with a competitive angiotensin II (AII) antagonist, [1-sarcosine, 8-isoleucine] angiotensin II. The angiotensin II antagonist was infused at a rate of 600 ng/kg/min for 30 min 1.5 hrs after intravenous injection of 40 mg of furosemide. Blood pressure was monitored and pre-infusion and post-infusion plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were determined. Pre-infusion PRA and PAC showed no significant differences among these three groups. In response to the AII antagonist infusion blood pressure rose in Groups I and II, but blood pressure responses in Group III were variable. Four out of the total 6 subjects had pressor responses and only one subject had a significant blood pressure reduction. In both Groups I and II, PRA decreased and PAC rose after infusion of the antagonist. In Group III, PRA decreased to a lesser degree and PAC showed no consistent change. These data suggest that the renin-angiotensin-aldosterone system in hypertensive women or oral contraceptives is different from that of the normotensive users. However, the pathophysiology of oral contraceptive induced hypertension is not homogenous and angiotensinogenic hypertension is uncommon.

1-Sarcosine-8-Isoleucine Angiotensin II↗
PubMed1975

Cyclic peptides of sarcosine. Syntheses and conformation.

A series of cyclic peptides of sarcosine with the general formula c-Sar-n, n=2-8, has been synthesized and conformational studies carried out both in solution and in the solid. The rings are conformationally very homogeneous and contain both cis and trans amide bonds. Their barriers to ring inversion are high; in the smaller rings this is attributed to steric hindrance, caused by the N-methyl-groups, whilst in the larger rings the folding of the chain in helical segments plays an important role.

Cyclization↗
PubMed1979

Blood pressure response to [1-sarcosine, 8-isoleucine] angiotensin II in patients with liver cirrhosis and ascites.

[1-Sarcosine, 8-Isoleucine] angiotensin II was given to 8 patients with cirrhosis and ascites and 7 cirrhotic patients without ascites on a regular diet. The 3 ascitic patients with high plasma renin activity (PRA) gave a depressor response, but the other ascite patients with normal or low PRA gave a pressor response or no response. All the non-ascitic patients gave a pressor response. There was an inverse correlation between the PRA before infusion and the change in blood pressure induced by this compound. In the patient with the highest PRA, who had ascites of a few days' duration, a marked reduction in blood pressure was observed on infusion of this compound. These results suggest that the renin-angiotensin system might be involved in maintenance of a normal blood pressure in some patients with cirrhosis and ascites, whose ascites is presumably in an early stage.

Aldosterone↗
PubMed1975

The effect of 1-sarcosine, 8-leucyl angiotensin II on glycerol-induced acute renal failure.

Several studies have suggested that increased activity of the renin-angiotensin system plays an important role in the pathogenesis of acute renal failure. An analog of angiotensin II, 1-sarcosine, 8-leucyl angiotensin II (AIIA), a potent antagonist of the pressor response of angiotensin II (AII), was injected (16 mug/200 gm) or infused (1.5 mug/200 gm/min) intravenously into glycerol treated (8 ml/kg) rats to evaluate the involvement of the renin-angiotensin system as a mediator in the pathogenesis of acute renal failure. Dehydrated animals, whether untreated, given AIIA, or saline became progressively azotemic and died with 72 hours after glycerol administration. Plasma renin activity, as measured by radioimmunoassay, decreased below dehydrated control levels at one hour after glycerol administration (7.45 ng/ml/hr +/- 1.29 (SE) to 3.24 +/- 0.64), and progressively increased to a maximum 9.9 +/- 0.98) at 17 hours; there was no difference between dehydrated control levels and those obtained 24 and 48 hours after glycerol. Nondehydrated glycerol treated rats were studied as above. These animals developed a non-lethal form of acute renal failure, the severity of which was also unaffected by AIIA administration. These observations indicate that AIIA neither prevents nor alters the development of glycerol induced acute renal failure.

Acute Kidney Injury↗