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At least 73 records · Page 4Linked to original sources
PubMed1986

Glycine solution as an irrigating agent during transurethral prostatic resection. Glycine concentrations in blood plasma.

In 17 men undergoing transurethral resection of the prostate (TURP), an isosmotic solution of 2.2% glycine was used for irrigation. The plasma glycine concentration was determined before and immediately after TURP and 2, 6, 24 and 48 hours later. The serum concentrations of sodium, albumin and prostatic acid phosphatase protein (PAP) were used as indicators of fluid absorption. Calculation of the absorbed fluid volume was based on the plasma concentration of glycine, and the disappearance rate of glycine from plasma was estimated. The mean disappearance rate (T 1/2) was 85 min, which was midway between previously observed rates for sorbitol and mannitol. The observed plasma glycine increase after TURP correlated well with fall in serum sodium and rise in serum PAP, with the blood loss during and up to 15 min after TURP, and also with the weight of the resected tissue. The plasma glycine level, highest immediately after TURP, normalized 24-48 hours postoperatively. No signs of ammonia intoxication or marked serum urea increase were seen in these patients, although some had very high plasma glycine values after TURP (mean 10.2, maximum 23 mmol/l) as compared with the preoperative levels (mean 0.2 mmol/l). There was some increase of plasma serine (a normal metabolite of glycine) after TURP. The authors conclude that the irrigating fluid should have a minimal concentration of glycine, near to the level of haemolysis onset, to minimize the plasma dilution effects, including hyponatraemia, and the appearance of metabolites when the irrigating fluid is absorbed.

Acid Phosphatase↗
PubMed1990

Glycinergic contacts in the outer plexiform layer of the Xenopus laevis retina characterized by antibodies to glycine, GABA and glycine receptors.

Electrophysiological experiments have predicted a direct synaptic input from glycinergic interplexiform cells (IPCs) to GABAergic horizontal cells in the Xenopus retina. However, previous ultrastructural studies failed to demonstrate this input. Here, we used three immunocytochemical approaches to investigate this issue. First, double-label postembedding immunocytochemistry with GABA- and glycine-like immunoreactivity (GABA-LI and glycine-LI) was used to study possible interactions of the glycinergic IPC with GABAergic horizontal cells. Processes postsynaptic to glycine-LI IPC terminals in the outer plexiform layer (OPL) fell into two groups, small microtubule-filled processes and larger electron-lucent processes with sparse microtubules and occasional mitochondria. In no case did we find glycine-LI synapses onto GABA-LI cells or processes. Second, pre-embedding immunocytochemistry was used to label GABA-LI cells and processes in the OPL. GABA-LI was sparse in horizontal cell axons and more intense in horizontal cell somas and in small processes. In agreement with our first set of experiments, GABA-LI profiles did not receive input from conventional synapses. Third, we localized glycine-receptor-like immunoreactivity (GlyR-LI) to several types of apparent synapses in the OPL. As expected, it was found at IPC synapses. Unexpectedly, GlyR-LI was also subsynaptic at photoreceptor synapses onto second order neurons, both at ribbon and basal junction type synapses. At least some of the GlyR-LI photoreceptor synapses were from cones. Also, GlyR-LI was apposed to photoreceptors and to unidentified small diameter processes, where no other indication of synaptic input was evident. Because glycine-LI is not found in photoreceptors, we suggest that glycine receptors at photoreceptor synapses are stimulated by glycine that diffuses from other sites, possibly from IPCs. This interpretation is consistent with available physiological studies of glycinergic effects in this retina.

Animals↗
PubMed1986

Inhibition of glycine oxidation by pyruvate, alpha-ketoglutarate, and branched-chain alpha-keto acids in rat liver mitochondria: presence of interaction between the glycine cleavage system and alpha-keto acid dehydrogenase complexes.

Pyruvate, alpha-ketoglutarate, and branched-chain alpha-keto acids which were transaminated products of valine, leucine, and isoleucine inhibited glycine decarboxylation by rat liver mitochondria. However, glycine synthesis (the reverse reaction of glycine decarboxylation) was stimulated by those alpha-keto acids with the concomitant decarboxylation of alpha-keto acid added in the absence of NADH. Both the decarboxylation and the synthesis of glycine by mitochondrial extract were affected similarly by alpha-ketoglutarate and branched-chain alpha-keto acids in the absence of pyridine nucleotide, but not by pyruvate. This failure of pyruvate to have an effect was due to the lack of pyruvate oxidation activity in the mitochondrial extract employed. It indicated that those alpha-keto acids exerted their effects by providing reducing equivalents to the glycine cleavage system, possibly through lipoamide dehydrogenase, a component shared by the glycine cleavage system and alpha-keto acid dehydrogenase complexes. On the decarboxylation of pyruvate, alpha-ketoglutarate, and branched-chain alpha-keto acids in intact mitochondria, those alpha-keto acids inhibited one another. In similar experiments with mitochondrial extract, decarboxylations of alpha-ketoglutarate and branched-chain alpha-keto acid were inhibited by branched-chain alpha-keto acid and alpha-ketoglutarate, respectively, but not by pyruvate. NADH was unlikely to account for the inhibition. We suggest that the lipoamide dehydrogenase component is an indistinguishable constituent among alpha-keto acid dehydrogenase complexes and the glycine cleavage system in mitochondria in nature, and that lipoamide dehydrogenase-mediated transfer of reducing equivalents might regulate alpha-keto acid oxidation as well as glycine oxidation.

3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)↗
PubMed1997

Characterization of glycine release mediated by glycine transporter 1 stably expressed in HEK-293 cells.

We constructed a cell line which stably expresses glycine transporter 1 (GlyT1) proteins. The cell line showed significant [14C]glycine uptake and could keep steep glycine concentration gradient between intracellular and extracellular space (in > out). Using this cell line, we investigated glycine release mediated by this transporter. The [14C]glycine release was enhanced by extracellular glycine and sarcosine, a selective inhibitor of the transporter, in a dose-dependent manner. In addition, the replacement of extracellular Na+ with Li+ or extracellular Cl- with acetate- markedly increased the release. Furthermore, we investigated the effects of extracellular Ca2+ and K+. The removal of these ions also showed enhancement of the release. These results suggest that glycine transporter 1 protein, which might be involved in the NMDA receptor neurotransmission, can release glycine into the extracellular space in the vicinity of synapses, and that the release might be influenced by the extracellular substrate concentration and ion composition in the synaptic cleft.

Amino Acid Transport Systems, Neutral↗
PubMed2005

Cytoprotection by glycine against ATP-depletion-induced injury is mediated by glycine receptor in renal cells.

It is known that glycine protects mammalian cells against ischaemic cell injury by preventing cellular membrane leakage. However, the molecular mechanisms have not yet been clearly elucidated. The purpose of the present study was to clarify whether GlyR (glycine receptor) acts as a key mediator in cytoprotection of glycine. cDNA encoding human GlyRa1 (a1-subunit of glycine receptor) was transfected into HEK-293 cells. The membrane integrity of the cells with or without GlyRa1 was examined by the uptake of marker compounds, the release of LDH (lactate dehydrogenase) and the exclusion of Trypan Blue. Glycine prevented the permeability of 70 kDa dextrans and 140 kDa LDH in the cells in which GlyR was expressed under conditions of ATP depletion. The inhibition of endogenous GlyR expression by RNA interference attenuated the cytoprotection by glycine. Furthermore, the mutation of Tyr202 to phenylalanine in GlyRa1 blocked the glycine-mediated cytoprotection, while the mutation of Tyr202 to leucine abolished the cytoprotection by strychnine. Our results suggested that the cytoprotection of glycine against ATP-depletion-induced injury might be mediated by GlyR.

Adenosine Triphosphate↗
PubMed2006

Oral administration of glycine in the prevention of restenosis after coronary angioplasty. A double blind placebo controlled randomized feasibility trial evaluating safety and efficacy of glycine in the prevention of restenosis after angioplasty.

OBJECTIVES: Evaluation of safety, feasibility, and efficacy of oral administered glycine in prevention of angiographic restenosis six months after percutaneous coronary intervention (PCI). BACKGROUND: The amino acid glycine modulates immunological response and enhances the production of endothelial derived nitric oxide (EDNO) factor. This factor has been shown to possess anti-atherosclerotic properties, actions of which are thought to reduce neo-intimal hyperplasia. Furthermore, glycine significantly elevates arginine serum levels. This amino acid has been extensively studied for its effects on the endothelium, nitric oxide (NO) metabolism and effects on several biochemical pathways interfering with the process of restenosis after PCI. METHODS: A prospective double blind placebo controlled randomized study evaluated safety and feasibility of chronic oral administration of glycine. In addition, the efficacy was determined by evaluation of six months angiographic restenosis rates. RESULTS: 214 patients scheduled for elective PCI were randomized to receive glycine or placebo. At follow-up, there was no significant difference in side effects and in major adverse cardiac events (MACE) between both groups. Six-month angiograms revealed similar restenosis rates for the glycine group (17.5%) and for the placebo group (20.2%) (P = 0.82). CONCLUSION: Chronic oral administration of glycine was safe and feasible and had similar side effects compared to placebo. However, chronic oral administration of glycine did not lead to a significant reduction in restenosis rates at six months after elective PCI.

Administration, Oral↗
PubMed1986

The glycine receptor: pharmacological studies and mathematical modeling of the allosteric interaction between the glycine- and strychnine-binding sites.

The displacement by glycine of 3H-strychnine binding to rat spinal cord membranes cannot be explained by a simple competitive interaction. Indeed, protein-modifying reagents can completely abolish the inhibition of 3H-strychnine binding by glycine and other agonists, whereas the interaction of strychnine itself and other related compounds with the binding site is unimpaired. Moreover, glycine cannot inhibit completely saturable 3H-strychnine binding, the extent of its maximum inhibitory effect depending on the ionic composition of the medium. Hill coefficients less than 1 (whose magnitude also depends on the assay medium) were obtained from glycine displacement curves. These properties are consistent with a mathematical model of two different, but mutually interacting, binding sites for strychnine and glycine on the glycine receptor. The effect of ions and protein-modifying reagents might be explained in this model as modifications of the mechanisms that mediate the allosteric interaction, and/or the affinity of glycine for the receptor. The agonists beta-alanine and taurine and the new antagonists, THAZ, iso-THAZ, and 4,5-TAZA, also seem to interact with a site different from the strychnine-binding site, probably the glycine-binding site.

Allosteric Regulation↗
PubMed2000

Chronic glycine treatment desensitizes the behavioral response to 1-aminocyclopropanecarboxylic acid (ACPC), a partial agonist at the strychnine-insensitive glycine site of the NMDA receptor complex.

Chronic treatment with 1-aminocyclopropanecarboxylic acid (ACPC) but not with dizocilpine or imipramine produces desensitization to the behavioral response in ACPC challenge in the forced swim test (forced swim test). The mechanism by which ACPC produces this effect is unclear and may depend upon either its functional antagonist or its agonist properties at the NMDA receptor. We now report that chronic treatment with glycine or ACPC desensitizes the behavioral effect of challenge with ACPC in the forced swim test. The desensitization of the acute effects of ACPC cannot be explained by the presence of residual glycine because 24 h after the last of 14 daily glycine injections (i.e. the time of forced swim test) cortical and hippocampal glycine concentrations were unchanged. Likewise, the affinity of glycine to displace specific [3H]5,7-DCKA binding to glycine sites of the NMDA receptor complex was unchanged by chronic glycine administration. These results support the hypothesis that antidepressants produce adaptation of the NMDA receptor complex by mechanisms other than simply increasing synaptic glycine concentrations. Moreover, these results indicate that the behavioral adaptation in the forced swim test induced by chronic treatment with ACPC results from its agonist properties.

Amino Acids↗
PubMed1991

Assay of plasma glycine by HPLC with electrochemical detection in patients undergoing glycine irrigation during gynaecological surgery.

A method for the measurement of plasma glycine by HPLC with electrochemical detection after derivatization with phenylisothiocyanate (PITC) is described. The absorption of glycine in eighteen women undergoing intrauterine glycine irrigation during transcervical resection of endometrium was assessed by measurement of plasma glycine before, immediately after and 24 h after surgery. The plasma glycine concentration was normal in all women before surgery (range 120-386 mumol/l) but had risen dramatically in some patients after surgery (range 180-24,800 mumol/l) before returning to normal levels over the following 24 h (range 173-553 mumol/l). No clinical consequences were observed despite the large increases in plasma glycine; mild hyponatraemia occurred in only one patient. These findings, albeit in a limited number of patients, support the hypothesis that the symptoms sometimes associated with the use of glycine buffers are most likely due to water overload with hyponatraemia rather than a toxic affect of glycine itself.

Adult↗
PubMed1996

Isovaleric acidemia: response to a leucine load after three weeks of supplementation with glycine, L-carnitine, and combined glycine-carnitine therapy.

OBJECTIVE: To assess the effectiveness of glycine and carnitine therapy on isovaleryl conjugate excretion in isovaleric acidemia (IVA). STUDY DESIGN: Urinary isovalerylglycine (IVG) and isovalerylcarnitine (IVC) were measured from 12-hour urine specimens collected overnight from an 8-year-old patient with IVA (who had no residual activity of isovaleryl-CoA dehydrogenase in fibroblasts) before and during 3-week courses of supplementation with glycine alone (250 mg/kg per day), L-carnitine alone (100 mg/kg per day) therapy, and both of these agents combined, with a 2 gm leucine challenge performed at the end of each treatment period. RESULTS: Isovalerylglycine was the predominant metabolite excreted throughout the study, and its mean value doubled with glycine treatment. Isovalerylcarnitine excretion was minimal without carnitine supplementation. L-Carnitine therapy was associated with a 50% decline in excretion of IVG without a fully compensatory increase in IVC. The readdition of glycine to the carnitine regimen resulted in an increase in IVG excretion. Leucine challenge resulted in a 2.7- and 2.4-fold increase of IVG and IVC excretion, respectively, during L-carnitine therapy but not during glycine supplementation, and a 3.5- and 4-fold increase in excretion of both metabolites during glycine plus L-carnitine therapy. Total conjugate excretion was highest after a leucine load during combined glycine and L-carnitine therapy. CONCLUSIONS: Combined glycine and L-carnitine therapy maximally increases isovaleryl conjugate excretion during metabolic stress but not under stable conditions.

Amino Acid Metabolism, Inborn Errors↗
PubMed1984

Glycine pools and turnover rates in leukaemia patients measured with [15N]glycine.

Turnover parameters for plasma glycine were measured by administration of a single dose of [15N]glycine to overnight fasted healthy volunteers, nine patients with chronic leukaemia, one patient with acute monocytic leukaemia and one patient with chronic myeloid leukaemia before and after chemotherapy. Gas chromatography-mass spectrometry was used to determine plasma [15N]glycine enrichment. Pool sizes and turnover rate constants were estimated from time-decay curves for isotope enrichment. Turnover rate constants and metabolic clearance rates of plasma glycine in leukaemia patients were elevated in comparison with data for healthy volunteers. The increased rates of glycine disappearance from the circulation were not accompanied by a depletion in glycine pool size. Turnover rate constants fell during chemotherapy and were within the normal range during remission. There was a significant positive correlation between glycine turnover rate constants and leucocyte counts. The increase in glycine turnover rate constants may be related to proliferation of the neoplastic cells.

Female↗