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Biomedical subjects

C Gimenez

Publications and source records attributed to C Gimenez.

At least 37 records · Page 2Linked to original sources
PubMed1987

Effects of systematically administered lithium on tryptophan transport and exchange in plasma-membrane vesicles isolated from rat brain.

The effect of lithium on the sodium-dependent high-affinity system for tryptophan uptake was examined in plasma membrane vesicles derived from rat brain. We demonstrated that Na+ could be replaced by lithium in the external medium and the presence of lithium produced an increase in the Vmax of the tryptophan transport whereas it had no significant effect on the Km for the substrate. Plasma membrane vesicles derived from synaptosomes obtained from long-term lithium-treated rats are able to accumulate tryptophan to a greater extent than normal rats and maintain a more negative membrane potential than controls. Our data support the idea that the stimulation by lithium of the high-affinity uptake system for tryptophan by maintaining adequate membrane potentials across the membrane, could lead to the stabilization of serotonin production, as has been demonstrated in long term-lithium treatment.

Animals↗
PubMed1986

Characterization of glycine uptake in plasma membrane vesicles isolated from cultured glioblastoma cells.

C6 glioblastoma cells in culture were employed to isolate plasma membrane vesicles. After disruption of the glioblastoma cells by homogenization, membrane fractions were obtained by centrifugation on a discontinuous Ficoll density gradient. Fragmented membranes were found mainly in vesicular form. Transport of glycine has been demonstrated in membrane vesicles, using artificially imposed ion gradients as the sole energy source. The uptake of glycine is strictly dependent on the presence of Na+ and Cl- in the medium, and the process can be driven either by an Na+ gradient (out greater than in) or by a Cl- gradient (out greater than in) when the other essential ion is present. The process is stimulated by a membrane potential (negative inside) as demonstrated by the effect of ionophore valinomycin and anions with different permeabilities. The kinetic analysis shows that glycine is accumulated by two systems with different affinities.

Biological Transport↗
PubMed1986

Developmental studies on the uptake of tyrosine by synaptosomes and plasma membrane vesicles derived from rat brain. Effect of thyroid hormones.

The uptake of L-tyrosine at various stages of development was examined in synaptosomes and in plasma membrane vesicles derived from rat brain. The total uptake has two components, Na+-dependent and Na+-independent, respectively. The Na+-dependent component of the transport system appears around the 5th postnatal day and increases with age. The affinity of the transport system for tyrosine does not vary substantially during development. The Vmax increases more than six-fold between day 15 and adulthood. Plasma membrane vesicles derived from T3-treated rats accumulate more tyrosine than those obtained from the control animals. The results support the view that thyroid hormones during development promote the establishment of the systems implicated in neurotransmission in the developing nervous system.

Aging↗
PubMed1985

Ontogenetic studies on tryptophan transport into plasma membrane vesicles derived from rat brain synaptosomes: effect of thyroid hormones.

The uptake of tryptophan at various stages of development was examined in plasma membrane vesicles derived from rat brain. The total uptake has two components Na+-dependent and Na+-independent respectively. The Na+-dependent component of the transport system appears around the 5th postnatal day and increases with the age. The Km value of the system does not vary during development. The Vmax increases five-fold between 14 and 35 day of postnatal life. Plasma membrane vesicles derived from T3-treated rats are able to accumulate nearly three-fold more tryptophan than nontreated rats. The results support the idea that thyroid hormones at the earlier stages of life, promote the establishment of neurotransmission in the developing nervous system.

Aging↗
PubMed1984

beta-Alanine transport into plasma membrane vesicles derived from rat brain synaptosomes.

Transport of beta-alanine has been demonstrated in membrane vesicles isolated from rat brain, using artificially imposed ion gradients as the sole energy source. The uptake of beta-alanine is strictly dependent on the presence of Na+ and Cl- in the medium, and the process can be driven either by an Na+ gradient (out greater than in) or by a Cl- gradient (out greater than in) when the other essential ion is present. The process is stimulated by a membrane potential (negative inside) as demonstrated by the effect of ionophore valinomycin and anions with different permeabilities. beta-Alanine uptake is inhibited by the presence of GABA.

Alanine↗
PubMed1984

Thromboembolism with low profile bioprosthesis.

Low profile bioprosthesis late follow-up indicates a low incidence of thromboembolism. For the entire series of 415 consecutively operated patients (rigid and flexible stents) the actuarial probability of freedom at 6 years is 90.3% (87.8% for MVR and 92.27% for AVR and 95.24% for MVR + AVR). The linearized incidence for MVR, is 2.5 +/- 0.62 per one hundred patients per year. For AVR this is 1.2 +/- 0.49 per one hundred patients per year. The probability of freedom of thromboembolism of the new flexible stent series (247 patients) at 48 months is 90.92% for MVR, 96.6% for AVR and 100% for MVR + AVR. Endocarditis for the entire series of patients (rigid/flexible stents) at 6 years is low: the linearized incidence for both MVR and AVR is 0.54 per one hundred patients per year. Tissues degeneration, after 5 years follow-up, in patients over 35 years old carrying LPB mounted on flexible stents was not observed. In the series of MVR patients, 17/209 presented thromboembolic complications. In the group of 17 patients, 88% had atrial fibrillation before surgery and 47% of the same group were on warfarin anticoagulation therapy when the embolic accident occurred. The indications for permanent anticoagulation therapy following bioprosthetic MVR in patients with chronic atrial fibrillation is still uncertain.

Actuarial Analysis↗
PubMed1983

Inhibition by L-phenylalanine of tryptophan transport by synaptosomal plasma membrane vesicles: implications in the pathogenesis of phenylketonuria.

Phenylalanine is accumulated in the genetically linked deficiency phenylketonuria. The effect of L-phenylalanine on the transport of tryptophan was studied using membrane vesicles from rat-brain synaptosomes. Phenylalanine at similar concentrations to those found in phenylketonuric patients competitively inhibits tryptophan uptake, with a Ki of the same order as the Km for tryptophan. This inhibition could be responsible for the depletion of serotonin found in phenylketonuria.

Animals↗
PubMed1981

Glycine transport into plasma-membrane vesicles derived from rat brain synaptosomes.

1. Transport of glycine has been demonstrated in membrane vesicles isolated from rat brain, using artificially imposed ion gradients as the sole energy source. 2. The uptake of glycine is strictly dependent on the presence of Na+ and Cl- in the medium, and the process can be driven either by an Na+ gradient (out greater than in) or by a C1- gradient (out greater than in) when the other essential ion is present. 3. The uptake of glycine is stimulated by a membrane potential (interior negative), as demonstrated by the effects of the ionophores valinomycin and carbonyl cyanide m-chlorophenylhydrazone and anions of different permeabilities. 4. The kinetic analysis shows that glycine is accumulated by two systems with different affinities. 5. The presence of ouabain, an inhibitor (Na+ + K+)-activated ATPase, does not affect glycine transport. 6. The existence of a high-affinity, Na+-dependent glycine-uptake system in membrane vesicles derived from rat brain suggests that this amino acid may have a transmitter role in some areas of the rat brain.

Animals↗
PubMed1979

Thyroid hormones and the precocious induction of hepatic glucokinase in the neonatal rat.

1. Oral intubation of glucose is more effective than intraperitoneal injection in inducing the premature appearance of hepatic glucokinase in suckling rats. 2. The inducing effect of glucose is enhanced by treatment of the animals 12 h or more earlier with 1 microgram triiodothyronine/g body weight. 3. Low but significant activities of glucokinase appear at the normal time of development in hypothyroid neonatal rats. Intubation of glucose into 13-day-old and 24-day-old hypothyroid results in the rapid appearance of glucokinase similar to that in normal animals treated likewise. 4. The enhancing effect of thyroid hormones on glucokinase induction by glucose does not necessarily mean that the normal postnatal increase in plasma thyroid hormones is essential for the normal appearance of glucokinase activity at the time of weaning. Other possible explanations are discussed.

Animals↗
PubMed1977

Experimental phenylketonuria: metabolic studies in rat liver.

The "in vivo" effects of L-phenylalanine on the gluconeogenic pathway in the liver of fasted rats with experimentally induced phenylketonuria-like characteristics have been investigated. Significant increases of the fructose 6-phosphate, glucose 6-phosphate and glucose concentrations were observed. The study of the effect of L-phenylalanine on the cytoplasmic and mitochondrial redox state and energy charge showed an increase in the mitochondrial NAD+/NADH ratio while the energy charge was virtually unchanged. The effects of phenylalanine and its metabolic derivatives (phenylacetate, phenylethylamine, phenyl-lactate, o-hydroxyphenylacetate and phenylpyruvate) on the activity of lactate dehydrogenase (EC 1.1.1.27), malate dehydrogenase (EC 1.1.1.37) and 3-hydroxybutyrate dehydrogenase (EC 1.1.1.30) in rat liver have been also investigated. Phenylpyruvate inhibited the lactate dehydrogenase activity with a Ki of 5.3 mM. Phenylpyruvate also inhibited both the mitochondrial (Ki = 4 mM) and cytoplasmic (Ki = 5 mM) malate dehydrogenase activities. Phenylpyruvate, phenylacetate and o-hydroxyphenylacetate inhibited the 3-hydroxybutyrate dehydrogenase activity with Ki values of 0.7, 6.0 and 9.5 mM respectively.

Animals↗
PubMed1976

Effect of phenylalanine metabolites on the activities of enzymes of ketone-body utilization in brain of suckling rats.

1. The effects of phenylalanine and its metabolites (phenylacetate, phenethylamine, phenyl-lactate, o-hydroxyphenylacetate and phenylpyruvate) on the activity of 3-hydroxybutyrate dehydrogenase (EC 1.1.1.30) 3-oxo acid CoA-transferase (EC 2.8.3.5) and acetoacetyl-CoA thiolase (EC 2.3.1.9) in brain of suckling rats were investigated. 2. The 3-hydroxybutyrate dehydrogenase from the brain of suckling rats had a Km for 3-hydroxybutyrate of 1.2 mM. Phenylpyruvate, phenylacetate and o-hydroxyphenylacetate inhibited the enzyme activity with Ki values of 0.5, 1.3 and 4.7 mM respectively. 3. The suckling-rat brain 3-oxo acid CoA-transferase activity had a Km for acetoacetate of 0.665 mM and for succinyl (3-carboxypropionyl)-CoA of 0.038 mM. The enzyme was inhibited with respect to acetoacetate by phenylpyruvate (Ki equals 1.3 mM) and o-hydroxyphenylacetate (Ki equals 4.5 mM). The reaction in the direction of acetoacetate was also inhibited by phenylpyruvate (Ki equals 1.6 mM) and o-hydroxyphenylacetate (Ki equals 4.5 mM). 4. Phenylpyruvate inhibited with respect to acetoacetyl-CoA both the mitochondrial (Ki equals 3.2 mM) and cytoplasmic (Ki equals 5.2 mM) acetoacetyl-CoA thiolase activities. 5. The results suggest that inhibition of 3-hydroxybutyrate dehydrogenase and 3-oxo acid CoA-transferase activities may impair ketone-body utilization and hence lipid synthesis in the developing brain. This suggestion is discussed with reference to the pathogenesis of mental retardation in phenylketonuria.

Acetyl-CoA C-Acetyltransferase↗