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E A Moja

Publications and source records attributed to E A Moja.

15 recordsLinked to original sources
PubMed1992

[The clinical implications of the use of an amino acid mixture without tryptophan in liver cirrhosis].

The ingestion of an amino acid mixture lacking tryptophan causes a rapid fall of plasma tryptophan in healthy subjects. This is because amino acids elicit protein synthesis and endogenous tryptophan is incorporated into new proteins. If protein synthesis is the mechanism through which tryptophan-free solution decrease blood tryptophan, it may be interesting to study tryptophan levels after a tryptophan-free mixture in subjects with impaired protein synthesis. In the present paper we show that in 27 cirrhotics the administration of a tryptophan-free solution caused a fall of total plasma tryptophan that began significantly later than in 14 control subjects, the delay being significantly proportional to the severity of the disease. The difference between control and cirrhotic subjects was due to the bound fraction of plasma tryptophan. The diagnostic and clinical usefulness of our findings are discussed.

Amino Acids↗
PubMed1991

Decrease in plasma tryptophan after a tryptophan-free amino acid solution. A comparison between cirrhotic and control subjects.

In healthy subjects the administration of an amino acid mixture devoid of tryptophan causes a marked decrease of plasma tryptophan. This is because amino acid mixtures induce protein synthesis and tryptophan in blood is incorporated into newly synthesized proteins. We hypothesized that a tryptophan-free mixture could differently affect plasma tryptophan levels in subjects with an impaired protein synthesis such as chronic liver patients. We studied tryptophan levels after a tryptophan-free amino acid solution in controls and cirrhotics fasting 12 hours. Plasma total tryptophan fell to 91% of the initial level 60 minutes after the administration of the diet, to 71% after 120, and to 50% after 210' in controls. In cirrhotics the solution caused a decrease of plasma tryptophan that began significantly later than in controls, the delay being proportional to the severity of the disease. Cirrhotics were subdivided into two groups in accordance to the Pugh modification of the Child-Turcotte criteria. Total plasma tryptophan was 100% of base line levels after 60', 88% after 120', and 65% after 210' in less severe clinical condition; total plasma tryptophan was 102% of base line levels after 60', 98% after 120', and 75% after 210' in more severe clinical condition.

Adult↗
PubMed1991

Cycloheximide blocks the fall of plasma and tissue tryptophan levels after tryptophan-free amino acid mixtures.

The hypothesis that incorporation of tryptophan (TRY) into proteins is the mechanism underlying the decrease in plasma and tissue TRY levels after a TRY-free amino acid mixture was investigated. Rats fasted 15 hours were pretreated with saline or with the protein synthesis inhibitor cycloheximide (CHEX) and treated with saline or a TRY-free amino acid mixture. In a first experiment, in saline pretreated rats the TRY-free mixture caused a decrease of 49% in total plasma TRY, of 64% in free plasma TRY, of 66% in brain TRY and of 42% in liver TRY. After 5 mg/kg of CHEX the same TRY-free diet caused a decrease of 5% in total plasma TRY, 14% in free plasma TRY, 18% in brain TRY and 9% in liver TRY. In a second experiment, the TRY-free diet caused a 43% decrease of total plasma TRY in saline pretreated animals and a decrease of 15%, 6% and 2% respectively after the pretreatment with 0.3, 1.0 and 5.0 mg/kg of CHEX. In brain TRY, the TRY-free diet caused a 62% decrease in saline pretreated rats and a decrease of 38%, 20% and 19% respectively after the pretreatment with 0.3, 1.0 and 5.0 mg/kg of CHEX. Since 5.0 mg/kg of CHEX almost completely block protein synthesis and since doses of CHEX from 0.3 to 5.0 mg/kg cause a dose-dependent inhibition of protein synthesis, our data support the hypothesis that protein synthesis is the mechanism through which TRY-free mixtures decrease TRY levels.

Amino Acids↗
PubMed1991

Effects of tryptophan depletion on Poggendorff illusion, corner Poggendorff illusion, and attention.

The effects of a tryptophan-free amino acid mixture on Poggendorff illusion, corner Poggendorff illusion, and attention were investigated with 12 male subjects who ingested either a balanced amino acid mixture or a tryptophan-free mixture, the latter known to cause a marked depletion of brain tryptophan and serotonin. No significant difference between the two mixtures on the perceptual illusions was found.

Adult↗
PubMed1990

An increase in strength of tilt aftereffect associated with tryptophan depletion.

The effects of a tryptophan-free amino acid mixture on tilt aftereffect, movement aftereffect, and the Mueller-Lyer illusion were studied. 12 male subjects ingested either a balanced amino acid mixture or a tryptophan-free mixture which causes a marked depletion of brain tryptophan and serotonin. The tryptophan-free mixture significantly increased the strength of tilt aftereffect but had no effect on movement aftereffect or the Mueller-Lyer illusion. These results were discussed with reference to the pharmacological activity of serotonin and its influence on the strength of lateral inhibition in mammalian brains.

Adult↗
PubMed1989

Dose-response decrease in plasma tryptophan and in brain tryptophan and serotonin after tryptophan-free amino acid mixtures in rats.

Rats fasted 15 hours were treated p.o. with increasing amounts (660 and 1320 mg/kg body weight) of a mixture containing a fixed proportion of seven essential amino acids (L-phenylalanine 13.6%, L-leucine 6.0%, L-isoleucine 12.1%, L-methionine 12.1%, L-lysine 30.3%, L-threonine 10.6%, L-valine 15.2%) and lacking tryptophan. The mixtures produced a dose-response decrease of free (by 34% after the lower dose and by 58% after the higher dose of the mixture) and total (by 10 and 31%) plasma tryptophan and of brain tryptophan (by 38 and 65%), serotonin (by 17 and 41%) and 5-hydroxyindole acetic acid (by 21 and 49%). The mechanisms of these changes are discussed.

Amino Acids↗
PubMed1988

Decrease in plasma tryptophan after tryptophan-free amino acid mixtures in man.

Male healthy subjects, fasting 12 hours, ingested increasing amounts of a mixture containing a fixed proportion of seven essential amino acids (L-isoleucine 11.5%, L-leucine 18.0%, L-lysine 13.1%, L-methionine 18.0%, L-phenylalanine 18.0%, L-threonine 8.2%, L-valine 13.1%) and lacking tryptophan. The diets produced a rapid fall in plasma tryptophan which was proportional to the total amount of the amino acids ingested. Following the highest dose administered (36.6 g) plasma tryptophan fell to a minimum of about 35% the initial level and remained markedly reduced at 6 hours after treatment. The mechanism of this decrease and its potential clinical relevance are discussed.

Adult↗
PubMed1978

Testosterone-attenuated stereotype and hyperactivity induced by beta-phenylethylamine in pargyline-pretreated rats.

Testosterone pretreatment (1.0-4.0 mg/kg) attenuated, in a dose-response fashion, the induction of stereotyped behavior and hyperactivity by pargyline (0.25, 4.0 mg/kg) and beta-phenylethylamine (8.0, 16.0 mg/kg) in preubertal, male rats. The dyskinetic movements induced by pargyline and beta-phenylethylamine were proposed as a possible animal model for tardive dyskinesias. Attenuation by testosterone of these effects suggested an hormonal involvement consistent with the reported predominant occurrence of tardive dyskinesias in women and in the elderly.

Animals↗
PubMed1977

Dose response and time course effects of N,N-dimethyltryptamine on disruption of rat shuttlebox avoidance.

N,N-Dimethyltryptamine (DMT) was given (ip) in different doses (0.25, 0.5, 1.0, 2.0, 4.0, 8.0 mg/kg) in a randomized order to a group of ten rats (Fisher 344/Mai) who were trained to a high, stable base line of conditioned avoidance responding in the shuttlebox. DMT produced dose-dependent disruptive effects, as a sigmoid function, with 1.0 mg/kg the minimal dose causing disruption and progressively more disruption with increasing doses, reaching a plateau at the highest dose. The disruptive effects were time-related, with onset and peak 8 min after injection, gradual decline thereafter, and disappearance by about 25-30 min. Both the threshold dose and time course for the disruptive effects correspond closely to what has been previously reported for DMT's psychological effects in humans.

Animals↗
PubMed1976

Dose-response effects of beta-phenylethylamine on stereotyped behavior in pargyline-pretreated rats.

We studied the dose-response and the time-course effect of beta-phenylethylamine (4.0-64.0 mg/kg, ip) on stereotyped behavior and motor activity in male Sprague-Dawley rats pretreated 2 hr eariler with pargyline (0.25-8.0 mg/kg, iv). Stereotyped behavior, defined as repetitive, nongoal-directed head movements and sniffing, and changes in motor activity were observed immediately after injection of beta-phenylethylamine for a 1 hr period. With increasing doses of pargyline pretreatment, beta-phenylethylamine produced, in a dose-response relationship, progressively more stereotyped behavior accompanied by increased motor activity. Without pargyline pretreatment, only 64.0 mg/kg beta-phenylethylamine induced behavioral changes. Stereotyped behavior and increased motor activity had an onset at 4-6 min after the injection of beta-phenylethylamine, peak at 10-30 min, and gradual decline in the next 10-20 min. These results are discussed in terms of a possible relationship with the degree of inhibition of Type a and Type B monoamine oxidase acused by the different doses of pargyline.

Animals↗
PubMed1976

A study of the EEG sleep patterns and the sleep and dream experience of a group of schizophrenic patients treated with sulpiride.

The modifications of spontaneous sleep in schizophrenic patients following N-ethyl-2(2-methoxy-5-sulfamido-benzamidomethyl)-pyrrolidine (sulpiride, Dobren) administration are reported in this study. No significant modifications in the quantitative distribution of the various sleep phases (LST, SWS, REM) were observed, while a significant percent increase of SWS was noted, together with a significant decrease in the number of awakenings during the night and an increase of the sleep onset time. The patients' own difficulty to fall asleep, however, decreased significantly, and also a significant increase of dream recall could be observed.

Adult↗