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A Gharib

Publications and source records attributed to A Gharib.

50 records · Page 3Linked to original sources
PubMed1986

Possible involvement of the S-adenosyl-L-homocysteine metabolites, adenosine and L-homocysteine, in sleep in rats.

The effects of i.p. injections of adenosine (Ado) and homocysteine at 17.00 h were tested on the rat sleep-waking cycle. Administration of 7 and 50 mg/kg of Ado resulted in a significant increase in sleep in otherwise saline male rats during the environmental-dark period (18.00-06.00 h). Increments of paradoxical sleep were maximal with the smaller dose of Ado. The larger dose increased slow-wave sleep during the first 2 h. In contrast, administration of homocysteine (7 mg/kg) had no effect while a larger dose (50 mg/kg) induced a slight but significant long-lasting decrease of paradoxical sleep. These results were compared with those previously obtained with S-adenosyl-L-homocysteine (SAH), an intracellular precursor of Ado and L-homocysteine. It is proposed that the reported hypnotic action of exogenous SAH in rats could be mediated by Ado receptors.

Adenosine↗
PubMed1986

Differential pulse voltammetry in vivo with working carbon fiber electrodes: 5-hydroxyindole compounds or uric acid detection?

Differential pulse voltammetry was performed in rats chronically implanted with carbon fiber electrodes in the caudate (n.Cd) and raphe dorsalis (n.RD) nuclei. The electrochemical signal obtained at the +300 mV potential (peak 3) in animals implanted for more than one week (long term chronic conditions, greater than 7 days) could be dependent upon the extracellular fraction of 5-hydroxyindolacetic acid (5-HIAA) since a single injection of Pargyline is sufficient to suppress it in n.Cd and n.RD. This result was obtained despite the tendency of Pargyline to increase n.Cd and n.RD endogenous concentrations of Uric Acid (UA) measured by High Performance Liquid Chromatography (HPLC). In contrast, in animals implanted for less than one week (short term chronic conditions, less than 7 days) peak 3 recorded in the same structure could be dependent upon extracellular fractions of 5-HIAA and UA since consecutive injections of Pargyline and Allopurinol are necessary to suppress this signal. The source of extracellular UA measured in brain by voltammetry, in such short term chronic conditions, might result from surgical trauma.

Animals↗
PubMed1985

Phospholipid methylase activity, [3H]S-adenosyl-L-homocysteine binding, and S-adenosyl-L-methionine and S-adenosyl-L-homocysteine levels in rat brain during maturation.

The changes in activity of phospholipid methyltransferase I and [3H]S-adenosyl-L-homocysteine ([3H]SAH) binding were determined in cortical membrane preparations from newborn rats and rats 1, 2, and 8 months old. The activity of phospholipid methyltransferase I and the [3H]SAH binding were significantly greater (respectively, +30 and +40%) in newborn rats than in 1-, 2-, and 8-month-old rats. The methylated products at days 1 and 30 were identical. These changes in methyltransferase activity may be correlated with variations in concentration of S-adenosyl-L-methionine (SAM) and SAH. The endogenous SAM level was higher and the SAH level was lower in newborn compared with adult rats. These data suggested that the processes of methylation were favored in newborn rats. The modifications observed after treatment with L-homocysteine reinforced this hypothesis.

Animals↗
PubMed1985

[Differential pulse voltammetry: focus on the measurement of 5-hydroxyindole compounds and uric acid in the brain].

The electrochemical signal obtained at the +300 mV potential (peak 3) in rats implanted for more than one week could be dependent upon extracellular fraction of 5-hydroxyindolacetic acid (5-HIAA) since a single injection of Pargyline is sufficient to suppress it in caudate and raphe dorsalis nuclei. In contrast, in rats implanted for less than one week, this signal could be dependent upon extracellular fractions of 5-HIAA and uric acid since consecutive injections of Pargyline and Allopurinol are necessary to suppress it.

Animals↗
PubMed1984

Autoradiographic localization of [14C]8-S-adenosyl-L-homocysteine in rat brain.

Following intracarotid injection of [14C]8-S-adenosyl-L-homocysteine ( [14C]SAH) in the rat, radioactivity was localized by autoradiographic detection in the circumventricular organs, such as the pineal gland, choroid plexuses and area postrema, which lie outside the blood-brain barrier. HPLC analysis indicated a decrease of [14C]SAH radioactivity in these structures from 1 to 45 min, after injection. These results are discussed and related to the known pharmacological properties of SAH.

Animals↗
PubMed1983

A comparison of the effects of S-adenosyl-L-homocysteine on sleep in normal and pinealectomized rats.

S-adenosyl-L-homocysteine (SAH) was administered to normal and pinealectomized rats previously implanted with electrodes for polygraphic recording. In normal rats, injected at 17.00 h, 7 mg/kg SAH induced a significant increase of paradoxical sleep (PS) during the night. When injected at 09.00 or 19.00 h, no effect was observed. In pinealectomized rats, SAH had no significant effect on PS amounts but seemed to resynchronize the PS rhythm. Thus, the pineal gland plays an important role in SAH effect. The results are discussed with reference to different mechanisms within the rat pineal gland and a possible implication of beta-adrenergic receptors.

Animals↗
PubMed1983

In vivo elevation of mouse brain S-adenosyl-L-homocysteine after treatment with L-homocysteine.

Intraperitoneal coadministration of adenosine and L-homocysteine markedly increased S-adenosyl-L-homocysteine in whole mouse brain, but further investigations showed that this elevation could also be produced following administration of L-homocysteine alone. The noted increase was maximal (+1325%) 10 min after treatment, remaining at about this level for 30-40 min before returning to control values after 180 min. Cerebral adenosine levels were decreased after treatment with L-homocysteine, adenosine, or these two substances in combination.

Adenosine↗
PubMed1982

S-adenosyl-L-homocysteine: simplified enzymatical preparation with high yield.

S-adenosyl-L-homocysteine hydrolase catalyses the synthesis of S-adenosyl-homocysteine (AdoHcy) from adenosine (Ado) and L-homocysteine (L-Hcy) in the absence of other enzymes, such adenosine deaminase, using Ado or L-Hcy as a substrate. Studies concerning the effect of substrates and enzyme concentrations with enzyme from beef liver, an inexpensive enzyme source, allowed the determination of the smallest amount of enzyme leading to total conversion to AdoHcy for the highest Ado and L-Hcy concentrations. Washing out the blood, homogenization of beef liver slices at pH 4.9 and precipitation with between 40% and 50% saturated (NH4)2SO4 eliminated contamination of tissue by blood adenosine deaminase. This enzyme preparation transforms Ado only into AdoHcy in the presence of L-Hcy. In a 1 1 final volume, an amount of enzyme preparation corresponding to at least 18.5 mg of fresh liver causes the total transformation of 60 mM Ado in the presence of 90mM L-Hcy after 40 hours incubation at 37 degrees C and pH 6.8. After purification by two crystallizations, the AdoHcy yield, based upon the Ado incubated, is about 80% of theory (1.0 g of AdoHcy per g of fresh beef liver).

Adenosylhomocysteinase↗
PubMed1982

The regional concentrations of S-adenosyl-L-methionine, S-adenosyl-L-homocysteine, and adenosine in rat brain.

The concentrations of S-adenosyl-L-methionine (SAM), S-adenosyl-L-homocysteine (SAH), and adenosine (Ado) were determined in whole brain and rat brain regions by HPLC. The whole brain contains, respectively, 22 nmol, 1 nmol, and 65 nmol of SAM, SAH, and Ado per g of wet tissue. Their distribution indicated that SAM and SAH levels are highest in brainstem, whereas the Ado level is highest in cortex. With aging the SAM concentrations decrease in whole brain, brainstem, and hypothalamus (-25%) and SAH levels increase by 90% in striatum and by 160% in cerebellum, while Ado levels are increased in all regions by 100--180%.

Adenosine↗
PubMed1977

A simple radiochemical assay of thromboxane B2, 12-hydroxyeicosatetraenoic acid (HETE) and 12-hydroxyheptadecatrienoic acid (HHT) synthetized by human platelets.

A simple radiochemical assay of thromboxane B2, 12-hydroxyeicosatetraenoic acid (HETE) and 12-hydroxyheptadecatrienoic acid (HHT) produced by platelets from arachidonic acid has been described. Moreover, this assay is suitable for measuring thromboxane A2 trapped as 11-mono-O-methylthromboxane B2 and minor products such as prostaglandins E2, F2alpha and D2. The advantage of this technique is discussed as to its ease and specificity.

Arachidonic Acids↗
PubMedDate not supplied

Pharmacokinetics and metabolism of S-adenosyl-L-homocysteine, in rats and dog.

Tissue distribution, metabolism and excretion of 14C-S-adenosyl-L-homocyteine were investigated in rat after oral and intraperitoneal administration. The radioactivity was distributed rapidly to the tissues. The urine was the major route of excretion: respectively 32% and 52% of radioactivity were excreted in 48 h urine after oral and intraperitoneal administration. Analysis of urine by HPLC showed that the major part of the radioactivity could be identified as uric acid. Absorption and pharmacokinetic parameters were determined in dog after oral and intravenous administration. The experimental data were fitted to a biexponential equation from a two-compartment open model.

Animals↗
PubMedDate not supplied

Delta-sleep-inducing peptide stimulates melatonin, 5-methoxytryptophol and serotonin secretion from perifused rat pineal glands.

The pineal gland is known to synthesize numerous indolamines. Since delta-sleep-inducing peptide (DSIP, a tryptophan nonapeptide) is found in the pineal gland, its effect on the secretion of indolamines was investigated. DSIP stimulated melatonin (MEL), 5-methoxytryptophol (5-ML) and serotonin (5-HT) synthesis and release, whereas it did not affect pineal cyclic AMP levels. The stimulatory effect of DSIP on MEL secretion was dose dependent between 5 x 10(-6) and 10(-4) M, whereas the minimal effective concentration of DSIP on 5-ML secretion was higher than 10(-5) M. The effect of DSIP (10(-4) M) was compared to the effect of isoproterenol (ISO, 10(-6) M) on MEL and 5-HT release. ISO stimulated MEL secretion and concomitantly decreased 5-HT release. With regard to kinetic characteristics, the effect of DSIP (10(-4) M) on MEL release was faster and of shorter duration than the effect of ISO (10(-6) M; 2 and 4 h, respectively). At 10(-4) M, DSIP potentiated the ISO-induced increase of MEL secretion. The DSIP-stimulated release of MEL was not significantly altered when the pineal glands were treated with 10(-5) M propranolol (a beta-adrenergic antagonist), 10(-5) M prazosin (an alpha 1-adrenergic antagonist) or 10(-5) M naloxone (an opioidergic antagonist). This study demonstrates that the DSIP-induced secretion of indolamines from rat pineal glands may not be elicited through the well-known noradrenergic or opioid systems.

Animals↗