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S Esteban

Publications and source records attributed to S Esteban.

At least 19 recordsLinked to original sources
PubMed2006

Antioxidant response and oxidative damage in brain cortex after high dose of pilocarpine.

Pilocarpine is a cholinergic agonist capable to induce seizures and an epilepticus-like state in rodents. This status epilepticus (SE) is an useful animal model to study the development and understanding of the neuropathology, behavioural and electroencephalographic alterations of human temporal lobe epilepsy. It has been suggested a relationship between SE and reactive oxygen species (ROS) that can result in seizure-induced neurodegeneration. The aim of this study was to evaluate the existence of oxidative damage and the changes in the antioxidant system in cortex after administration of a high pilocarpine dose. Rats were injected with pilocarpine (350 mg/kg i.p.) or with saline as control and 2h after the animals were sacrificed. Malondialdehyde (MDA) levels, as marker of lipid peroxidation, significantly increased (64%) after pilocarpine treatment evidencing oxidative damage. Antioxidant enzyme activities--catalase (CAT), glutathione peroxidase (GP) and superoxide dismutase (SOD)--significantly increased in response to pilocarpine (28%, 28% and 21%, respectively). GP and Mn-SOD gene expression were induced by pilocarpine treatment. Vitamin E concentration in brain cortex decreased (15%) as result of pilocarpine administration. In conclusion, the high dose of pilocarpine, used in the present study, induces oxidative damage and increases antioxidant enzyme activities and expression in brain cortex. Moreover, increased lipid peroxidation produces the consumption of Vitamin E.

Animals↗
PubMed2006

Antioxidant response analysis in the brain after pilocarpine treatments.

Cholinergic and gabaergic systems play an important role generating electroencephalographic activity and regulating vigilance states. Pilocarpine is a cholinergic agonist commonly used to induce seizures and an epilepticus-like state in rodents. A relationship between status epilepticus and reactive oxygen species has been also suggested which could result in seizure-induced neurodegeneration. The aim of this study was to evaluate the existence of oxidative damage as well as the antioxidant enzyme response in cortex and hippocampus after the administration of an intraperitoneal (350 mg/kg) and an intracerebroventricular (360 microg, 1 microl) pilocarpine injection in rats. The GABA agonist muscimol (1 mg/kg, i.p.), with described neuroprotective properties, was used as a negative control. Only systemic pilocarpine induced oxidative damage. Malondialdehyde levels, as a marker of lipid peroxidation (LP), increased in both regions (55-56%). Catalase (52-80%) and superoxide dismutase (53-60%) activities also rose in both regions but glutathione peroxidase activity only increased in cortex (45%). Glutathione reductase and caspase-3 activity did not change. In conclusion, systemic pilocarpine produced oxidative brain damage, whereas local pilocarpine brain injection had no effects. Moreover, the enzymatic determinations performed in this study are a good tool to study brain injury in pharmacological manipulations such as the ones used in short recording EEG studies.

Animals↗
PubMed2006

Improved circadian sleep-wake cycle in infants fed a day/night dissociated formula milk.

On the basis of the circadian nutritional variations present in breast milk, and of the implications for the sleep/wake cycle of the nutrients present in infant formula milks, we designed a formula milk nutritionally dissociated into a Day/Night composition. The goal was to improve the bottle-fed infant's sleep/wake circadian rhythm. A total of 21 infants aged 4-20 weeks with sleeping difficulties were enrolled in the three-week duration study. The sleep analysis was performed using an actimeter (Actiwatch) placed on an ankle of each infant to uninterruptedly record movements during the three weeks. The dissociated Day milk, designed to be administered from 06:00 to 18:00, contained low levels of tryptophan (1.5g/100g protein) and carbohydrates, high levels of proteins, and the nucleotides Cytidine 5 monophosphate, Guanosine 5 monophosphate and Inosine 5 monophosphate. The dissociated Night milk, designed to be administered from 18.00 to 06.00, contained high levels of tryptophan (3.4g/100g protein) and carbohydrates, low levels of protein, and the nucleotides Adenosine 5 monophosphate and Uridine 5 monophosphate. Three different milk-feeding experiments were performed in a double-blind procedure covering three weeks. In week 1 (control), the infants received both by day and by night a standard formula milk; in week 2 (inverse control), they received the dissociated milk inversely (Night/Day instead of Day/Night); and in week 3, they received the Day/Night dissociated formula concordant with the formula design. When the infants were receiving the Day/Night dissociated milk in concordance with their environment, they showed improvement in all the nocturnal sleep parameters analyzed: total hours of sleep, sleep efficiency, minutes of nocturnal immobility, nocturnal awakenings, and sleep latency. In conclusion, the use of a chronobiologically adjusted infant formula milk seems to be effective in improving the consolidation of the circadian sleep/wake cycle in bottle-fed infants.

Bottle Feeding↗
PubMed2005

Degradation of wine industry wastewaters by photocatalytic advanced oxidation.

Wine industry wastewaters contain a high concentration of organic biodegradable compounds as well as a great amount of suspended solids. These waters are difficult to treat by conventional biological processes because they are seasonal and a great flow variation exists. Photocatalytic advanced oxidation is a promising technology for waters containing high amounts of organic matter. In this study we firstly investigated the application of H2O2 as oxidant combined with light (artificial or natural) in order to reduce the organic matter in samples from wine industry effluents. Secondly, we studied its combination with heterogeneous catalysts: titanium dioxide and clays containing iron minerals. The addition of photocatalysts to the system reduces the required H2O2 concentration. Although the H2O2/TiO2 system produces higher efficiencies, the H2O2/clays system requires a H2O2 dosage between three and six times lower.

Catalysis↗
PubMed2003

Dualism and uniformism in sleep.

The phenomenological evidence for distinguishing between REM and NREM sleep is overwhelming. However, this difference has only been found thanks to electrophysiological analytical methods, and is practically non existent in phenotypic terms, i.e., observable with the naked eye. It is well accepted that the selective pressure determining evolutionary changes can only work upon phenotypic differences. Hence, it follows that the differences between REM and NREM could not have been selected through evolution and this implies that, in functional terms, both states could be equivalent.

Animals↗
PubMed2001

The imidazoline receptor ligand 2-(2-benzofuranyl)-2-imidazoline is a dopamine-releasing agent in the rat striatum in vivo.

2-BFI (2-(2-benzofuranyl)-2-imidazoline) is a prototypical I2-imidazoline receptor ligand. In vivo, however, 2-BFI (1-20 mg/kg) decreased the synthesis of dopa/dopamine (DA) in rat striatum through mechanisms not related to interaction with I2-imidazoline receptors or to inhibition of the enzyme monoamine oxidase. The aim of this study was to unravel the mechanism underlying this potent effect of 2-BFI in brain. In vitro 2-BFI showed very low affinity for D2-dopamine receptors (K(i)=47 microM), and in vivo the drug (7 mg/kg) decreased the synthesis of striatal dopa/DA similarly in control rats (43%) and in rats pre-treated with alpha-methyl-para-tyrosine (50%) or cocaine (51%), indicating that this effect was not the result of D2-dopamine autoreceptor direct stimulation, inhibition of the enzyme tyrosine hydroxylase or blockade of neuronal DA reuptake. In DA-depleted (reserpine-treated) rats, however, 2-BFI did not inhibit significantly (11%), the synthesis of dopa/DA in the striatum, indicating that the effect of 2-BFI was indirectly mediated by endogenous DA through the activation of D2-dopamine autoreceptors. In conclusion, the I2-imidazoline receptor ligand 2-BFI is also a DA releasing agent in brain, and consequently a DA indirect agonist in vivo.

Adrenergic Uptake Inhibitors↗
PubMed1999

Effects of imidazoline receptor ligands on monoamine synthesis in the rat brain in vivo.

This study was designed to assess the effects of imidazoline drugs on putative presynaptic imidazoline receptors modulating brain monoamine synthesis in vivo. The accumulation of 3,4-dihydroxyphenylalanine (dopa) and 5-hydroxytryptophan (5-HTP) after decarboxylase inhibition was used as a measure of the rate of tyrosine and tryptophan hydroxylation in various brain regions of naive rats and after irreversible alpha2-adrenoceptor inactivation with EEDQ (1.6 mg/kg, i.p., 6 h). Clonidine (1-3 mg/kg), moxonidine (1-10 mg/kg) and rilmenidine (10 mg/kg) (mixed I1/alpha2 agonists) decreased dopa and 5-HTP synthesis in the cerebral cortex (14%-81%), hippocampus (27%-84%) and/or striatum (29%-56%), but these inhibitory effects were abolished in N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (EEDQ)-treated rats. Similarly, the stimulatory effect of efaroxan (mixed I1/alpha2 antagonist; 10 mg/kg) on dopa synthesis in the cortex (77%) and hippocampus (57%) was abolished by EEDQ. The selective I1-ligand 2-endo-amino-3-exoisopropylbicyclo-heptane (AGN-192403; 5-10 mg/kg) did not modify dopa or 5-HTP synthesis in any brain region in naive or EEDQ-treated rats. Idazoxan (mixed I2/alpha2 antagonist; 20 mg/kg) increased dopa synthesis in the cortex (111%) and hippocampus (87%), but the stimulatory effects were abolished by EEDQ. Moreover, idazoxan and efaroxan decreased 5-HTP synthesis in the cortex (12%-34%) and hippocampus (30%-34%) in a manner sensitive to blockade by the 5-HT1A receptor antagonist WAY 100135. The selective I2-igands 2-(2-benzofuranyl)-2-imidazoline (2-BFI; 20 mg/kg) and 2-styryl-2-imidazoline (LSL 61122; 10 mg/kg) did not alter the synthesis of dopa or 5-HTP in the cortex or hippocampus. In striatum, 2-BFI (1-20 mg/kg) dose-dependently decreased dopa synthesis (ED50: 5.9 mg/kg), reduced dopamine levels (6%-36%) and increased those of its metabolites DOPAC (15%-95%) and HVA (24%-74%). The inhibitory effect of 2-BFI on dopa/dopamine synthesis in striatum remained unchanged after alkylation of imidazoline receptors with isothiocyanatobenzyl imidazoline (IBI; 60 mg/kg, 6 h) or blockade of these receptors with 2-(2-ethyl 2,3-dihydro-2-benzofuranyl)-2-imidazole (KU-14R; 7-20 mg/kg). Therefore, most imidazoline drugs modulated the synthesis of brain monoamines through interaction with alpha2-adrenoceptors or 5-HT1A receptors. The results do not provide functional evidence for the existence of presynaptic imidazoline receptors regulating the synthesis of monoamines in the rat brain.

5-Hydroxytryptophan↗
PubMed1999

Activation and desensitization by cyclic antidepressant drugs of alpha2-autoreceptors, alpha2-heteroreceptors and 5-HT1A-autoreceptors regulating monamine synthesis in the rat brain in vivo.

The effects of antidepressant drugs on the synthesis of noradrenaline and serotonin (5-HT) were assessed using the accumulation of 3,4-dihydroxyphenylalanine (dopa) and 5-hydroxytryptophan (5-HTP) after decarboxylase inhibition as a measure of the rate of tyrosine and tryptophan hydroxylation in the rat brain in vivo. Three inhibitory synthesis-modulating receptors were investigated simultaneously: the alpha2C-autoreceptor modulating dopa/noradrenaline synthesis, and the alpha2A-heteroreceptor and 5-HT1A-autoreceptor modulating 5-HTP/5-HT synthesis. Acute treatment (2 h, i.p.) with desipramine (1-10 mg/kg), protriptyline (0.3-10 mg/kg) and nisoxetine (3-10 mg/kg), selective NA reuptake blockers, dose-dependently decreased dopa synthesis in cortex (15%-40%) and hippocampus (20%-53%). Fluoxetine (1-10 mg/kg) and zimelidine (1-10 mg/kg), selective 5-HT reuptake blockers, did not alter dopa synthesis. Fluoxetine and zimelidine dose-dependently decreased 5-HTP synthesis in cortex (14%-43%) and hippocampus (27%-54%). Desipramine and protryptyline did not alter 5-HTP synthesis in cortex but in hippocampus it was decreased (36%). Repeated desipramine (10 mg/kg for 1-21 days) or fluoxetine (3 mg/kg for 3-21 days) treatment resulted in a time-dependent loss in their ability to decrease dopa or 5-HTP synthesis. Desipramine (1-21 days) did not alter 5-HTP synthesis in cortex, but in hippocampus it was decreased (21%-37%, days 1-14) followed by recovery to control values (day 21). Fluoxetine (3-21 days) did not alter brain dopa synthesis. To further assess the desensitization of alpha2C-autoreceptors, alpha2A-heteroreceptors and 5-HT1A autoreceptors regulating the synthesis of dopa/NA or 5-HTP/5-HT after chronic desipramine and fluoxetine, the effects of clonidine (agonist at alpha2-auto/heteroreceptors) and 8-OH-DPAT (agonist at 5-HT1A-autoreceptors) were tested. In saline-treated rats, clonidine (1 mg/kg, 1 h) decreased dopa and 5-HTP synthesis in cortex (58% and 54%) and hippocampus (54% and 42%). In desipramine-treated rats (10 mg/kg, 21 days), but not in fluoxetine-treated ones (3 mg/kg, 14 days), the effect of clonidine was attenuated in cortex (12% and 18%) and only for dopa synthesis in hippocampus (31%). In saline-treated rats, 8-OH-DPAT (1 mg/kg, 1 h) decreased 5-HTP synthesis in cortex (63%) and hippocampus (75%). In fluoxetine-treated rats, but not in desipramine-treated ones, this inhibitory effect was markedly attenuated in cortex (26%) and hippocampus (9%). These findings indicate that acute treatment with cyclic antidepressant drugs results in activation of inhibitory alpha2C-autoreceptors, alpha2A-heteroreceptors and/or 5-HT1A-autoreceptors regulating the synthesis of dopa/NA and/or 5-HTP/5-HT in brain, whereas chronic treatment with these drugs is followed by desensitization of these presynaptic receptors.

5-Hydroxytryptophan↗
PubMed1998

Trypanosoma cruzi: Tc52 released protein-induced increased expression of nitric oxide synthase and nitric oxide production by macrophages.

Trypanosoma cruzi target molecules that might regulate the host immune responses have not yet been fully identified. In the present study, we demonstrate that the parasite-released molecule (Tc52) was able to synergize with IFN-gamma to stimulate nitric oxide production by macrophages. This synergistic effect was also observed at the level of inducible nitric oxide synthase gene expression. Furthermore, Tc52 was also shown to induce gene expression for IL-1alpha, IL-12, and IL-10. Moreover, the combination of Tc52 and IFN-gamma down-regulates IL-1alpha and IL-10 gene expression, but not IL-12. Isotype profiles and Tc52 or anti-CD3-induced T cell proliferation were also analyzed, indicating that active immunization with Tc52 partially relieves the immunosuppression observed during the acute phase of the disease. Moreover, under conditions of experimental infection, the Tc52 appears immunologically silent, failing to elicit Ab response and lymphocyte proliferation during the initial acute phase infection. Following active immunization, Tc52 was capable of stimulating T cell proliferation and Ab production with a predominance of IgG1, IgG2a, IgG2b, IgG3, and to a lesser extent IgA. Taken together, these results demonstrate that T. cruzi Tc52-released Ag could be involved in the immunoregulatory processes. The immune response against Tc52 that appears late in the T. cruzi infection may play a role in the modulation of its biological function(s).

Animals↗
PubMed1996

Kinetic constants of alpha-methyl-D-glucoside transport in the chick small intestine during perinatal development.

The kinetic parameters of alpha-methyl-D-glucoside (alpha Glc1Me) have been determined in the small intestine in order to establish developmental and regional changes in the apical transport in embryos and newly hatched chicks. Results show that the apparent Michaelis constant (Km) values did not change during the period studied in each region of the small intestine. However, the ileum showed a smaller Km than that of the duodenum and jejunum, indicating an increase of the affinity of the carrier in the distal portion of the intestine and a significant contribution of the ileum to overall sugar absorption in the perinatal period. There were important changes in the diffusional component and in the mediated transport system capacity during this period, as well as in the different regions of the intestine. Significant increases in the maximal rate of transport (Vmax) were observed in all regions during the embryonic period until the second day after hatching, followed by a decline during the first week. During all the period studied, Vmax values from the jejunum were significantly greater than those from both the duodenum and the ileum at every age studied showing that the jejunum is the segment that is best suited for Na(+)-mediated uptake. Such changes which occur when the need for nutrients for rapid development are at their highest are not solely a result of diet composition, but rather in accordance with a genetic programme.

Animals↗
PubMed1996

The alpha 2-adrenoceptor antagonist idazoxan is an agonist at 5-HT1A autoreceptors modulating serotonin synthesis in the rat brain in vivo.

The in vivo effects of the alpha 2-adrenoceptor idazoxan, rauwolscine and phentolamine on alpha 2-auto/heteroreceptors and 5-HT1A autoreceptors modulating the synthesis of dopa/noradrenaline and 5-HTP/serotonin were assessed in rats, using the accumulation of dopa and 5-HTP after decarboxylase inhibition as a measure of the rate of tyrosine and tryptophan hydroxylation. The acute administration of idazoxan (0.1-40 mg/kg) induced a pronounced dose-dependent increase in the synthesis of dopa in the cerebral cortex (22-86%) and hippocampus (8-80%), as a consequence of the powerful blockade of alpha 2-autoreceptors. However, idazoxan did not increase the synthesis of 5-HTP in these brain regions, as it would have been expected by the concurrent blockade of alpha 2-heteroreceptors on serotonergic terminals. Instead, idazoxan decreased the synthesis of 5-HTP in the cerebral cortex (13-33%) and hippocampus (25-48%), suggesting that these inhibitory effects were mediated through activation of 5-HT1A autoreceptors. Similar results were obtained for rauwolscine. Pre-treatment of rats with the selective 5-HT1A receptor antagonist WAY100135 (10 mg/kg) fully antagonized the inhibitory effects of idazoxan (10 mg/kg) on 5-HTP synthesis, but it did not prevent the stimulatory effects of idazoxan on dopa synthesis. The results indicate that idazoxan is a potent and specific agonist at 5-HT1A autoreceptors modulating brain serotonin synthesis in vivo.

Animals↗
PubMed1996

Alpha 2-autoreceptors and alpha 2-heteroreceptors modulating tyrosine and tryptophan hydroxylase activity in the rat brain in vivo: an investigation into the alpha 2-adrenoceptor subtypes.

The subtype determination of auto- and hetero-alpha 2-adrenoceptors modulating the synthesis of noradrenaline (NA) and serotonin (5-HT), respectively, was assessed using the accumulation of 3,4-dihydroxyphenylalanine (dopa) and 5-hydroxytryptophan (5-HTP) after decarboxylase inhibition as a measure of the rate of tyrosine and tryptophan hydroxylation in the rat brain in vivo. In the cerebral cortex and hippocampus, Org 3770 (non-selective alpha 2-adrenoceptor antagonist, 0.5-10 mg/kg, i.p.) increased (43%-58%) and clonidine (non-selective alpha 2-adrenoceptor agonist, 1 mg/kg) decreased (37%-49%) the synthesis of dopa. Also the antagonist ARC 239 (alpha 2B/C selective, 5-40 mg/kg) increased the synthesis of dopa in cortex (39%-46%) and hippocampus (17%-85%). In contrast, the antagonist BRL 44408 (alpha 2D selective, 1-10 mg/kg) did not increase the synthesis of dopa in cortex, and increased it modestly in hippocampus only. The agonist guanoxabenz (alpha 2B/C selective, 0.03-3 mg/kg) decreased the synthesis of dopa in both brain regions (20%-65%), whereas the agonist oxymetazoline (alpha 2D selective, 0.1-3 mg/kg) failed to do so. These results indicated that the alpha 2-autoreceptors that modulate the synthesis of dopa/NA are probably associated with the alpha 2B/C-subtypes. In cortex and hippocampus, clonidine decreased (35%-53%) the synthesis of 5-HTP but Org 3770 failed to induce the opposite effect (except the 2 mg/kg dose in cortex). BRL 44408 markedly increased the synthesis of 5-HTP in cortex (113%-148%) but not in hippocampus. Similarly, also ARC239 increased the formation of 5-HTP in cortex (36%-48%) but not in hippocampus, where it was decreased (30%-55%). Oxymetazoline decreased the synthesis of 5-HTP in hippocampus (28%-30%) but failed to do so in cortex. Guanoxabenz in the low dose range (0.03-0.3 mg/kg) did not decrease the synthesis of 5-HTP in any brain region. These results indicated that the alpha 2-heteroreceptors that modulate the synthesis of 5-HTP/5-HT may well be different from the proposed alpha 2B/C-autoreceptors modulating the synthesis of dopa/NA. These alpha 2-heteroreceptors appear to be associated with the alpha 2D-subtype.

Adrenergic alpha-Agonists↗
PubMed1994

Oxytocic effect of trypsin on the isolated rat uterus.

To study the oxytocic effect of trypsin, we measured the force of isometric contraction in uteri isolated from estrogenized rats exposed to trypsin (8.8 x 10(-10) to 1.7 x 10(-6) mol/L) either alone or in the presence of receptor antagonists to angiotensin II [saralasin ([Sar1,Ala8]angiotensin II) or DuP 753 (losartan)] or to kinins (D-[Arg0,Hyp3,Thi5,8,D-Phe7]-bradykinin). We found that saralasin or DuP 753, but not the kinin antagonist, displaced the dose-response curve to the right. Exposure to exogenous angiotensin I desensitized the preparation to further doses of either angiotensin I or II or trypsin, without altering the effects of oxytocin or bradykinin. Enalaprilat (an angiotensin I converting enzyme inhibitor) or pepstatin A (a renin inhibitor) also displaced the dose-response curve to trypsin to the right, without altering the effects of oxytocin or angiotensin II. Our results indicate that the response to trypsin is mediated by an agent produced from a substrate present in the uterus and acting on the angiotensin II type 1 receptor and are consistent with both renin and angiotensin I converting enzyme being involved in its mechanism of action, thus supporting the notions that the renin-angiotensin system may be important in the late stages of pregnancy and that serine proteases existing in the uterus may contribute to its activation.

Angiotensin I↗
PubMed1991

Effect of cafeteria diet on the gastrointestinal transit and emptying in the rat.

1. When gastrointestinal transit and emptying of intraluminal contents were studied using a radioactive tracer marker [( 14C]PEG-4000), the fastest gastric transit and the slowest overall transit time were observed in female Wistar rats (1-3 months old) after they were fed a cafeteria diet (a hypercaloric diet). 2. The small intestine length of cafeteria fed rats was higher than lean rats, whereas the stomach and large bowel length showed no difference between cafeteria and lean rats. 3. A state of mild obesity was obtained after rats were fed a cafeteria diet. This obesity was demonstrated by the highest body weight and the highest gain of white adipose tissue in rats fed a cafeteria diet.

Animals↗
PubMed1991

Gastrointestinal emptying in the final days of incubation of the chick embryo.

1. The gastrointestinal (GI) emptying of the chick embryo was studied in days 19 and 20 of incubation using radioactive (14C-PEG-4000) and coloured (Evans Blue dye) tracer markers. 2. Following administration by oral cannula, the percentages of tracer marker recovered in the yolk sac and the GI tract showed the existence of a GI motor pattern in both 19 d and 20 d chick embryos and suggested that the fluids drunk by the chick embryo during the final days of incubation could have reached the yolk sac from the GI tract via the vitelline diverticulum.

Animals↗