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Biomedical subjects

C Ríos

Publications and source records attributed to C Ríos.

At least 37 records · Page 2Linked to original sources
PubMed1998

Nitric oxide synthase inhibition prevents acute quinolinate-induced striatal neurotoxicity.

Quinolinic acid (QUIN) is an endogenous excitotoxin acting on N-methyl-D-aspartate (NMDA) receptors, that leads to neurotoxic damage resembling the alterations observed in Huntington's disease. Two major end-points of QUIN induced neurotoxicity are both circling behavior (CB) and lipid peroxidation (LP). Recently, nitric oxide (NO) has been implicated as a mediator of cell injury in some neurological disorders, thus, NO as a free radical might be involved in QUIN-induced neurotoxicity and oxidative stress. In the present study we evaluated the possible role of NO on QUIN-induced neurotoxicity, by measuring nitric oxide synthase activity (NOS), before and after QUIN-induced damage and by evaluating the effect of NOS inhibition on acute QUIN-induced CB and LP. Rats were striatally microinjected with QUIN (240 nmol/microl). QUIN administration increased NOS activity by 327% as compared to control values and this enhancement was inhibited by i.v. pretreatment with a NOS inhibitor the N(G)-nitro-L-arginine methyl ester (L-NAME) (10 mg/kg). QUIN-induced CB was also attenuated by pretreatment of rats with 1, 5, 10 and 15 mg/kg of L-NAME by -37, -55, -62 and -74% vs QUIN respectively. Similarly, L-NAME also reduced by 32% the QUIN-induced LP. These findings suggest that enhanced NOS activity may participate in QUIN-induced neurotoxicity and oxidative stress.

Animals↗
PubMed1997

Effect of p-chlorophenylalanine (PCPA) on sleep and monoamines content in the brain of a lizard species.

Administration of PCPA, a specific inhibitor of serotonin synthesis, induced a significant decrease of total sleep time in the lizard Ctenosaura pectinata. This effect was exerted on both quiet sleep and active sleep, but it was more intense on active sleep. Reduction in the amount of active sleep was due to a decrease in the number of the episodes not in their mean duration, since this parameter increased significantly from 5.97 s, under control conditions, to 11.77 s, 10.66 s and 8.85 s at 24, 48 and 72 h after PCPA injection, respectively. Neurochemical analysis showed a significant decrease in the amount of serotonin in the analyzed brain stem structures 12 h after PCPA administration. The possible participation of serotonergic mechanisms in the regulation of reptilian sleep is discussed.

Animals↗
PubMed1997

Brain capillary lesions produced by cocaine in rats.

In the last 20 years, acute and chronic cocaine addiction has increased among young and adult people. The effects of cocaine on brain vasculature of young animals have not been histologically studied in depth. In the present study, we report the lesions of brain capillaries, including the choroid plexus, produced by chronic cocaine administration, in adult Wistar rats receiving i.p., 30 mg/kg/day of aqueous cocaine hydrochloride solution. Rats were sacrificed after several days of treatment. Histopathological examination of capillaries from different brain regions and cerebellum was performed using light microscopy. At 7 days, there were initial signs of dilatation, rupture and thrombosis of capillaries. At 15 days of treatment small interstitial oedema and hemorrhages by rupture of the basal membrane of the capillaries was found. At 30 days of treatment, many capillaries from different areas showed fibroid endothelial thickening, and wall fibrosis become evident after 60 days of daily cocaine. In numerous places (cortex, gray nucleus: thalamus, caudate, hippocampus and cerebellum) we observed capillaries with an occluded lumen probably due to fibrosis or thrombi after 90 days of treatment. In the latter treatment, capillaries from the choroid plexuses had their lumen dilated and the epithelial cells vacuolated or necrotic. We hypothesize that the chronic administration of cocaine in rats induced brain lesions in part as a result of capillary disruption and subsequent extravasation of erythrocytes to brain parenchyma.

Animals↗
PubMed1997

Cadmium levels in maternal, cord and newborn blood in Mexico City.

Blood samples were withdrawn from n = 49 mothers and their children at the moment of birth to assess blood cadmium levels of the mother, the newborn and the cord. A questionnaire was applied to the mothers in order to obtain data about possible sources of cadmium exposure. Maternal blood cadmium was found significantly correlated (r2 = 0.578) with cord blood cadmium levels, while cord blood was correlated (r2 = 0.499) with newborn blood cadmium. Nevertheless, maternal blood cadmium and newborn blood cadmium were not correlated at all (r2 = 0.047). Previous smoking habits of the mother increased maternal blood cadmium concentrations significantly, but it did not modify cadmium concentrations of either the cord or the newborn. The latter result suggests the existence of a placental barrier for cadmium. Birthweight was found to be inversely associated (P < 0.06) only with cord blood cadmium levels. The results of the study suggest that cord blood cadmium holds information about both maternal and newborn cadmium status and also about cadmium effects on birthweight.

Adolescent↗
PubMed1997

Effects of N omega-nitro-L-arginine and L-arginine on quinolinic acid-induced lipid peroxidation.

The effects of a nitric oxide synthase inhibitor, N omega-nitro-L-arginine (L-NARG), and a nitric oxide precursor, L-arginine (L-ARG), on the lipid peroxidation induced by quinolinic acid (QUIN, an NMDA receptor agonist), were both tested in synaptosomal fractions from whole rat brain. Baseline of lipid peroxidation was found at 2.43 +/- 0.24 fluorescence units/mg protein or 14.27 +/- 1.24 nmoles of TBARS/mg protein (100%). QUIN (100 microM)-induced lipid peroxidation in synaptosomes (256% and 166% vs. control, as measured by lipid fluorescent products and thiobarbituric acid-reactive substances, respectively) was inhibited by concentrations of 10, 40, 100, 200 and 400 microM of L-NARG (74%, 58%, 56%, 48% and 48% vs. quinolinate value, respectively). Coincubation of synaptosomes with QUIN plus L-ARG (100 microM), which alone resulted a potent pro-oxidant (277% vs. control), increased the lipoperoxidative effect induced by QUIN alone in 120% (290% vs. control). Synaptosomes simultaneously exposed to QUIN (100 microM) plus L-ARG (100 microM) plus L-NARG (200 microM) showed levels of lipid peroxidation similar to those of quinolinate alone. These findings suggest that nitric oxide may contribute to the oxidative damage induced in vitro by QUIN.

Animals↗
PubMed1997

Metallothionein inducers protect against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine neurotoxicity in mice.

1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is a drug that induces parkinsonism in human and non-human primates. Free radicals are thought to be involved in its mechanism of action. Recently, the participation of metallothionein as scavenger of free radicals has been proposed. In this work, we studied the effect of metallothionein inducers in MPTP neurotoxic action. Male swiss albino mice were pretreated either with cadmium (1 mg/kg) or dexamethasone (5 mg/kg), two well-known inducers of metallothionein synthesis, and 5 hours later with an MPTP administration (30 mg/kg). Treatment schedule was repeated daily for either 3 or 5 consecutive days. All animals were killed 7 days after the last administration, and striatal dopamine and homovanillic acid contents were analyzed as an end-point of MPTP neurotoxicity. Striatal dopamine content of cadmium plus MPTP-treated animals (3-days) increased by 32%, and 48% (5-days) vs MPTP-alone animals. Dexamethasone plus MPTP-treated group also showed increased dopamine levels 28% (3-days) and 43% (5-days). MPTP treatment reduced striatal metallothionein concentration (49% vs control animals). Dexamethasone and cadmium increased metallothionein concentrations in MPTP-treated groups, by 77% and 82% respectively. Results suggest that metallothionein induction provide a significant resistance factor against the deleterious effect of MPTP.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1997

Neuroprotective effect of dapsone against quinolinate- and kainate-induced striatal neurotoxicities in rats.

We tested the ability of dapsone, a well-known antibiotic and antiinflammatory drug, to attenuate both the quinolinic acid (an NMDA agonist of glutamate receptors)- and kainic acid (a non-NMDA agonist of glutamate receptors)-induced in vivo neurotoxicities in rats. Circling behaviour and striatal gamma-aminobutyric acid (GABA) depletion were considered as behavioural and neurochemical end-points of brain toxicity. Rotation behaviour, evaluated six days after the intrastriatal injection of quinolinic acid (130 +/- 19 ipsilateral turns/hr), was attenuated by doses of 12.5 mg/kg and 25 mg/kg of dapsone (50 +/- 9 and 63 +/- 9 turns/hr, respectively). Striatal GABA levels (237.3 +/- 15.1 micrograms/g in control rats), found depleted at day 7 after quinolinic acid (98.3 +/- 8.6 micrograms/g), were also protected by dapsone at doses of 12.5 and 25 mg/kg (167.7 +/- 19.5 and 236.4 +/- 46.6 micrograms/g, respectively). No protective effects were observed on quinolinic acid-induced neurotoxicity, as evaluated by both parameters, at lower doses of dapsone (6.25 and 9.375 mg/kg). The action of dapsone, at the dose of 12.5 mg/kg, was also measured on kainic acid-induced depletion of the striatal GABA levels. Animals treated with dapsone + kainic acid (182.8 +/- 27.1 micrograms/g) showed significant attenuation of GABA depletion, as compared to rats treated with kainic acid alone (122.2 +/- 19.9 micrograms/g). These findings provide evidences to suggest that dapsone is acting as a neuroprotective agent against excitotoxicity induced by glutamate receptor agonists.

Animals↗
PubMed1996

Systemic DL-kynurenine and probenecid pretreatment attenuates quinolinic acid-induced neurotoxicity in rats.

Kynurenine (KYN) is the precursor of kynurenic acid (KYNA), an endogenous antagonist of the glycine site of the NMDA (N-methyl-D-aspartate) receptor. Probenecid (PROB), blocks the excretion of KYNA from the extracellular fluid. KYNA antagonizes the toxic action of quinolinic acid (QUIN), an endogenous NMDA receptor agonist. In this study, we tested the effect of the systemic administration of KYN and PROB, either alone or in combination, on QUIN-induced circling behavior and gamma-aminobutyric acid (GABA) depletion in rats. Circling behavior and GABA depletion induced by QUIN were both partially prevented by PROB (200 and 300 mg/kg) and KYN (300 and 450 mg/kg) treatments. Lower doses of drugs administered separately were nonprotective. However, when administered in combination, doses of 150 or 300 mg/kg KYN plus 100 mg/kg PROB significantly protected animals against QUIN neurotoxicity. These findings suggest a role of KYN and PROB as promoters of KYNA-mediated NMDA receptor antagonism, via an increase of kynurenate in brain extracellular spaces.

Animals↗
PubMed1996

Quinolinic acid neurotoxicity: in vivo increased copper and manganese content in rat corpus striatum after quinolinate intrastriatal injection.

Copper and manganese, two essential metals involved in physiological and physiopathological processes in the brain, were measured in corpora striata of rats 7 days after intrastriatal injection of quinolinic acid (QUIN, 240 nmol/l microliters), an N-methyl-D-aspartate (NMDA) receptor agonist with toxic activity. Seven days after QUIN administration, copper and manganese contents were assessed by graphite furnace atomic absorption spectrophotometry. Total copper content was increased by 152% in QUIN-treated rats (18.74 +/- 2.05 micrograms/g) as compared to control animals (7.44 +/- 1.15 micrograms/g), whereas manganese striatal levels were enhanced by 35% (0.30 +/- 0.02 microgram/g) vs. control values (0.22 +/- 0.02 microgram/g). Quinolinate-induced striatal increase in copper and manganese levels were prevented by 23% (9.18 +/- 1.43 micrograms/g) and -0.45% (0.22 +/- 0.03 microgram/g) vs. control values, respectively, in rats pretreated with an NMDA receptor antagonist, dizocilpine (MK-801, 10 mg/kg, i.p.), 60 min before QUIN administration. As an index of QUIN neurotoxicity, striatal GABA levels were also measured 7 days after QUIN injection. GABA content was decreased by-55% in QUIN-lesioned rats (96.37 +/- 8.92 micrograms/g), whereas MK-801 was able to block QUIN-induced GABA depletion by 2% (219.37 +/- 10.60) vs. control values (214.2 +/- 21.88 micrograms/g). These findings suggest that increased concentrations of transition metals can be mediated by selective overactivation of NMDA receptors and might be a consequence of neural loss as well as glial response to damage.

Analysis of Variance↗
PubMed1996

Changes in transition metal contents in rat brain regions after in vivo quinolinate intrastriatal administration.

Total copper and manganese contents were measured in five rat brain regions 7 days after a unilateral striatal injection of quinolinic acid (QUIN, 240 nmol/ 1 microliter), an endogenous N-methyl-D-aspartate (NMDA) receptor agonist. Concentrations of both transition metals were evaluated in tissue of brain cortex, hippocampus, corpus striatum, midbrain and cerebellum of saline- and QUIN-treated rats using graphite furnace atomic absorption spectrophotometry. Increases in copper content were observed after QUIN striatal injection in cerebellum, hippocampus, midbrain and corpus striatum (37, 55, 71 and 152% as compared against control values, respectively) but not in brain cortex. Manganese levels were found enhanced only in corpus striatum of QUIN-treated rats by 35% vs. control values, but not in all other brain regions analyzed. QUIN-induced increases in regional copper content were partially prevented in hippocampus, midbrain and striatum (17, 57, and 23% vs. control, respectively) by pretreatment of rats with an NMDA receptor antagonist, dizocilpine (MK-801, 10 mg/kg, i.p.), administered 60 min before QUIN microinjection. The same protective effect of dizocilpine was observed against QUIN-induced enhancement of striatal manganese content (-0.45% vs. control). These findings resemble those changes observed in postmortem Huntington's disease brains and suggest that alterations in regional content of copper, but not in manganese, may be a consequence of the spreading of QUIN-induced neurotoxic events into the striatal tissue to the neighboring regions of the brain, by action of QUIN on NMDA receptors.

Animals↗
PubMed1996

Humoral and cellular immune response within the subarachnoid space of patients with neurocysticercosis.

To study the immune response within the subarachnoid space in patients with neurocysticercosis, we measured the cerebrospinal fluid contents of immunoglobulins A, E, G, and M in 38 patients and the contents of the proinflammatory cytokines TNF-alpha, IL-1b, IL-6 and IFN-gamma in 17 patients. The same measurements were made in 30 neurological patients without inflammatory or immune-mediated disorders. Each immunoglobulin and cytokine, including the gender and age of the patient, was compared by multiple regression analysis with the CSF contents of cells, protein and ELISA for cysticercal antigens. A direct correlation was found of IgM with cell content (p < 0.058) and with ELISA values (p < 0.027); of age with protein content (p < 0.006); of IL-6 with protein content (p < 0.018) and of IL-1b with ELISA values (p < 0.004). An inverse correlation was found of glucose with ELISA values (p < 0.008). A complex function of the immune response within the subarachnoid space was observed: mean values of IgG, IgM, IgE and interleukins 1b and 6 were increased, whereas values of IgA, TNF-alpha and IFN-gamma were similar to those of controls.

Antigens, Helminth↗
PubMed1995

Short-term manganese pretreatment partially protects against 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine neurotoxicity.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is a neurotoxin that induces parkinsonism in human and non-human primates. Its mechanism of action is not fully elucidated. Recently, the participation of trace metals, such as manganese, on its neurotoxic action has been postulated. In this work, we studied the effect of manganese administration on the neurochemical consequences of MPTP neurotoxic action. Male Swiss albino mice were treated with manganese chloride (MnCl2.4H2O; 0.5 mg/ml or 1.0 mg/ml of drinking water) for 7 days, followed by three MPTP administrations (30 mg/kg, intraperitoneally). Seven days after the last MPTP administration, mice were sacrificed and dopamine and homovanillic acid contents in corpus striatum were analyzed. Striatal concentration of dopamine was found increased by 60% in mice pretreated with 0.5 mg/ml and 52% in the group treated of 1.0 mg/ml as compared versus animals treated with MPTP only. Homovanillic acid content in both groups treated with manganese was the same as those in control animals. The results indicate that manganese may interact with MPTP, producing an enhancement of striatal dopamine turnover, as the protective effect of manganese was more pronounced in the metabolite than in the neurotransmitter.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1994

Dapsone attenuates kainic acid-induced seizures in rats.

We tested the ability of dapsone (4,4'-diamino-diphenyl sulfone) to attenuate kainic acid-induced seizures. We observed that 9.375 and 12.5 mg/kg doses of dapsone administered 30 min before a single kainic acid (10 mg/kg) i.p. injection were able to decrease the time of electroencephalographic seizures by 52% and 82%, respectively, as compared with rats administered with 10 mg/kg kainic acid only. The 12.5 mg/kg dose of dapsone was also able to diminish both kainic acid-evoked body and head shakes (58%) and kainic acid-induced mortality (75%). These results suggest that dapsone could be used in clinical trials as anticonvulsant.

Animals↗
PubMed1994

Thallium distribution in organs and brain regions of developing rats.

The concentration of thallium in body organs and brain regions was studied in rats as a function of the animals age from newborn to 20-days old. Thallium was analyzed at different times after a single sublethal i.p. injection of the metal (16 mg/kg). The results indicate that the brain is less permeable to thallium in the older animals, suggesting that reduced thallium transport into the brain is related to the establishment of the blood-brain barrier in the rats. Differences between weanling and newborn rats were also found in regard to regional distribution of thallium in the brain as the older animals showed a region-dependent distribution while newborn rats presented an homogeneous content of thallium among all regions.

Aging↗
PubMed1994

Combined D-penicillamine and prussian blue as antidotal treatment against thallotoxicosis in rats: evaluation of cerebellar lesions.

Rats were treated with a single dose of thallium acetate (32 mg/kg i.p.) and the antidotal effect of D-penicillamine and prussian blue given alone or in combination was assessed by means of evaluation of the thallium-induced cerebellar histological lesions. After thallium poisoning (24 h), antidotes were administered for 4 days as follows: D-penicillamine (DP) 25 mg/kg, i.p. twice daily; prussian blue (PB), 50 mg/kg p.o., twice daily. Mortality among the treatment groups was as follows: control, 87.5%; DP, 100%; PB, 56.25%; DP+PB, 25%. Three days after these treatments, rats treated with the combination DP+PB presented a significantly lower number of altered Purkinje cells in cerebellum as compared with those of the thallium alone treated animals, indicating adequate protection by this antidote treatment against thallium neurotoxicity. Prussian blue protected against thallium-induced neurotoxicity to a lesser extent as compared with the effects obtained by the DP+PB protection. DP did not protect against thallium-induced alterations of Purkinje cells. These results confirm the efficacy of the combined antidotal treatment of DP and PB against thallium toxicity in rats, and support the possible application in human cases of thallotoxicosis.

Animals↗
PubMed1994

Use of lead-glazed ceramics is the main factor associated to high lead in blood levels in two Mexican rural communities.

Two isolated rural communities of Mexico were studied to assess the possible relationship between lead-glazed ceramics use and lead exposure. Women from these communities (n = 98) were asked to participate by filling out a general-purpose and exposure questionnaire in order to assess the individual contribution of ceramics to lead exposure. Blood samples were withdrawn to measure lead in blood and erythrocytic zinc protoporphyrin levels. Results were analyzed by multiple regression in order to find predictors of the dependent variables. Significant association between lead in blood and erythrocytic zinc protoporphyrin levels was identified with the following variables: storage in lead-glazed ceramics, cooking in lead-glazed ceramics, and meat and cheese consumption. The adjusted regression models explained 20-23% of the variance of the dependent variables (lead in blood and erythrocytic zinc protoporphyrin). A significant association (r2 = .38) was observed between lead in blood and lead in food prepared in lead-glazed ceramics in a subsample of 28 women. Results indicate that lead-glazed ceramics use may be the main predictor of lead in blood and erythrocytic zinc protoporphyrin levels in the rural communities studied.

Adolescent↗