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C Ríos

Publications and source records attributed to C Ríos.

At least 55 records · Page 3Linked to original sources

MK-801, an N-methyl-D-aspartate receptor antagonist, blocks quinolinic acid-induced lipid peroxidation in rat corpus striatum.

In this study, we evaluate the possible participation of lipid peroxidation (LP) in the neurotoxic events that follow after quinolinic acid (QUIN) microinjection into the rat corpus striatum. Two hours after QUIN (240 nmol/microliters) intrastriatal administration, lipid peroxidation was found increased by 32% vs. control as measured by thiobarbituric acid-reactive substances (TBARS). At the same time tested, the enhancement in LP was of 55% vs. control as measured by lipid fluorescent products (LFP) formation (a second index of lipid peroxidation employed). The increase of QUIN-induced lipid peroxidation was completely abolished by pretreatment of rats with an N-methyl-D-aspartate (NMDA) receptor antagonist, MK-801 (10 mg/kg, i.p.), 60 min before QUIN microinjection. Results suggest an NMDA receptor involvement in the QUIN-induced oxidative processes.

Animals↗

[Dilated cardiomyopathy and hypereosinophilia in a young female patient].

A 23-year-old white woman was admitted because of cardiac failure (functional class II), palpable purpura and hypereosinophilia. A month before, she had been operated due to right femoral embolus. In this occasion, enhanced cardiac size on X-ray film of the chest and 12,300 eosinophils/mm3 were observed. She was asthmatic from her childhood. The laboratory data did not detect an etiology of hypereosinophilia. Serologic test for collagenous diseases, Chagas, hydatidosis, toxocariasis, Coxsackie B 1-6 and cytomegalovirus were not considered reactive. Three parasitologic stool examinations were negative. Duodenal sounding was negative. Myocardial dilatation was confirmed by mode M and B echocardiogram (60 mm left ventricular diastolic diameter), and by 99Tc radiocardiogram (left ventricular ejection fraction -LVEF-: 29% and right VEF: 15%). On the 25th day of treatment with 16-beta-methyl-prednisone (1 mg/K/d), eosinophil count was reduced to 300/mm3. On the 45th day, clinical improvement, dilatation reduction on echocardiogram and a 32% LVEF were observed. On the 10th month, the patient has no signs or symptoms of cardiac failure under treatment. Although endomyocardial biopsy was not performed but considering the low prevalence of myocardial dilatation at such an age, it is possible to postulate that the patient has undergone the initial necrotic stage (dilated cardiomyopathy) and the intermedial thrombotic stage (femoral embolus) of the eosinophilic endomyocardial disease.

Adult↗

Osteochondral lesions in developing rats intoxicated with thallium twenty four hours after birth.

An i.p. injection of a solution of thallium acetate in deionized water at a dose of 32 mg/kg, in 24-h-old rats, produces morphological and biochemical alterations in both cartilaginous and osseous tissues. From the beginning, there are alterations in the cartilaginous cell as well as in chrondrine, osteoblasts, osseous tissue and bone marrow. Rats were sacrificed at 24, 48, and 72 h and also at 7 days. Two animals survived for 50 days. One showed total irreversible alopecia while the other one had partial alopecia with discrete recovery. Both showed a low weight and a size of 8 cm. Microscopically, degenerative changes were produced consisting of alteration and death of many cartilaginous cells, uneven metachromasia and the chondrine and decrease of the growth cartilage, scanty bone trabeculae with few osteoblasts. The bone marrow showed few myeloblasts and megakaryocytes. Progressive cellular damage throughout the 50 days of survival represents a response of the thallium ionic accumulation and recycling in cellular mitochondria of all the body's cells. This appeared in our study as irreversible and progressive osteochondral alterations with atrophy of the skin and its adnexa, hyalinization of elastic and collagenous fibers with intense interstitial edema.

Alopecia↗

Differential role of serotonin and noradrenaline on anxiety reduction after ejaculation in the rat.

As previously reported, a reduction in anxiety after ejaculation was observed. In a previous report it was demonstrated that the GABA-benzodiazepine system is involved in the mediation of this reduction in anxiety. The anxiety levels were measured using a defensive burying model. This work was performed to elucidate the serotonin and noradrenaline participation in the mediation of this phenomenon. Two experiments were made. In the first experiment the serotonergic neurotoxin 5,7-dihydroxytryptamine (5,7-DHT, 10 micrograms/10 microliters) was intracerebroventricularly injected. Five days after its administration the behavioral tests were performed. In the second experiment, the noradrenergic neurotoxin N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP4, 50 mg/kg X 2) was IP administered. The neurochemical data reveal a drastic reduction in various brain areas respective monoamine levels after these treatments. The lesion produced by 5,7-DHT was able to reverse the reduction in anxiety in copulating males, but produced no changes in noncopulating animals. This finding supports the idea that the serotonergic system is involved in the reduction of anxiety observed after ejaculation. The results of the DSP4 experiment suggest that there is not a direct participation of the noradrenergic system in the anxiety reduction observed after ejaculation.

5,7-Dihydroxytryptamine↗

Patterns of mental health utilization among island Puerto Rican poor.

BACKGROUND: This paper describes utilization of mental health services by poor Puerto Ricans living on the island. It examines the utilization rates, within health sectors, and settings for the provision of mental health services. METHODS: Data are based on an islandwide probability sample of 18- to 64-year-old respondents living in low socioeconomic areas. We assessed need with the Psychiatric Symptom and Dysfunction Scales. RESULTS: Approximately one-third of our study population (31.5%) met criteria for need. Of these, only 32% had received any mental health care in the past year. Need was significantly associated with use of physical or mental health services for mental health problems. We found those who needed services to be five times more likely than those who did not need services to have used one or both sectors of care at least once in the past year. Among the first group 21.8% used the physical health sector to deal with mental health problems in contrast with 17.9% who sought care in the mental health sector. In the physical health sector, subjects used the public and private settings equally. In the mental health sector, 70% of subjects used the public setting. CONCLUSIONS: This suggests the nonpsychiatric physician as a main provider for mental health treatment.

Adolescent↗

Determination of lithium in rat brain regions and synaptosomes by graphite furnace atomic absorption spectrophotometry.

A graphite furnace atomic absorption spectrophotometric method for the analysis of very low concentrations of lithium in brain tissue and subcellular fractions is described. The method has a picogram sensitivity and shows a precision value of 10.1% expressed as the per cent variation coefficient for the tissue analysis of the metal. Lithium concentration in eight regions of the rat brain and regional synaptosomal lithium contents were analyzed with the method described. Results from these determinations show that lithium is heterogeneously distributed among rat brain regions 24 hr after a single s.c. lithium administration; hypothalamus, corpus striatum and midbrain were the regions with the highest lithium accumulation. Lithium is homogeneously concentrated in the synaptosomes obtained from rat brain regions. The method proposed may be considered adequate for trace lithium analysis in pharmacological studies of the metal.

Animals↗

Brain regional thallium distribution in rats acutely intoxicated with Tl2SO4.

The content of thallium in seven body organs and eight brain regions of rats acutely exposed to Tl2SO4 was compared. Rats received a single i.p. injection of Tl2SO4 at three doses: 16, 32 and 48 mg/kg. At 24 h after treatment, thallium content in kidney was higher than in all other organs studied and whole brain had the lowest thallium concentration. A thallium differential distribution was found among brain regions. The highest thallium concentration was found in the hypothalamus and the lowest in the cortex. This distribution pattern was similar with the three doses used. Time course of thallium accumulation in brain was found to be considerably more rapid in the hypothalamus than in other regions, particularly the cortex, suggesting differences in thallium entry into brain parenchyma. Thallium brain regional differential distribution might be related to some of the symptoms of thallium central neurotoxicity.

Animals↗

Changes in lipid peroxidation induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine and 1-methyl-4-phenylpyridinium in mouse brain homogenates.

We studied the effect of the Parkinson-inducing drug 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and of its metabolite 1-methyl-4-phenylpyridinium (MPP+) on lipid peroxidation in mouse brain homogenates in vitro. MPTP (0.35-1.4 mM) inhibited both spontaneous and Fe2+-induced peroxidation in a dose-dependent manner. MPP+, on the other hand, produced a slight enhancement of lipid peroxidation at 1.4 and 2.1 mM concentrations. These results are discussed in terms of the possible mechanisms of MPTP and MPP+ neurotoxicity.

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

Thallium increases monoamine oxidase activity and serotonin turnover rate in rat brain regions.

The effect of thallium acetate administration on monoaminergic pathways was studied in male Wistar rats using 30 mg/kg and 50 mg/kg acute IP doses. We found that thallium activated both monoamine oxidase (MAO) activity and serotonin turnover rate in rat brain regions, that may contribute to the neuronal damage mechanism of the agent. MAO activity in midbrain and pons was increased at both doses (at 30 mg/kg dose by 27.7% and 37%; at 50 mg/kg dose by 48% and 47%, respectively vs. control group). Serotonin turnover rate in pons was also increased at the 30 mg/kg dose (172%) while midbrain and pons serotonin turnover was increased only at the 50 mg/kg dose (56% and 166%, respectively vs. control group). Dopamine turnover rate was not significantly changed. The results indicate that thallium induced a significant increase in pons and midbrain MAO activity and also in serotonin turnover rate as compared with control animals, and this could led to behavioral and toxic alterations in the rats intoxicated with thallium.

Animals↗

Prevalence of acute intermittent porphyria in a Mexican psychiatric population.

BACKGROUND: Acute intermittent porphyria is a hereditary error of porphyrin metabolism in which the main metabolic defect is caused by a decrease in porphobilinogen deaminase activity. Previous work has demonstrated a higher prevalence of acute intermittent porphyria in the psychiatric patient population than in the general population. The goal of this study was evaluate 300 psychiatric patients and 150 control subjects to detect acute intermittent porphyria by measurement of porphobilinogen (PBG) deaminase activity in blood. METHODS: Screening for porphobilinogen deaminase activity was carried out by fluorometric measurement of porphyrins synthesized during 1 h in blood and the measurement of delta-aminolevulinic acid and porphobilinogen in urine. RESULTS: We found two psychiatric patients, one male and one female, with decreased porphobilinogen deaminase activity. When the families of these patients were studied, one brother was found to have an abnormality. Among controls, a woman was found to have the abnormality and her father was found to have typical features of the disease. CONCLUSIONS: These results indicate a prevalence of porphyria in Mexican psychiatric patients similar to controls, and that measurement of PBG deaminase activity is a good tool for defining acute intermittent porphyria carriers.

Acute Disease↗

Retinal lesions in rat fetuses prenatally exposed to cocaine.

The increased use of cocaine in the United States and worldwide has created great concern about its effects on fetuses and neonates of pregnant cocaine abusers. The effects on neonates are varied: fetal growth delay, microcephaly, abnormal neurological functions, microphthalmia, and maternal obstetric complications. In this study, the effect of prenatal cocaine administration was studied microscopically in the retina of rat fetuses. Twenty-five pregnant Wistar rats were injected i.p. with an aqueous cocaine solution using a 30 mg/kg daily dose for 45 days. Control group rats (15 pregnant animals) received saline solution for the same period. Day 0 of gestation was the day after mating. Dosing began on this day. The rats were killed on gestation day 21 and fetuses were obtained for examination. The histopathological light and electron microscope studies of the retinas showed interstitial oedema, areas depleted of cells, necrosis, and hyperchromatic ganglion cells. There also was a significantly lower number of retinal cells compared to control fetuses. In four cases, teratogenic lesions of the retina were observed whereas no changes were present in control fetuses. Results indicate that development of retina in fetuses prenatally exposed to cocaine was altered by cocaine exposure.

Animals↗

Effects of lead-arsenic combined exposure on central monoaminergic systems.

Lead acetate (116 mg/kg/day), arsenic (11 or 13.8 mg/kg/day as sodium arsenite), a lead-arsenic mixture or vehicle were administered to adult mice through gastric intubation during 14 days. Then, the regional content of norepinephrine (NE), dopamine (DA), serotonin (5-HT), 3,4 dihydroxyphenyl-acetic acid (DOPAC), 5-hydroxyindole-3-acetic acid (5-HIAA), arsenic, and lead were quantified. Compared with the accumulation after single element exposures, the mixture elicited a higher accumulation of lead and a lower arsenic accumulation in the brain. Compared to controls, lead induced only an augmentation of DOPAC (200%) in the hypothalamus. By contrast, the mixture provoked increases of DOPAC in the hypothalamus (250%), DA and 5-HIAA in the striatum (67 and 187%, respectively) and NE decreased in the hypothalamus (45%). Although these alterations were similar to those produced by arsenic alone, the mixture provoked a 38% decrease of NE in the hippocampus and increases of 5-HT in midbrain and frontal cortex (100 and 90%, respectively) over control values, alterations that were not elicited by either metal alone. These results demonstrate an interaction arsenic/lead on the central monoaminergic systems of the adult mouse.

3,4-Dihydroxyphenylacetic Acid↗