Biomedical subjects

C Ríos

Publications and source records attributed to C Ríos.

At least 19 recordsLinked to original sources

PubMed2003

Natural soil gamma radioactivity levels and resultant population dose in the cities of Zacatecas and Guadalupe, Zacatecas, Mexico.

The study of natural gamma radioactivity was made to determine the concentrations of natural radionuclides in soil. Twenty soil samples collected in the cities of Zacatecas and Guadalupe and their suburban areas in the Mexican state of Zacatecas were analyzed by gamma-ray spectrometry to determine the activity concentrations of 226Ra, 232Th, and 40K. Gamma-spectrometry measurements were made using a hyperpure germanium detector surrounded with shielding material to reduce the background counting rate. The GammaVision-32 MCA emulation software was used for gamma-ray spectrum analysis and the TRUMP card of 2k as a MCA emulator. Conversion factors were used to calculate the dose to the population from outdoor exposure to terrestrial gamma rays. The measured activity concentration of 226Ra varies from 11 to 38 Bq kg(-1), the activity concentration of 232Th varies from 8 to 38 Bq kg(-1). The activity concentration of 40K is in the range 309-1,049 Bq kg(-1). The overall population mean outdoor terrestrial gamma dose rate is 44.94 nGy h(-1).

Background Radiation↗

PubMed2001

Enhanced brain regional lipid peroxidation in developing rats exposed to low level lead acetate.

Neurotoxicity associated with lead exposure may be the result of a series of small perturbations in brain metabolism, and, in particular, of oxidative stress. Some studies have suggested a lead-induced enhancement on lipid peroxidation as a possible mechanism for some toxic effects of lead. However, there are no reports about the association between lipid peroxidation enhancement and brain lead content. In this study, we determined the concentration of lead and the formation of lipid fluorescence products in the blood, as well as in the parietal cortex, striatum, hippocampus, thalamus, and cerebellum of rats exposed prenatally and postnatally to variable concentrations of lead acetate through drinking water. Pregnant Wistar rats were intoxicated throughout gestation with solutions containing either 320 or 160 ppm of lead. The pups were treated after birth in the same way until 45 days of age. Control animals received deionized water for the same period of time. The developing rats were sacrificed at postnatal day 45 and lead level was assessed biochemically in the blood and different brain regions. Results showed that blood lead levels were increased in a dose-dependent manner. In the brain, lead accumulated preferentially in the parietal cortex, striatum, and thalamus as compared to the control group, while lipid fluorescence products were significantly increased in the striatum, thalamus, and hippocampus of the treated animals. These data suggest that in the brain of rats exposed to lead acetate, lead produces a neurotoxic effect with a complex correlation with both lead regional content and lipid peroxidation.

Animals↗

PubMed2001

Participation of manganese-superoxide dismutase in the neuroprotection exerted by copper sulfate against 1-methyl 4-phenylpyridinium neurotoxicity.

Neurodegenerative effects of 1-methyl-4-phenylpyridinium (MPP+), the main metabolite of the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) include enhancement of lipid peroxidation in the striatum of mice, associated to overproduction of free radicals. Copper acts as a prosthetic group of several copper-dependent antioxidant enzymes, and we previously showed the neuroprotective effect of CuSO4 pretreatment against the MPP+-induced neurotoxicity. In those studies, acute administration of CuSO4 (2.5 mg/kg) blocked MPP+-induced striatal lipid peroxidation, suggesting the activation of Cu-dependent proteins that defend neurons from damage elicited by free radicals. In the present study, we evaluated the activity of superoxide dismutase in mice pretreated with CuSO4 16 h or 24 h prior to MPP+ administration. Copper administration produced a specific and significant increase in manganese superoxide dismutase activity in both the CuSO4/saline (fivefold increase) and the CuSO4/MPP+ groups of animals (sevenfold increase). The Na2SO4/MPP+ group showed a twofold increase in manganese superoxide dismutase activity versus control levels. The results suggest that the load of copper activating manganese-dependent superoxide dismutase could be responsible for neuroprotection against the MPP+ insult.

1-Methyl-4-phenylpyridinium↗

PubMed2001

Histopathological alterations in the brain regions of rats after perinatal combined treatment with cadmium and dexamethasone.

Industrial and environmental exposure to cadmium (Cd) is well known to produce multiorgan toxicity in humans. Metallothionein (MT) is a cellular ligand for Cd. MT has been shown to protect against Cd-induced toxicity in many organs, including brain. In this study, we described the histopathological alterations in parietal cortex, striatum, hippocampus and cerebellum of rats following perinatal combined exposure to cadmium and dexamethasone (Dx), a drug known to induce MT synthesis in brain. Wistar rats of 13 days of age were treated for 5 days, as follows; (1) saline solution, (2) CdCl(2) 1 mg/kg per day, (3) Dx 2 mg/kg per day, (4) CdCl(2) 1 mg/kg per day + Dx 2 mg/kg/day. Rats were killed on either 18 or 28 days of age. The content of Cd in parietal cortex, striatum, hippocampus and cerebellum at 18 days old age increased 58.3-, 9.4-, 18.3- and 11.3-fold, while at 28 days of age in the same regions the increases were 6.6-, 5.8-, 25.3- and 11.3-fold in the Cd treated rats, respectively. No lesions were observed in the brain of control rats. Rats treated with Dx at 28 days of age showed interstitial edema in the four regions. Cd-treated rats at 28 days of age showed lesions in the four studied regions. In general, Dx treatment attenuated all Cd-induced lesions.

Animals↗

PubMed2001

Quinolinic acid induces oxidative stress in rat brain synaptosomes.

The oxidative action of quinolinic acid (QUIN), and the protective effects of glutathione (GSH), and 2-amino-5-phosphonovaleric acid (APV), were tested in rat brain synaptosomes, Reactive oxygen species (ROS) formation was quantified after the exposure of synaptosomes to increasing concentrations of QUIN (25-500 microM). The potency of QUIN to induce lipid peroxidation (LP) was tested as a regional index of thiobarbituric acid-reactive substances (TBARS) production, and the antioxidant actions of both GSH (50 microM) and APV (250 microM) on QUIN-induced LP were evaluated in synaptosomes prepared from different brain regions. QUIN induced concentration-dependent increases in ROS formation and TBARS in all regions analyzed, but increased production of fluorescent peroxidized lipids only in the striatum and the hippocampus, whereas both GSH and APV decreased this index. These results suggest that the excitotoxic action of QUIN involves regional selectivity in the oxidative status of brain synaptosomes, and may be prevented by substances exhibiting antagonism at the NMDA receptor.

2-Amino-5-phosphonovalerate↗

PubMed2001

Striatal manganese accumulation induces changes in dopamine metabolism in the cirrhotic rat.

Manganese (Mn) is an essential metal that, in excess, causes an extrapyramidal syndrome consisting in tremor, rigidity and akinesia. Recently, Mn was found to accumulate in brains of cirrhotic patients who also present motor abnormalities. Manganese alters dopaminergic transmission promoting an increase in the turnover of dopamine (DA). In this study, we studied the changes in dopamine and its main metabolite homovanillic acid (HVA) to evaluate DA turnover following administration of manganese to bile-duct obstructed rats. Some groups of rats were treated with manganese chloride in two concentrations: 0.5 and 1 mg/ml of Mn2+ in their drinking water. Four weeks after surgery and treatment with manganese, striatal Mn, DA and HVA were assessed. Marked increases (P<0.05) of striatal manganese content were observed in cirrhotic rats treated and untreated with manganese, these augments were dependent on the Mn concentration in water. Striatal contents of DA in cirrhotic rats diminished by 30% (P<0.05), administration of 0.5 mg/ml of manganese in drinking water to these rats returned dopamine to the basal level and 1 mg/ml of manganese increased dopamine content by 27%. The relationship of Mn content and DA turnover (HVA:DA) in the same animal showed a positive and statically significant correlation (P<0.05), with differences in slope for sham (b1=0.1528) and cirrhotic rats (b1=0.0174). These results suggest that manganese brain accumulation observed in liver failure could be a key element to understand dopamine metabolism in cirrhotic condition of humans.

Animals↗

PubMed2001

Comparative analysis of superoxide dismutase activity between acute pharmacological models and a transgenic mouse model of Huntington's disease.

We examined the activity of striatal superoxide dismutase (SOD) in two acute pharmacological models of Huntington's disease (HD), and compared it with SOD activity in the striata of mice transgenic for the HD mutation. Total SOD, and Cu/ZnSOD activities increased in young transgenic mice, but decreased in older (35 week) mice. We consider that the increased enzyme activity represents a compensatory mechanism to protect cells from free radical-induced damage, but the system becomes insufficient in older animals. Major decreases in SOD activity were also observed both after quinolinic acid and 3-nitropropionic acid intrastriatal injections. The present results indicate that in both types of HD models striatal oxidative damage occurs, and that it is associated with alterations in the cellular antioxidant system.

Animals↗

PubMed2000

Subchronic administration of sublethal doses of thallium to rats: effects on distribution and lipid peroxidation in brain regions.

Occupational exposure to thallium (Tl+) is known to be responsible for severe neurological manifestations in humans, including ataxia and paralysis; however, little is known yet about the precise mechanism of toxicity elicited by this heavy metal at sublethal doses and its brain distribution after chronic or subchronic exposures resulting from environmental contamination. In order to evaluate the levels of Tl in rat brain regions after a subchronic administration (30 days) of sublethal doses of Tl (I) acetate: 0.8 mg/kg (1/40 of LD(50)), 1.6 mg/kg (1/20 of LD(50)), we measured the concentrations of Tl by atomic absorption spectrophotometry. A possible role of oxidative injury in the pattern of toxicity exerted by Tl in the same brain regions, was also studied. Lipid peroxidation (LP) as a current marker of oxidative stress, was estimated by the generation of lipid fluorescent products. Higher concentrations of Tl were observed in brain tissue from adult rats treated with 1.6 mg/kg, as compared to those treated with 0.8 mg/kg. However, no differential distribution of Tl among regions was observed after administration of 0.8 mg/kg dose to rats, nor after 1. 6 mg/kg dose. We also found significant changes in LP both in corpus striatum and cerebellum from rats treated daily with 0.8 mg/kg Tl, whereas all regions from rats treated with 1.6 mg/kg Tl exhibited enhanced LP as compared to control. These findings suggest an active role of free radicals and oxidative events involved in the pattern of toxicity after exposure to sublethal doses of Tl, which are associated with regional susceptibility of the brain to this metal.

Animals↗

PubMed2000

Striatal oxidative damage parallels the expression of a neurological phenotype in mice transgenic for the mutation of Huntington's disease.

We examined the degree of oxidative damage to the brain of mice transgenic for the mutation responsible for Huntington's disease. We found that there is a progressive increase in striatal lipid peroxidation (LP), that parallels the worsening of the neurological phenotype. We consider that these transgenic mice may provide an interesting system to test treatments aimed at protecting cells from damage induced by free radicals.

Animals↗

PubMed2000

Role of glutathione in Thiobencarb resistance in the European eel Anguilla anguilla.

Glutathione-dependent defense against xenobiotic toxicity is a multifaceted phenomenon that has been well characterized in mammals. In the present study, eels of species Anguilla anguilla were exposed to 15 ppm of the herbicide thiobencarb (S-4-chlorobenzyl diethylthiocarbamate) for 96 h. Eels exposed to the pesticide were grouped in 24-h intervals according to their time of death, while surviving intoxicated eels constituted another group (live animals). Glutathione content (GSx, GSH, GSSG) was determined in liver and muscle tissues of the dead and live (intoxicated) animals and compared to control values (nonexposed eels). The fish that died before 96 h of exposure were considered susceptible to thiobencarb, while those dead after 96 h and the surviving ones were called resistant. Hepatic glutathione (GSH) content in susceptible eels was lower than that in the control fish, while resistant eels presented GSH levels threefold higher than those of controls. Muscle glutathione levels in dead eels were practically unaffected, but there was a significant decrease in GSH levels in the surviving intoxicated eels. These results indicate that the eels that were able to induce glutathione synthesis in the liver due to the presence of thiobencarb in the medium demonstrated a greater longevity than those who lost glutathione homeostasis.

Animals↗

PubMed2000

MPTP decreases MT-I mRNA in mouse striatum.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is a drug that induces parkinsonism in humans and non-human primates. Free radicals are thought to be involved in its mechanism of action. Recently, metallothionein has been proposed to play a role as a scavenger of free radicals. In the present work, we studied the effect of MPTP neurotoxicity on brain metallothionein-I (MT-I) mRNA expression. Male C-57 black mice were treated with MPTP (30 mg/kg, i.p., daily) for 3 or 5 days. All animals were killed by cervical dislocation 7 days after the last MPTP dose. The brains were removed quickly and immediately frozen, and quantitative in situ hybridization was performed using MT-I cDNA probe. MT-I mRNA content in striatum, a region which is known to be highly predisposed and sensitive to MPTP-induced oxidative stress, decreased by 30% (3 days) and 39% (5 days) respectively, after the last MPTP administration. These results suggest that MT-I gene expression is decreased in MPTP neurotoxicity. It is suggested that the reduction of MT, an anti-oxidant and a free radical scavenger, in the striatum by MPTP enables the neurotoxin to exert maximal oxidative damage to the striatum.

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

PubMed2000

Arteries of the hindfoot of the llama (Lama glama).

The objective of this study was to describe the arterial distribution of the hindfoot of the llama (Lama glama). Ten adult llamas, preserved in 6% formalin solution at 0 degree C, were dissected. The arterial system was perfused with a solution of 14% coloured plaster; the venous system was perfused with a solution of 17% coloured industrial gelatin. Angiographies were also obtained. In the llama, the arterial distribution is of the saphenous type and this simple sort of irrigation could be used as a didactic model. The caudal branch of the saphenous artery divides into the small lateral plantar artery and the larger medial plantar artery, which continues as the plantar common digital artery III, and it is the main blood supply of the hindfoot. The dorsal pedal artery is underdeveloped and the perforating tarsal artery does not exist in this species. The plantar common digital artery III divides into the plantar proper digital II, III and IV. Branches from the plantar proper digital artery III supply the digits. We compared the arterial distribution of the hindfoot of the llama with that of other domestic animals including the one-humped camel (Camelus dromedarius).

Angiography↗

PubMed1999

Dapsone prevents morphological lesions and lipid peroxidation induced by quinolinic acid in rat corpus striatum.

Increasing doses of dapsone were tested on rats administered intrastriatally with quinolinic acid in order to evaluate a possible protective action of this drug on the striatal lesions produced after the excessive activation of N-methyl-D-aspartate receptors. Morphological lesions were evaluated 7 days after the intrastriatal injection of quinolinate (240 nmol/microl) by light microscopy, and the ratio of neuronal damage per field was also estimated as a quantitative index of the striatal toxicity. Quinolinate alone produced extensive necrosis and loss of striatal neurons. No protective effects on the striatal tissue from quinolinate-treated rats were observed at lower doses of dapsone (6.25 and 9.375 mg/kg). However, at higher doses (12.5 and 25 mg/kg), dapsone prevented significantly the striatum from quinolinate toxicity. Dapsone alone had no effect on the striatal tissue from control rats. A single dose of dapsone (12.5 mg/kg) was tested also on the index of lipid peroxidation 2 h after the striatal injection of quinolinate, resulting in a significant protection (78% vs. QUIN). Findings of this study, in accordance with our previous reports, demonstrate the ability of dapsone to prevent the neuronal damage associated with the excitatory action of quinolinate via overactivation of NMDA receptors, and provide evidences to support the hypothesis that this drug is acting against the pattern of toxicity elicited by agonists of glutamate receptors.

Animals↗

PubMed1999

Intrauterine lead exposure and preterm birth.

The objective of this study was to determine the risk of preterm birth in relation to umbilical cord blood lead levels (UCL) among primiparous and multiparous women. A case-cohort study was performed in Mexico City during 1995. A total of 459 full-term births was compared with 161 preterm births (before 37 gestational weeks). Mothers were interviewed before the delivery about their reproductive histories and other related factors of preterm birth. Lead was determined by atomic absorption spectrophotometry. Lead levels were higher in primiparous women who had a preterm birth than in primiparous women with a full-term birth (9.77+/-2.0 microgram/dl vs 8.24+/-2.15 microgram/dl); this difference was marginally significant. After adjusting for other known preterm birth risk factors, the frequency of preterm birth was almost three times higher among women who had UCL levels greater or equal to 5.1 microgram/dl compared to those who had UCL levels lower than 5.1 microgram/dl. This difference was not observed among multiparous women. Our results suggest that intrauterine lead exposure may be associated with preterm birth in first deliveries but not in subsequent ones.

Adolescent↗

PubMed1999

Nomega-nitro-L-arginine, a nitric oxide synthase inhibitor, antagonizes quinolinic acid-induced neurotoxicity and oxidative stress in rat striatal slices.

Nitric oxide (NO) is a potential contributor to neurotoxicity following overactivation of N-methyl-D-aspartate (NMDA) receptors. In this work we investigated the effect of Nomega-nitro-L-arginine (L-NARG 25, 50, or 100 microM), a selective inhibitor of nitric oxide synthase (NOS) -the synthetic enzyme of NO- on quinolinic acid (QUIN 100 microM)-induced neurotoxicity (measured as lactate dehydrogenase (LDH) leakage) in rat striatal slices. Oxidative stress was also measured both as lipid peroxidation and as the levels of reduced (GSH) and oxidized (GSSG) glutathione, in an effort to elucidate a possible participation of NO in the toxic mechanisms involved in NMDA receptor-mediated neuronal injury. The action of L-arginine (L-ARG 100 or 200 microM), a well-known NO precursor, was also tested on QUIN-induced neurotoxicity and oxidative stress. Results showed that QUIN produced significant changes in both cell damage (177%) and oxidative injury (203% in lipid peroxidation, 68% in GSH, and 123% in GSSG) as compared to control values. All these effects were antagonized by adding L-NARG to the incubation media, whereas L-ARG alone, or in combination with QUIN, significantly enhanced both lipid peroxidation and LDH leakage. Moreover, the protective effects of L-NARG on QUIN-induced lipid peroxidation were reversed by addition of an excess of L-ARG to the media. These findings indicate that NO is probably mediating the mechanism of neurotoxicity produced by QUIN, which may be of potential value to explain the molecular basis of neurodegenerative processes linked to QUIN-mediated NMDA receptor overactivation.

Animals↗

PubMed1999

[Lead elimination by traditional curing].

OBJECTIVE: To evaluate traditional acidic curing as a preventive method for reducing lead content of glazed ceramic ware. MATERIAL AND METHODS: In 27 ceramic ware pieces from four states in Mexico, the level of residual lead was determined through atomic absorption spectrophotometry after four washings with acetic acid 3%. RESULTS: The lead content of the vinegar washing diminished proportionally with the number of washings, although it remained highly above the permissible levels of this metal (2.5-7.0 p.p.m.). CONCLUSIONS: Traditional acidic curing of glazed ceramic ware is not a useful preventive measure for reducing lead exposure.

Cooking and Eating Utensils↗

PubMed1998

Increase of striatal dopamine release by cadmium in nursing rats and its prevention by dexamethasone-induced metallothionein.

Repeated daily intraperitoneal (i.p.) administrations of cadmium (CdCl2, 1 mg/kg per day for 5 days) increased striatal dopamine (DA) release (180% of controls) and turnover (150% of controls) in 13-day-old rats. Cd treatment also increased striatal metallothionein (MT) content (161%), Cd (127%) and lipid peroxidation (LPO, 190%). In addition, Cd treatment decreased striatal tyrosine hydroxylase (TH) activity (-28%), and such an effect may result from D-2 receptor blockade as a consequence of excessive dopamine release, since sulpiride (a specific D-2 receptor antagonist) administration to Cd-treated rats abolished the effect of Cd on TH. No effect was observed on striatal monoamine oxidase (MAO) activity. Dexamethasone (Dx) treatment increased striatal MT content and caused no effect on either DA release or turnover. However, Dx administration prevented the effects caused by Cd, including the increased DA release and enhanced striatal lipid peroxidation. These results indicate that toxic effects on the brain are to be expected as a result of Cd exposure and that Dx administration can attenuate them.

Animals↗

PubMed1998

Interaction between isoniazid and diverse vasodilators: role of decreased cerebral GABA.

OBJECTIVE: To determine if the interaction between isoniazid and hydralazine, consisting of increased hypotension accompanied by bradycardia, occurs with other vasodilators. METHODS: Blood pressure and heart rate responses to a number of vasodilators were determined in rats under chloralose-urethane, pretreated or not with 250 mg/kg of isoniazid. The influence of this dose of isoniazid on GABA levels in the hypothalamus and pons-medulla was assessed in other groups of rats. RESULTS: Increased hypotension and bradycardia following i.p. isoniazid were observed with dipyridamole, prazosin, pinacidil and hydralazine given i.v. Bradycardia without increased hypotension appeared with papaverine and verapamil, while increased hypotension with unchanged heart rate was observed with minoxidil and captopril. Isoniazid decreased GABA in the hypothalamus and pons-medulla. CONCLUSIONS: At the high dose used, isoniazid interacts with various vasodilators, irrespective of their mechanism of action. The interaction could be due to the influence of the drug on GABA levels at cardiovascular regulatory sites.

Animals↗