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Biomedical subjects

R Barroso-Moguel

Publications and source records attributed to R Barroso-Moguel.

At least 19 recordsLinked to original sources
PubMed2006

Morphometric analysis of brain lesions in rat fetuses prenatally exposed to low-level lead acetate: correlation with lipid peroxidation.

The effect of prenatal lead acetate exposure was studied microscopically together with the concentration of lead and lipid fluorescent products (LFP) in the brain of rat fetuses. Wistar rats were intoxicated with a lead solution containing either 160 or 320 ppm of lead acetate solution during 21 days through drinking water. The control group (ten rats) received deionized water for the same period. The rats were killed on gestation day 21 and fetuses were obtained; the placenta, umbilical cord and parietal cortex (Cx), striatum (St), thalamus (Th) and cerebellum (Ce) were collected for measuring tissue lead concentration, LFP as an index of lipid peroxidation and histopathologic examination. Lead contents were increased in placenta, umbilical cord, St, Th and Cx in both lead-exposed groups. Lead exposure increased (LFP) in placenta and umbilical cord, St, Th and Ce as compared to the control group. Histopathological examination showed severe vascular congestion in placenta, the Cx, St, Th and Ce with hyperchromatic and shrunken cells. Interstitial oedema was found in all regions studied of both lead exposed groups. The morphometric evaluation of the studied brain regions showed an absolute decrease in total cell number and increased number of damaged cells and interstitial oedema. Our results show that morphological changes in rat brain are correlated with increased lipid peroxidation, and the lead levels of the umbilical cord, however it is not clear whether oxidative stress is the cause or the consequence of these neurotoxic effects of lead.

Animals↗
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

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↗
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

Alveolar lesions induced by systemic administration of cocaine to rats.

In this work, alveolar lesions induced after systemic administration of cocaine (30 mg/kg per day, i.p.) to rats were evaluated both by light microscope analysis for morphological assessment as well as by measurement of the alveolar area as a quantitative index of the alveolar damage. Rats were examined after different times of exposure: 7, 15, 30, 45, 60 and 75 days. The histopathological evaluation of cocaine-treated rats revealed a remarkable thickening in some interalveolar septa, with interstitial hemorrhages, progressive thrombosis and transformation of reticular and elastic fibers into diffuse fibrosis. A significant decrease of the alveolar area was also observed. These findings are indicative of severe changes in capillaries, alveoli and bronchiole after cocaine exposure, which in turn may progressively disrupt the general function of the lungs. Differential mechanisms of systemic toxicity after cocaine exposure are 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↗
PubMed1995

Experimental nephropathy by chronic administration of cocaine in rats.

The recent and significant increase of cocaine abuse has emerged as a major public health problems. Cocaine abuse is frequently associated with multiorganic lesions, including renal failure. We report the light-microscopic features of the progression of renal lesions produced by chronic cocaine administration in rats. Male Wistar rats weighing 225-250 g were used. Twenty eight rats received an aqueous solution of cocaine hydrochloride (30 mg/kg/day i.p.) daily, while 28 control rats were injected i.p. daily with a saline solution. Rats from both groups were sacrificed after 7, 15, 30, 45, 60, 75 and 90 days of treatment. The histopathological study showed early changes on day 15, with damage to glomerular capillary walls and swelling of tubular epithelium, and lesions progressed to 90 days with development of glomerular atrophy and sclerosis. The tubular epithelial cells were necrotic and sloughed, and the lumen of papillary ducts contained destroyed red blood cell (RBC) casts. The interstitium had numerous foci of necrosis and haemorrhage. The results show that chronic treatment with cocaine in rats produce severe lesions both to glomerular, interstitium and tubular cells.

Animals↗
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↗
PubMed1992

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↗
PubMed1978

Innervation of the carotid body. An experimental quantitative study.

The innervation of the carotid body in the cat was studied by means of light- and electron-microscopic techniques. Sinus nerve resection, glossopharyngeal resection, bilateral cervical sympathectomy, excisions of two nerves, and injection of 6-hydroxydopamine (6-OH-DA) were performed in different groups of animals. It was found that resection of the sinus nerve produces a rapid phase of degeneration of intralobular fibers and synaptic boutons, followed by a reinnervation with a progressive reappearance of these elements. This reinnervation is retarded by sympathectomy and prevented by 6-OH-DA. It is therefore concluded that reinnervation is due to collateral regeneration of nearby sympathetic fibers. Resection of the sinus nerve produces an increase in the number of argentaffin cells and dense-cored vesicles in the cytoplasm of principal cells. These findings suggest the existence of efferent synaptic contacts between this nerve and principal cells. Part of the intralobular fibers and synaptic boutons degenerate after bilateral sympathectomy demonstrating that sympathetic axons connect synaptically to the principal cells. Sympathetic fibers reach the carotid body, not only from branches of the cervical plexuses but also from fibers running in the adventitia of the common carotid artery, and via glossopharyngeal and sinus nerves. The vagus nerve contributes a few fibers to the parenchymal lobules of the carotid body.

Animals↗