Search PubMed⌕ Search

Biomedical subjects

Laura Colín-Barenque

Publications and source records attributed to Laura Colín-Barenque.

7 recordsLinked to original sources

Hippocampal cell alterations induced by the inhalation of vanadium pentoxide (V(2)O(5)) promote memory deterioration.

Spatial memory may be severely impaired as a consequence of ageing and neurodegenerative diseases, conditions that include neuronal damage. Vanadium (V) is a metalloid widely distributed in the environment and exerts severe toxic effects on a wide variety of biological systems. Reports about V inhalation toxicity on the CNS are limited, thus the purpose of this study is to determine the effects of Vanadium pentoxide (V(2)O(5)) inhalation (0.02M) on the memory and its correlation with the cytology of the hippocampus CA1. Forty eight CD-1 male mice were trained in spatial memory tasks and inhaled 1h twice a week; after each inhalation animals were evaluated and sacrificed from 1 to 4 weeks, perfused and processed for Golgi method and for ultrastructure evaluation. The cytological analysis consisted in counting the number of dendritic spines of 20 pyramidal neurons of hippocampus CA1, as well as ultrastructural characteristics. Results show that V inhalation produces a time dependent loss of dendritic spines, necrotic-like cell death, and notorious alterations of the hippocampus CA1 neuropile, which correlate with spatial memory impairment. Our data suggest that V induces important cellular and functional alterations, fact that deserves special attention since the concentration's trend of this element in the atmosphere is increasing.

Administration, Inhalation↗

Ependymal epithelium disruption after vanadium pentoxide inhalation. A mice experimental model.

The blood-brain barrier (BBB) protects the CNS against chemical insults. Regulation of blood-brain tissue exchange is accomplished by ependymal cells, which possess intercellular tight junctions. Loss of BBB function is an etiologic component of many neurological disorders. Vanadium (V) is a metalloid widely distributed in the environment and exerts potent toxic effects on a wide variety of biological systems. The current study examines the effects of Vanadium pentoxide (V2O5) inhalation in mice ependymal epithelium, through the analysis of the brain metal concentrations and the morphological modifications in the ependymal cells identified by scanning and transmission electron microscopy after 8 weeks of inhalation, in order to obtain a possible explanation about the mechanisms that V uses to enter and alter the CNS. Our results showed that V2O5 concentrations increase from the first week of study, stabilizing its values during the rest of the experiment. The morphological effects included cilia loss, cell sloughing and ependymal cell layer detachment. This damage can allow toxicants to modify the permeability of the epithelium and promote access of inflammatory mediators to the underlying neuronal tissue causing injury and neuronal death. Thus, understanding the mechanisms of BBB disruption would allow planning strategies to protect the brain from toxicants such as metals, which have increased in the atmosphere during the last decades and constitute an important health problem.

Administration, Inhalation↗

Sex differences in bronchiolar epithelium response after the inhalation of lead acetate (Pb).

In order to identify if there were sex differences in lead (Pb) lung concentrations and in bronchiolar response after its inhalation, a mice inhalation model was conducted. Sixty CD-1 adult mice from each sex inhaled separately, lead acetate 0.1 M for 1 h, thrice weekly during 15 days. Animals were evaluated for Pb-lung concentrations by atomic absorption spectrometry and for morphological evaluation by scanning electron microscopy (SEM). Higher Pb-lung concentrations were determined in females, however, more cell damage was found in males, finding that correlated with an increased loss of the nonciliated bronchiolar cells (NCBC) more sloughing and necrosis. Differences in particle clearance, oxidative stress handling, cytokines pathway activation and cytochrome P450 enzymes activity, all influenced by sex hormones, might be a possible explanation for our findings. The relevance of further studies in this field is stressed, as well as its relation to the different development expected for each sex in disease evolution, possible complications and treatment response.

Administration, Inhalation↗

Bilateral increase of perforated synapses after unilateral dopamine depletion.

In recent years attention has been focused on perforated synapses considering their possible involvement in synaptic plasticity in the nervous system. It has been hypothesized that an increase in the number of synapses may represent a structural basis for the enduring expression of synaptic plasticity during some events that involve memory and learning; also it has been suggested that perforated synapses increase in number after some experimental situations. The aim of this study was to analyze whether the dopamine depletion produces changes in the synaptology of the corpus striatum of rats after the unilateral injection of 6-OHDA. The findings suggest that after the lesion, both contralateral and ipsilateral striata present a significant increment in the number of perforated synapses, suggesting brain plasticity that might be an intent to recuperate the contact surface lost after endogenous or exogenous aggressions.

Animals↗

Bromocriptine treatment in a murine Parkinson's model: ultrastructural evaluation after dopaminergic deafferentation.

The objective of this article was to identify the effects of bromocriptine on the ultrastructure of the caudate nucleus in rats with a 6-hydroxidopamine (6-OHDA) unilateral lesion of the substantia nigra pars compacta. Eighteen Wistar male rats were stereotactically lesioned with 6-OHDA (n=12), or sham lesioned (n=6). Two days after rotational behavior was tested, and 2 days later, 6 rats were treated with 0.3 mg/Kg bromocriptine orally for a month and 6 rats were kept for the same time without treatment. The neuropile of the sham operated and bromocriptine-treated rats was well preserved contrary to the non-bromocriptine-treated rats. Also, it was found that there was a significant difference in the number of synaptic endings with edema in caudate of bromocriptine-treated rats compared with non-treated rats; however, the size of the synaptic endings were different to those found in the sham lesioned rats. Also, as in the sham lesioned group, the bromocriptines showed more synaptic contacts with dendritic spines contrasting to the non-treated group. The results suggest that bromocriptine possesses antioxidant properties because it decreased the ultrastructural alterations after 6-OHDA lesion.

Animals↗

Inhaled vanadium pentoxide decrease gamma-tubulin of mouse testes at different exposure times.

Vanadium is an important environmental and industrial pollutant whose concentrations have increased in the last decades. Due to its status as reproductive toxicant and a microtubule damaging agent, the present study investigated by immunohistochemistry the effect of the inhalation of vanadium pentoxide on gamma-tubulin within somatic and testicular germ cells. Male mice inhaled vanadium pentoxide (V2O5) (0.02 M) 1 h/twice a week for 12 weeks. Our results demonstrated that vanadium accumulates in the testes starting with the initial inhalation (24 h), and this pattern remained until the last week of treatment. In general, vanadium was capable of significantly decreasing the percentage of gamma-tubulin in all analyzed testicular cells (Sertoli, Leydig and germ cells) starting with the first week of treatment. For all cell types studied, regression analysis revealed a negative and significant relationship between the percentage of immunopositive cells to gamma-tubulin and exposure time, showing a time dependent response in all cases. Our findings suggest that alterations on this protein might imply changes in microtubule-involved function such as cell division, which in the testes might lead to damage in the spermatogenesis, leading probably to infertility.

Administration, Inhalation↗

Single-cell gel electrophoresis assay of nasal epithelium and leukocytes from asthmatic and nonasthmatic subjects in Mexico City.

The prevalence of asthma--a chronic inflammatory respiratory disease--is increasing worldwide. One hypothesis suggests that this trend is related to enhanced exposure to air pollutants. Chronic inflammation generates oxidative stress, and cells involved in an allergic reaction are capable of producing reactive oxygen species that may predispose asthmatics to increased deoxyribonucleic acid (DNA) damage. The authors estimated DNA strand breaks by use of single-cell gel electrophoresis assay on 2 different cell types (i.e., nasal epithelial cells and leukocytes) sampled from asthmatic and nonasthmatic medical students in Mexico City. The authors found that asthmatic subjects had more DNA breaks in their nasal epithelial cells than did their nonasthmatic counterparts. In contrast, asthmatic subjects had less damage in their leukocytes than did nonasthmatic individuals. These findings suggest that the hyperreactivity of the nasal epithelium prevents systemic effects from air pollutants, as reflected by less DNA injury to leukocytes of the asthmatic group. Asthmatic's nasal epithelial cells were more sensitive to DNA damage than were those of nonasthmatics--perhaps as a consequence of increased fragility induced either by air pollution or by a chronic inflammatory response.

Adolescent↗