Biomedical subjects

Patricia Mussali-Galante

Publications and source records attributed to Patricia Mussali-Galante.

9 recordsLinked to original sources

PubMed2006

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↗

PubMed2006

Thrombocytosis induced in mice after subacute and subchronic V2O5 inhalation.

Reports about vanadium (V) inhalation toxicity on the hematopoietic system, specifically about coagulation are limited. Therefore, we decided to evaluate the effects of V with a complete blood count and morphologic analysis of platelets on blood smears. CD-1 male mice inhaled V2O5 0.02 M 1 h twice weekly over 12 weeks. Blood samples were obtained by direct heart puncture; Wright stained smears were used for platelet quantification. An increase in platelet count from the third week of exposure was observed, as well as the presence of megaplatelets. Our results demonstrate, for the first time, that V induces thrombocytosis and it might correlate with some thromboembolic diseases. Further analysis is needed to evaluate the functionality of these platelets as well as the cause of its increase.

Administration, Inhalation↗

PubMed2005

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↗

PubMed2005

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↗

PubMed2005

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↗

PubMed2005

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↗

PubMed2004

Metal mixture inhalation (Cd-Pb) and its effects on the bronchiolar epithelium. An ultrastructural approach.

The current study explores the effects of the inhalation of lead (Pb), Cd and its mixture (Pb-Cd) in a mice model, analysing metal concentrations in the lung, and the morphological modifications in the bronchiolar epithelium identified by scanning electron microscopy after eight weeks of inhalation. Our results indicate that metal concentrations in lung were higher compared to controls; however, Pb concentrations drastically decrease in the mixture. This reduction was also observed in the inhalation chamber. The main changes observed in the bronchiole were mostly in the mixture. The modifications were mainly given by Cd alone and in the mixture, with a decreased number of nonciliated bronchiolar cells and an increased number of bundles of dividing cells. The additive effect of Pb-Cd is suggested, as the extensive damage observed was more evident when mice were exposed to the mixture, and the results endured more research in the area of inhaled mixtures.

Administration, Inhalation↗

PubMed2003

Nasal cytology and genotoxic damage in nasal epithelium and leukocytes: asthmatics versus nonasthmatics.

BACKGROUND: The best example of a chronic inflammatory respiratory disease is asthma, a disease which has an increasing prevalence worldwide. This chronic inflammation is also related to the generation of oxidative stress since the cells involved in the allergic reaction are capable of producing reactive oxygen species (ROS), and this might predispose asthmatics to increased genotoxic damage. METHODS: A respiratory symptomatology questionnaire was self-applied by asthmatic and nonasthmatic students. A single cell gel electrophoresis assay in two different cell types (nasal epithelial cells and leukocytes) was performed, and the cytology of the nasal smears stained with HE was evaluated. RESULTS: Both groups reported having a runny nose. Asthmatics had greater DNA damage in the nasal epithelial cells in contrast to nonasthmatics. In leukocytes no statistical significance in DNA damage was identified. Metaplasia was evident in asthmatics that also showed eosinophils and neutrophils as well as goblet cells and mucus at a higher frequency compared with nonasthmatics. CONCLUSIONS: Nasal symptoms did not correlate with genotoxic damage, since they were reported in both groups. Nasal epithelial cells of asthmatics are more sensitive to genotoxic damage, and chronic inflammatory response. Also the activity of eosinophils might mediate the DNA damage through the generation of ROS.

Adult↗

PubMedDate not supplied

Ultrastructural modifications in the mitochondrion of mouse Sertoli cells after inhalation of lead, cadmium or lead-cadmium mixture.

CD-1 mice inhaled 0.01 M lead acetate, 0.006 M cadmium chloride or Pb-Cd mixture during 1h twice a week during 4 weeks. Testes were processed for transmission electron microscopic analysis. The percentage of damaged mitochondria was related to exposure time and the type of metal inhaled, noticing more damage when the mixture was administered. A dose-time relationship was found. Cadmium chloride caused the most severe mitochondrial alteration compared to lead acetate, whereas the mixture was more aggressive compared with each metal alone. Our results suggest that the changes in Sertoli cell could lead to a transformation process that may interfere with spermatogenesis.

Administration, Inhalation↗