Memory deterioration in an oxidative stress model and its correlation with cytological changes on rat hippocampus CA1

Avila-Costa, Marı́a Rosa; Colı́n-Barenque, Laura; Fortoul, Teresa I.; Machado‐Salas, Jesús; Espinosa-Villanueva, Jesús; Rugerio-Vargas, Concepción; Rivas‐Arancibia, Selva

doi:10.1016/s0304-3940(99)00458-9

Cited by 74 publications

(38 citation statements)

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“…Using the Third National Health and Nutrition Examination Survey (NHANES III) cohort, an association between annual ozone exposure and decreased cognitive function and short-term memory was observed in the adult population (Chen & Schwartz, 2009). Memory impairment was also observed in rats exposed to ozone acutely -exposure for 4 hours to 400-1000 ppb (Dorado-Martínez et al, 2001;Rivas-Arancibia et al, 2000;Avila-Costa et al, 1999) -and sub-chronically, 250 ppb for 15-90 days, 4 hours a day (Rivas-Arancibia et al, 2010). Exposure to ozone has also been associated with oxidative injury to various brain regions in the rat, including the striatum, substantia nigra, cerebellum, olfactory bulb, frontal and prefrontal cortex, either through acute high dose exposures (1 ppm for 4 hours: RivasArancibia et al, 2000), or longer duration low dose challenges (7-60 day exposure to 250 ppb ozone for 4 hours a day: Rivas-Arancibia et al, 2010;Martínez-Canabal et al, 2008;Mokoena et al, 2010;Guevara-Guzmán et al, 2009).…”

Section: Experimental and Panel Studiesmentioning

confidence: 99%

A rapid assessment of the impact of hazard reduction burning around Sydney, May 2016

Broome¹,

Johnston

Horsley

et al. 2016

Medical Journal of Australia

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This document presents answers to 24 questions relevant to reviewing European policies on air pollution and to addressing health aspects of these policies. The answers were developed by a large group of scientists engaged in the WHO project "Review of evidence on health aspects of air pollution -REVIHAAP". The experts reviewed and discussed the newly accumulated scientific evidence on the adverse effects on health of air pollution, formulating science-based answers to the 24 questions. Extensive rationales for the answers, including the list of key references, are provided. The review concludes that a considerable amount of new scientific information on the adverse effects on health of particulate matter, ozone and nitrogen dioxide, observed at levels commonly present in Europe, has been published in recent years. This new evidence supports the scientific conclusions of the WHO air quality guidelines, last updated in 2005, and indicates that the effects in some cases occur at air pollution concentrations lower than those serving to establish these guidelines. It also provides scientific arguments for taking decisive actions to improve air quality and reduce the burden of disease associated with air pollution in Europe.This publication arises from the project REVIHAAP and has been co-funded by the European Union. Keywords AIR POLLUTANTS AIR POLLUTION -ADVERSE EFFECTS ENVIRONMENT AND PUBLIC HEALTH EVIDENCE BASED PRACTICE GUIDELINES HEALTH POLICYAddress requests about publications of the WHO Regional Office for Europe to: Publications WHO Regional Office for Europe Scherfigsvej 8 DK-2100 Copenhagen Ø, Denmark Alternatively, complete an online request form for documentation, health information, or for permission to quote or translate, on the Regional Office web site (http://www.euro.who.int/pubrequest). © World Health Organization 2013All rights reserved. The Regional Office for Europe of the World Health Organization welcomes requests for permission to reproduce or translate its publications, in part or in full.The designations employed and the presentation of the material in this publication do not imply the expression of any opinion whatsoever on the part of the World Health Organization concerning the legal status of any country, territory, city or area or of its authorities, or concerning the delimitation of its frontiers or boundaries. Dotted lines on maps represent approximate borderlines for which there may not yet be full agreement.The mention of specific companies or of certain manufacturers products does not imply that they are endorsed or recommended by the World Health Organization in preference to others of a similar nature that are not mentioned. Errors and omissions excepted, the names of proprietary products are distinguished by initial capital letters.All reasonable precautions have been taken by the World Health Organization to verify the information contained in this publication. However, the published material is being distributed without warranty of any kind, either express or implied. ...

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Section: Experimental and Panel Studiesmentioning

confidence: 99%

A rapid assessment of the impact of hazard reduction burning around Sydney, May 2016

Broome¹,

Johnston

Horsley

et al. 2016

Medical Journal of Australia

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“…In addition, some studies have proposed a neuronal defense mechanism in which the cell tries to decrease the membrane surface exposed to free radicals, with the inal purpose to try to control the balance in the intraneuronal medium [63]. All these changes afect the number of synapses and the metabolic interaction between astrocytes and neurons.…”

Section: Free Radicals and Diseasesmentioning

confidence: 99%

Oxidative Stress, Inflammation, and Formation of Beta‐ Amyloid 1‐42 in Brain

Rivas‐Arancibia¹,

Rodrı́guez-Martı́nez²,

Méndez‐García³

et al. 2016

Free Radicals and Diseases

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Alzheimer's disease is characterized by the pathognomonic presence of intracellular neuroibrillary tangles containing hyperphosphorylated tau protein and extracellular senile plaques primarily formed by -amyloid. Both the neuroibrillary tangles and the plaques formed by -amyloid 1-42 are the inal result of a chain of events that progressed along with the disease for a long time. Oxidative stress plays a fundamental role among those events as proven by the experiments carried out using animal models. This can be demonstrated since there are studies indicating that, although the formation ofamyloid is inhibited through diferent mechanisms using drugs or speciic antibodies), cognitive deicit is not prevented. In this chapter, we will focus on reviewing the role the chronic state of oxidative stress plays in the development of Alzheimer's disease and how the loss of redox balance induces a vicious cycle that may change normal signaling. As a consequence, there are alterations in multiple metabolic pathways that end up in the formation of hyperphosphorylated tau and insoluble -amyloid, leading to the advance of a progressive neurodegeneration process. This is characterized by neuronal dead, astrocytic changes, microglia activation, and the loss of brain repair.Keywords: oxidative stress, Alzheimer's disease, -amyloid 1-42, ozone, neurodegeneration © 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.© 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. . IntroductionDespite a great deal of studies and the eforts of researchers in the ield, the physiopathology of Alzheimer's disease AD) is not yet clear. There is neither an accurate early diagnosis nor an efective treatment that allows the patients to have beter life expectancies [1]. Perhaps one of the most important problems to solve is understand that when the diagnosis is made, the symptoms and the signs of Alzheimer's disease are the result of a long chain of events that took place during an extended period of time and that such symptoms and signs change with time [2].One can assume that intracellular signaling and metabolic changes found during the early stages of the disease are not the same as the ones found at more advanced stages. For this reason, recent postmortem studies fail to completely clarify the physiopathology of this disease. . Changes at cellular level caused by chronic oxidative stressAcute oxidative stress is reversible and it is present in a number of physiological and pathological mechanisms that are reversible as well. These mechanisms play a defensive role ...

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“…Além disso, alterações na memória de longo prazo e diminuição das espículas dendríticas no hipocampo foram encontradas em ratos tratados com colchicina. 14 As propriedades dinâmicas dos microtúbulos são moduladas por proteínas denominadas proteínas associadas aos microtúbulos (MAPs, do inglês microtubule associated proteins). 15 As MAPs podem ser divididas em três famílias distintas: MAP1, MAP2 e tau.…”

Section: Citoesqueleto E Seus Componentesunclassified

O papel das proteínas do citoesqueleto na fisiologia celular normal e em condições patológicas

Monteiro

Kandratavicius

Leite

2011

J. epilepsy clin. neurophysiol.

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RESuMOIntrodução: O citoesqueleto é uma complexa rede de proteínas que determina a forma da célula. Ele é fundamental para que ocorra a movimentação celular; proporciona o suporte estrutural e mobilidade de organelas intracelulares e a estrutura para movimentação e separação de cromossomos durante a divisão celular. Os componentes principais do citoesqueleto são os microfilamentos, os filamentos intermediários e os microtúbulos. Os microtúbulos são formados por dímeros de a e b tubulina que se associam à proteínas específicas, as proteínas asssociadas aos microtúbulos (MAPs). A associação diferencial entre estas proteínas possibilita ampla variedade na modulação de função dos componentes do citoesqueleto no meio celular. As MAPs expressas no sistema nervoso central (SNC), MAP2 e tau, possuem diferentes isoformas geradas por processamento alternativo. O objetivo da presente revisão é de descrever e discutir as principais funções das proteínas do citoesqueleto em condições normais e patológicas, com destaque na fisiopatologia das epilepsias. Resultados: As MAPs possuem funções essenciais nas células neuronais, agem principalmente na formação estrutural destas células, garantindo sua morfologia e regulando funções específicas. Alterações nos níveis de expressão de proteínas estruturais estão envolvidas em diversas patologias do SNC como a esquizofrenia, a epilepsia do lobo temporal, as displasias corticais e as desordens do desenvolvimento. Estudos com modelos animais de epilepsia e tecido humano proveniente de pacientes epilépticos têm mostrado que as crises epilépticas podem modificar a expressão das proteínas do citoesqueleto. Conclusões: Apesar do significativo conhecimento existente sobre o citoesqueleto e proteínas associadas aos microtúbulos, não se sabe exatamente os mecanismos responsáveis pelas modificações estruturais encontradas em algumas patologias. Além do papel bem estabelecido do citoesqueleto como componente estrutural e citoarquitetônico, sua participação como facilitador do tráfico intracelular de neurotransmissores e outras macromoléculas é função ainda a ser melhor explorada e compreendida. unitermos: citoesqueleto, proteínas associadas aos microtúbulos, epilepsia do lobo temporal, neuropatologia, desordens do neurodesenvolvimento. ABSTRACT The role of cytoskeleton proteins in normal cell physiology and in pathological conditionsIntroduction: The cytoskeleton is a complex network of protein fibers that determines the shape of cells. It is essential for the movements of cells and provides the structural support and movements of organelles within the cells, and the framework for moving and separating chromosomes during the cell division. The main components of the cytoskeleton are microfilaments, intermediate filaments and microtubules. Microtubules are assembled dimers of a and b tubulin that bind to specific proteins, the microtubules associated proteins (MAPs). Differential association between these proteins enables a wide variety in functional modulation of the cytoskeleton components in the...

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Memory deterioration in an oxidative stress model and its correlation with cytological changes on rat hippocampus CA1

Cited by 74 publications

References 16 publications

A rapid assessment of the impact of hazard reduction burning around Sydney, May 2016

A rapid assessment of the impact of hazard reduction burning around Sydney, May 2016

Oxidative Stress, Inflammation, and Formation of Beta‐ Amyloid 1‐42 in Brain

O papel das proteínas do citoesqueleto na fisiologia celular normal e em condições patológicas

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