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ToxSci Advance Access published online on October 15, 2009
Toxicological Sciences, doi:10.1093/toxsci/kfp252
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© The Author 2009. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org

Oxidative Stress Caused by Ozone Exposure Induces Loss of Brain Repair in The Hippocampus of Adult Rats

Selva Rivas-Arancibia*, Rosalinda Guevara-Guzmán*, Yolanda López-Vidal{dagger}, Erika Rodríguez-Martínez*, Margarete Zanardo Gomes{ddagger}, Mariana Angoa-Pérez* and Rita Raisman-Vozari{ddagger}

* Departamento de Fisiología, Universidad Nacional Autónoma de México, AP 70-250, CP 04510, México, D.F., México {dagger} Departamento de Microbiología y Parasitología, Universidad Nacional Autónoma de México, AP 70-250, CP 04510, México, D.F., México {ddagger} INSERM, UMRS 975, CRICM, Experimental Therapeutics of Neurodegeneration, Hôpital de la Salpêtrière, Paris, France

Corresponding author: Selva Rivas-Arancibia, Physiology Department, Faculty of Medicine, National Autonomous University of Mexico, CP 04510, AP 70-250, México City, Mexico. Phone number: +525556232500, FAX +525556232241 E-mail srivas{at}servidor.unam.mx

Received August 18, 2009; revision received October 8, 2009; accepted October 12, 2009


  Abstract

Oxidative stress is involved in many neurodegenerative diseases. Chronic ozone exposure causes a secondary increase of reactive oxygen species, which cause an oxidative-stress state in the organism. Ozone is one of the main components of photochemical pollution. Our purpose was to test that oxidative stress caused by chronic low doses of ozone, by itself, alters adult neurogenesis and causes progressive neurodegeneration in the hippocampus, which actions lead to the loss of brain plasticity in the mature central nervous system of rats. Animals were exposed to an ozone-free air stream and for 15, 30, 60, and 90 days to low doses of ozone to cause oxidative stress. Each group was then tested by 1) a spectrophotometer test to quantify lipid peroxidation levels, 2) immunohistochemistry testing against doublecortine, Neu-N, p53, microglia, and glial fibrillary-acidic protein (GFAP), 3) western blot tests for doublecortine and Neu-N, and 4) a one-trial passive avoidance test. Our results indicated that ozone causes an increase of lipid peroxidation levels, morphological changes in the nucleus and the cytoplasm, and cell swelling in neurons. The western blot shows a decrease for Neu-N and doublecortine. Activated and later phagocytic microglia and an increased number of astrocytes were found. There was a memory deficiency positively related to the amount of ozone exposure. These alterations suggest that oxidative stress caused by low doses of ozone causes dysregulation of inflammatory processes, progressive neurodegeneration, chronic loss of brain repair in the hippocampus, and brain plasticity changes in the rat analogous to those seen in Alzheimer's disease.

Key Words: oxidative stress; ozone; neurogenesis; neurodegeneration.


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