• Naira Pereyra-Muñoz, Concepción Rugerio-Vargas, Mariana Angoa-Pérez, Gabino Borgonio-Pérez, and Selva Rivas-Arancibia.
• Physiology Department, Faculty of Medicine, National Autonomous University of Mexico, CP 04510, AP 70-250, Mexico-City, Mexico.
• J. Chem. Neuroanat. 2006 Feb 1;31(2):114-23.

AbstractThe purpose of this work was to study if chronic low-dose ozone exposure could per se induce oxidative damage to neurons of striatum and substantia nigra. Thirty male Wistar rats were divided into three groups--Group 1: exposed to an air stream free of ozone; Group 2: exposed for 15 days to ozone; Group 3: exposed for 30 days to ozone. Ozone exposure was carried out daily for 4 h at a 0.25 ppm dose. Each group was then tested for (1) motor activity, (2) quantification of lipid peroxidation levels, (3) Klüver-Barrera staining, and (4) immunohistochemistry for tyrosine hydroxylase (TH), dopamine and adenosine 3',5'-monophosphate-regulated phosphoprotein of 32 kD (DARPP-32), inducible nitric oxide synthase (iNOS), and superoxide dismutase (SOD), to study neuronal alterations in striatum and substantia nigra. Results indicate that ozone exposure causes a significant decrease in motor activity. Ozone produced lipid peroxidation, morphological alterations, loss of fibers and cell death of the dopaminergic neurons. The DARPP-32, iNOS and SOD expression increased with repetitive ozone exposure. These alterations suggest that ozone causes oxidative stress which induces oxidative damage to substantia nigra and striatum of the rat.

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