Journal
JOURNAL OF CHEMICAL NEUROANATOMY
Volume 31, Issue 2, Pages 114-123Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.jchemneu.2005.09.006
Keywords
neuronal damage; oxidative stress; ozone; dopamine; striatum; substantia niga
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The 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) Kluver-Barrera staining, and (4) immunohistochemistry for tyrosine hydroxylase (TH), dopamine and adenosine 3 ',5 '-monophosphate-regulated phosphoprotein of 32kD (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. (c) 2005 Elsevier B.V. All rights reserved.
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