It has been proposed that molecules derived from reactions that occur between the ozone and the lung tissue mediate nonpulmonary effects caused by ozone exposure. Free radicals are among those proposed molecules that flow throughout the bloodstream to other organs producing lipid peroxidation. In order to elucidate on aspect of ozone toxicity mechanisms, we measured the thiobarbituric acid-reactive products (TBARS), as an index of lipid peroxidation, in a variety of brain regions in rats exposed to 1 ppm of ozone for 1, 3, 6, and 9h. Another group exposed to 9h of O(3) plus 3h of clean-air exposure was also included. The results showed an important increase in TBARS content in all the studied structures. Such effect seems to be transient. These findings indicates that acute ozone exposure can produce cerebral peroxidation as it has been found in rats exposed chronically, suggesting an involvement of free radicals in brain effects of ozone exposure.