Activity of nitric oxide synthase isoforms in acute brain oxidative damage induced by ozone exposure

Selective brain damage induced by ozone exposure. Ozone exposure induce superoxide radical (O●2) capable to produce an overproduction of proinflammatory markers as platelet-activating factor (PAF), tumor-necrotic factor (TNF) and gamma-interferon (IFɤ), as well as nitric oxide (NO) and peroxynitrite (ONOO), which reaching the brain tissue induce reactive oxygen species (ROS) and lipid peroxidation (LP). However, at the cerebral cortex of treated mice with the nitric oxide synthetase (NOS) inhibitor 7-Nitroindazole (7-NI), the LP expressed in Reactive Fluorescence Units (R.F.U./mg prot) showed significant decrease as compared to those treated with Solution Saline (SS), while the hippocampus (Hp) with Aminoguanidine (AMG) and the striatum (St) with L-G nitroarginine methyl ester (l-NAME) were also protected from the O3. Such effects indicated that the noxious effects of ozone over the central nervous system could occur as consequence of an overproduction of NO induced by an inflammatory reaction. [Display omitted] •The inhibition of NOS isoforms activity attenuates neuronal oxidative damage induced by ozone exposure.•The decrease in oxidative damage in the brain does not depend on the inhibition of a particular isoform.•The inhibition of the activity of the constitutive NOS isoforms decreases the damage in the cortex and the striatum.•In the hippocampus, inhibition of the iNOS isoform reduces oxidative damage.