Abstract NO2 is a well-known indoor and outdoor pollutant that may cause adverse health problems. Recently, accumulating but extremely limited evidences show that NO2 possibly express neurotoxicity and is responsible for various neurological disorders. In the present study, neurological hazard of NO2 and possible mechanisms were determined in rat pallium following a repetitive inhalation exposure with various concentrations (5, 10 and 20mg/m3). After 7-day exposure (6h/day), observable adverse effects were induced encompassing decreased ratio of brain to body weight, mild brain pathology, increased neuronal apoptosis, altered antioxidants (Cu/Zn-SOD, Mn-SOD, GPx and NO) activity and increasing formation of PCO. NO2 inhalation also induced augment of oncogenes (c-fos, c-jun) levels, and deregulation of apoptosis-related genes (p53, bax and bcl-2) expression. With all above data, the present report provided essential information for the characterization of the neurotoxic hazard of NO2 and related mechanisms, which is required in response to the general concern about the vulnerability of the neurological system to it.