Antioxidant and inflammatory response after acute nitrogen dioxide and ozone exposures in C57Bl/6 mice

Ozone (O-3) and nitrogen dioxide (NO2) are highly reactive and toxic oxidan t pollutants. The objective of this study is to compare chemokine, cytokine , and antioxidant changes elicited by acute exposures of O-3 and NO2 in a g enetically sensitive mouse. Eight-week-old C57BI/6J mice were exposed to 1 or 2.5 ppm ozone or 15 of 30 ppm NO2 for 4 or 24 h. Changes in mRNA abundan ce in lung were assayed by slot blot and ribonuclease protection assay (RPA ). Messages encoding metallothionein (Mt), heme oxygenase 1 (HO-1), and ind ucible nitric oxide synthase (iNOS) demonstrated increased message abundanc e after 4 and 24 h of exposure to either O-3 or NO2. Furthermore, increases in message abundance were of a similar magnitude for O-3 and NO2. Messages encoding eotaxin, macrophage inflammatory protein (MIP)-1 alpha, and MIP-2 were elevated after 4 and 24 h of exposure to I ppm ozone. Interleukin-6 w as elevated after 4 h of exposure to ozone. After 4 h of 2.5 ppm ozone expo sure, increased mRNAs of eotaxin, MIP-1 alpha: MIP-2, Mt, MO-1, and iNOS we re elevated to a higher magnitude than were detected after I ppm ozone. Mon ocyte chemoattractant protein (MCP-1) was elevated following 15 ppm NO2 exp osure. After 4 h of 30 ppm NO2 exposure, messages encoding eotaxin, MIP-1 a lpha MIP-2, and MCP-I were elevated to levels similar to those detected aft er ozone exposure. Our results demonstrate a similar antioxidant and chemok ine response during both O-3 and NO2 exposure. Induction of these messages is associated with the duration and concentration of exposure. These studie s suggest that these gases exert toxic action through a similar mechanism.