The concentration of IL-8 in nasal secretions is directly correlated with the severity of common cold symptoms in subjects with experimental RV colds. Preliminary data suggest that the elaboration of IL-8 by respiratory epithelial cells is mediated by changes in the oxidative state of the cell. The purpose of these studies was to describe the effect of RV infection on cellular redox enzyme activity and to determine the role of nitric oxide in RV-induced IL-8 elaboration. All studies were done in transformed respiratory epithelial cells (BEAS-2b). Total superoxide dismutase activity was increased in cells following RV challenge from 3.49 ±.24 to 4.42 ±.49 U/mg protein. This increase was due to a significant increase in CuZnSOD activity from 1.16 ±.31 to 2.55 ±.32 U/mg protein (p<0.05). This increase in activity was associated with an increased concentration of enzyme protein. In contrast, MnSOD, catalase, and glutathione peroxidase activities were not significantly different in RV challenged cells. Nitric oxide pathways do not appear to play a role in RV-induced IL-8 production. RV infection did not increase the concentration of nitrite in media supernatants, inhibitors of inducible nitric oxide synthetase did not affect IL-8 production by RV-challenged cells and treatment of the cells with nitric oxide donors did not stimulate IL-8 elaboration. The results of these studies suggest that changes in the oxidative state of BEAS-2b cells following RV infection are associated with induction of CuZnSOD. Nitric oxide does not appear to play a role in RV-induced IL-8 elaboration.