Smoke inhalation injury is associated with high incidence of pulmonary complications as it represents a major cause of mortality after major burn injury. Burn is associated with release of inflammatory mediators which ultimately cause local and distant pathophysiological effects. The present study investigated the effect of smoke inhalation or\and burn injury on the antioxidants status in the lungs in a rat model to simulate an inhalation injury as might be encountered by firefighters and burn victims. Seventy five rats were equally randomized to five groups: Sham group, smoke inhalation injury group, burn group, sham burn group, and smoke burn group. At the end of the exposure protocol rats were killed by cervical decapitation and the lungs were removed completely and processed for histopathological and biochemical analysis by measuring lung antioxidant enzyme activities: Malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GPs) level, as an index of lipid peroxidation. Grossly, results showed that rats´lungs in the smoke inhalation group and the smoke burn group showed multiple hemorrhagic spots. Light microscopic examination showed localized and diffuse alveolar hemorrhage. Two rats in the burn group had evidence of pneumonia and lung abscesses. Biochemically, results showed that both smoke inhalation and burn injury significantly elevated lung MDA and glutathione peroxidase levels when compared with controls. The combined smoke and burn group resulted in a more significant rise in both antioxidant levels indicating a higher level of lipid peroxidation. SOD level was significantly lowered on exposure to both conditions when compared to control. SOD level was significantly lower in the combined injury group when compared to either smoke or burn alone. In conclusion; the above data provide evidence that inhalation injury with and without burn decrease tissue antioxidant capacity and increase tissue peroxidative injury.