Protection by vitamin B-2 against oxidant-mediated acute lung injury

The effect of vitamin B-2 (riboflavin) on oxidant-mediated acute lung injur y has been examined in three different rat models. Pulmonary injury was ind uced by intravenous injection of cobra Venom factor (CVF), by the intrapulm onary deposition of IgG immune complexes, or by hind limb ischemia-reperfus ion. In each of the three models, injury was characterized by increases in vascular permeability (leakage of I-125-labeled bovine serum albumin), alve olar hemorrhage (extravasation of Cr-51-labeled rat erythrocytes), and neut rophil accumulation (myeloperoxidase activity). Intraperitoneal administrat ion of riboflavin at a dose of 6 mu moles/kg body weight reduced vascular l eakage by 56% in the CVF model, by 31% in the immune complex model, and by 53% in the lung injury model following ischemia-reperfusion of the hind lim bs. Similar treatment reduced hemorrhage by 76%, 51%, and 70% in the three models of lung injury. In the CVF model, riboflavin was also shown to decre ase products of lipid peroxidation (conjugated dienes) in lungs (by 45%) an d in plasma (by 74%). Neutrophil accumulation in the lungs was not influenc ed by riboflavin administration in any of the three models. The studies dem onstrate that riboflavin can mount a significant protection against oxidant -mediated inflammatory organ injury.