Abstract

Activation of transcription factor NF-?B (electrophoretic mobility shift assay) was investigated in the isolated perfused rat liver infused with 0.5 mg of colloidal carbon/ml for 5-20 min, in relation to carbon phagocytosis and carbon-induced O2 consumption. Experiments were carried out in control rats and in animals treated with the Kupffer cell inactivator gadolinium chloride (GdCl3). Carbon uptake and carbon-induced O2 consumption by perfused livers exhibited a linear increase as a function of the perfusion time, leading to constant O2/carbon uptake ratios, with low (0.04-0.15%) fractional sinusoidal lactate dehydrogenase release in the 5-20 min perfusion time studied. NF-?B DNA binding activity showed a maximal enhancement at 10 min of carbon perfusion, a response that was sustained at a lower extent at 15 and 20 min of carbon stimulation. After 10 min of carbon infusion, NF-?B activation, carbon-induced O2 consumption, and carbon uptake were diminished by 84%, 94%, and 64% by GdCl3 treatment (P < 0.05), respectively. It is concluded that the respiratory burst of carbon-stimulated Kupffer cells triggers NF-?B activation in the isolated perfused liver, a response that is elicited under optimal conditions of Kupffer cell function and organ viability.