Oxygen radical generation during ischemia-reperfusion in the isolated perfused rat liver monitored by enhanced chemiluminescence.

Using luminol- and lucigenin-enhanced chemiluminescence (Lm-CL and Lg-CL), we monitored oxygen radical generation during ischemia-reperfusion in the isolated perfused rat liver. Both enhanced chemiluminescence levels decreased during 30 min of ischemia and increased markedly at the onset of reperfusion. When the liver was subjected to another 30 min of ischemia, reperfusion caused a progressive increase in both types of enhanced chemiluminescence. Administration of superoxide dismutase (SOD) into the perfusate strongly attenuated Lm-CL, but had a limited effect on Lg-CL. Catalase (CAT) and allupurionol (ALP) failed to attenuate both types of enhanced chemiluminescence. Thus the predominant oxygen radicals in the liver during reperfusion is superoxide and the lack of effect of ALP on oxygen radical generation indicates that hypoxanthine-xanthine oxidase reaction is unlikely to be a primary source of oxygen radicals. The different response to SOD in Lm-CL and Lg-CL is considered to be based on the diffusion space of luminol and lucigenin in the tissue. The relationship between oxygen radical levels and tissue damage, and the site of oxygen radical detection are discussed.