SOURCE OF REACTIVE OXYGEN SPECIES IN ANTI-THY1 NEPHRITIS

In proliferative glomerulonephritis, both macrophages and mesangial ce lls generate reactive oxygen species (ROS), contributing to the develo pment of glomerular injury. We have attempted to determine which cell produces ROS during anti-Thyl nephritis (ATN) in rats. The generation of ROS was studied using luminol amplified chemiluminescence (GCL) on isolated glomeruli. Immunohistochemical studies used avidin-biotin com plex (ABC) to label macrophages and mesangial cells. Immediately after ATN induction, mesangiolysis and infiltration with ED-1 positive cell s (referred to as macrophage) was noted with a peak at day 1. After da y 4, mesangial proliferation appeared with a decrease of the ED-1 posi tive cells and a prominent increase of PCNA positive cells (regarded a s mesangial cells). In the early phase of ATN, GCL, reflecting ROS gen eration; increased along with the appearance of ED-1 positive cells. G CL subsequently decreased as mesangial cells increased This suggested that macrophage were the principal participants in ROS generation in t he early phase of ATN although mesangial cells cannot be completely di sregarded in the generation of ROS and development of glomerular injur y.