Abstract
In order to clarify the mechanism of pathophysiology of renal damage due to viral infection, we measured generation of superoxide anion (O-2) in isolated rat glomeruli under basal conditions, and also under inoculation with inactivated or live cox-sackievirus B4 (Cox. B4, 102 TCD50/0.1 ml) in the presence of phytohemagglutinin (PHA) or concana-valin A (Con A) as a stimulant. Release of O-2from isolated rat glomeruli was determined spectroscopically on the basis of SOD-inhibitable reduction of ferricytochromec.
Generation of O-2stimulated by PHA or Con A was increased, and was dose-dependant. Live Cox. B4 enhanced O-2generation in isolated rat glomeruli, while inactivated Cox. B4 did not. Furthermore, O-2generation in isolated rat glomeruli cultured with live Cox. B4 for 24 hours was more increased than with only medium under stimulation with PHA.
These results suggest that the enhancement of O-2generation during Cox. B4 infection is an important factor in the pathophysiology of renal damage due to viral infection.
