Postischemic functional impairment of the kidney is a severe problem following living or caddaveric renal transplantation. It is well estabilished that a substantial component of psotischemic injury is caused by oxygen free radicals generated
from
xanthine ozsidase at ischemi/a/reperfusion (I/R) through lipid peroxidation. Glutathione is well known as a radical scavenger of oxygen free radicals. Malonyldialdehyde (MDA) is a stable end product of lipid peroxidation. The present study was
undertaken to investigate whether the meassurement of levels of xanthine oxidase activity, glutathione, and Mda in renal tissue could be used as indicators fo freulal function following I/R injury. 50 male Sprague-Dawley were divided into 3
groups;
control group (N=10), allopurinol-pretreatment group (Group A, N=20) and no-pretreatment group (Group B, N=20) for in-vitro and in-vivo study. Animals in in-vitro study underwent bilateral renal ischemia for 60 min after pretreatment with
allopurinol in
group A and saline in group B, and left nepohrectomy was then performed for study of ischemic injry. After 30 min of right renalf reperfusion, right jnepohrectomy was then perfomed for IjR injury study. Xanthine oxidase activity, glutathione, and
MDA
were measured in nephrectomized kidney tissues. In-vivo renal function studies were performed in both group A and B with measurement of creatinine clearance (Ccr) at 7th day of experiments after renal ischemia for 60 min. The xanthine oxidase
activity
decreased significantly in group A, but increased significantly in group B. the type conversion ratio increased significantly in group B. Glutathione levels dedcreased significatly in group B compared to group A. MDA levels increased
significantly
in
group B compared to group A. Ccr decreased significantly in group B compared to group A. Thus, it is suggested that the measurement of levels of xanthine oxidase jactivity, glutathione, and MDA in renal tissue following ischemia/reperfusion
injury
could
be used as indicators of renal function.
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