Abstract
Purpose. In this research ACE activity (as a marker of epithelial injury) was studied in rats with gentamicin induced renal toxicity. Methods. Male Sprague-Dawley rats were sacrificed 1, 3, 5, and 7 days after gentamicin injection, 100 mg/kg/day for 1, 3, 5, and 7 consecutive days. ACE activity was measured in serum, kidney and lung. These data were compared with normal saline-treated rats. Histological scoring of renal cortical pathology was performed on days 1, 3, 5, and 7. Results. Treatment of rats with gentamicin resulted in renal damage evidenced by proteinuria, polyuria, and decreased creatinine clearance. The damage to the kidney proximal tubule was evident by (a) the histological analysis at light microscopy and (b) the augmentation in the urinary excretion of N-acetyl-β-d-glucosaminidase (NAG). Kidney ACE activity decreased while lung and serum ACE activity didn’t change until day 7. Lung ACE activity increased significantly on day 7. Kidney and serum ACE activity increased too. Blood pressure increased significantly on day 7. This corresponded well with the lung ACE activity increment. Conclusion. These data suggest that kidney ACE activity decreased significantly just one day after gentamicin administration and prior to kidney NAG decrease.
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