Renal oxidative injury after leukocyte transfer from ischemia-reperfusion-induced kidney damage in Balb/c mice.

The present study investigates the role of leukocyte transfer in the induction of kidney damage from mice that have undergone a severe renal ischemia-reperfusion insult into the intact recipient mice. First, Balb/c (inbred) mice were subjected to either sham operation (Sham donors) or bilateral renal IR injury (60 min ischemia-3 h reperfusion, IR donors). Leukocytes were isolated from blood and were transferred to two recipient groups: intact recipient mice received leukocytes from Sham donor group (Sham recipient) or from IR donor group (IR recipient). After 24 h, recipient mice were anesthetized for sample collections. Renal malondialdehyde increased and total glutathione concentration and superoxide dismutase activity decreased significantly in the IR recipient group compared to the Sham recipient group. BUN and plasma creatinine were significantly different between donor groups, but these parameters were not significantly different in the two recipient groups. In the IR donor group, there have been extensive changes in renal tissues comparing to Sham including severe destruction of the tubules, necrosis and tubular obstruction plus tubular flattening. IR recipient kidneys showed significant differences from their corresponding Sham group, demonstrating some degrees of injury including loss of brush borders from proximal tubules, cellular vacuolation and flattening of the tubules. However, less tissue damage was seen in this group comparing to IR donor kidneys. These findings showed that leucocytes transferred from post-ischemic mice induced oxidative stress and consequent damage to native kidneys, suggesting a role of leucocytes in the oxidative processes of reperfusion injury.

Antioxidant vitamins preserve superoxide dismutase activities in gentamicin-induced nephrotoxicity.

OBJECTIVE: The clinical use of gentamicin (G) is limited due to its known nephrotoxic actions. Generation of reactive oxygen species has been proposed as a causative factor of cell death in G-induced acute renal failure (ARF). Previous studies using superoxide dismutase (SOD) mimetics have indirectly suggested a role for the superoxide ion in G-induced ARF. In this study, we directly measured the enzyme activities using in situ isolated kidneys seeking to investigate the effects of antioxidant therapy on preservation of endogenous antioxidant levels in ARF. METHODS: Thirty-five male Sprague-Dawley rats were randomly assigned to 5 groups: control, Tyrode-perfused; G, gentamicin (200 mg/L) added to the perfusate; G + vitamin E (Vit E; 100 mg/100 g BW, IM); G + vitamin C (Vit C) added to the drinking water for 3 days (200 mg/L) and to the perfusate (100 mg/L); G + Vit E + Vit C. SOD activities were determined in renal tissues based on NAPDH oxidation at 340 nm by spectrophotometry. RESULTS: SOD activity was significantly reduced in the G group compared with the controls (P<.05). Administration of Vit E alone or in combination with Vit C significantly preserved enzyme activity levels compared with the G group (P<.05). CONCLUSION: Antioxidant vitamins have a role in preservation of renal endogenous antioxidant activities, namely SOD, in G-induced nephrotoxicity.