title: Renal oxidative injury after leukocyte transfer from ischemia-reperfusion-induced kidney damage in Balb/c mice.
abstract: 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.
authors.affiliation: Tehran University of Medical Sciences Department of Physiology, Faculty of Medicine Tehran Iran Tehran University of Medical Sciences Department of Physiology, School of Medicine Tehran 14176-13151 Iran.
authors.forename: Mehri
authors.initials: M
authors.lastname: Kadkhodaee
authors.forename: H
authors.initials: H
authors.lastname: Khastar
authors.forename: B
authors.initials: B
authors.lastname: Seifi
authors.forename: A
authors.initials: A
authors.lastname: Najafi
authors.forename: F
authors.initials: F
authors.lastname: Delavari
mesh_terms: D000818:Animals; D005978:Glutathione / Q000378:metabolism; D007668:Kidney / Q000098:blood supply* / Q000503:physiopathology; D007674:Kidney Diseases / Q000378:metabolism / Q000503:physiopathology*; D007687:Kidney Tubules, Proximal / Q000378:metabolism / Q000503:physiopathology*; D017708:Leukocyte Transfusion / Q000379:methods; D007962:Leukocytes / Q000378:metabolism / Q000502:physiology*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009336:Necrosis / Q000378:metabolism / Q000503:physiopathology; D018384:Oxidative Stress / Q000502:physiology*; D015427:Reperfusion Injury / Q000378:metabolism / Q000503:physiopathology*; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D013482:Superoxide Dismutase; D005978:Glutathione