title: In vivo imaging of oxidative stress in ischemia-reperfusion renal injury using electron paramagnetic resonance.
abstract: Oxidative stress during ischemia-reperfusion acute renal failure (IR-ARF) was noninvasively evaluated with in vivo electron paramagnetic resonance (EPR) imaging. Female ICR mice underwent left nephrectomy and 30-min ischemia-reperfusion of the right kidney. Oxidative stress was evaluated as organ reducing activity with the half-lives of the spin probe 3-carbamoyl-2,2,5,5-tetramethylpyrrolidine-1-oxyl (carbamoyl-PROXYL) using 1) conventional L-band EPR, which showed organ-reducing activity in the whole abdominal area; and 2) EPR imaging, which showed semiquantitative but organ-specific reducing activity. The results were compared with the reducing activity of organ homogenate and phosphatidylcholine hydroperoxide (PC-OOH) concentrations. Half-lives of carbamoyl-PROXYL in the whole upper abdominal area, measured by L-band EPR, were prolonged on day 3 after ischemia-reperfusion and recovered to the level of nontreated mice on day 7. This trend resembled closely that of serum creatinine and blood urea nitrogen concentration. The EPR imaging-measured carbamoyl-PROXYL half-life was also prolonged on day 3 in both the kidney and the liver. However, in the kidney this showed only partial recovery on day 7. In the liver, this convalescence was more remarkable. The ex vivo studies of organ reducing activity and PC-OOH agreed with the results from EPRI, but not with those from L-band EPR. These results indicate that renal reducing activity shows only partial recovery on day 7 after ischemia-reperfusion, when serum creatinine and blood urea nitrogen have recovered. EPR imaging is an appropriate and useful method for the noninvasive evaluation of oxidative stress in the presence of renal injury.
authors.affiliation: Dept. of Nephrology, Institute of Clinical Medicine, Univ. of Tsukuba, Tennodai, Tsukuba, Ibaraki, Japan 305-8575. aki-hira@md.tsukuba.ac.jp
authors.forename: Aki
authors.initials: A
authors.lastname: Hirayama
authors.forename: Sohji
authors.initials: S
authors.lastname: Nagase
authors.forename: Atsushi
authors.initials: A
authors.lastname: Ueda
authors.forename: Takaaki
authors.initials: T
authors.lastname: Oteki
authors.forename: Kenji
authors.initials: K
authors.lastname: Takada
authors.forename: Mami
authors.initials: M
authors.lastname: Obara
authors.forename: Mariko
authors.initials: M
authors.lastname: Inoue
authors.forename: Keigyou
authors.initials: K
authors.lastname: Yoh
authors.forename: Kouichi
authors.initials: K
authors.lastname: Hirayama
authors.forename: Akio
authors.initials: A
authors.lastname: Koyama
mesh_terms: D058186:Acute Kidney Injury / Q000473:pathology; D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D001806:Blood Urea Nitrogen; D003404:Creatinine / Q000097:blood; D003497:Cyclic N-Oxides / Q000378:metabolism; D003952:Diagnostic Imaging / Q000379:methods*; D004578:Electron Spin Resonance Spectroscopy / Q000379:methods*; D005260:Female; D006207:Half-Life; D007091:Image Processing, Computer-Assisted; D007668:Kidney / Q000378:metabolism / Q000473:pathology*; D008099:Liver / Q000378:metabolism; D051379:Mice; D008813:Mice, Inbred ICR; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000502:physiology*; D010713:Phosphatidylcholines / Q000378:metabolism; D011759:Pyrrolidines / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D015427:Reperfusion Injury / Q000473:pathology*
chemical_list: D000975:Antioxidants; D003497:Cyclic N-Oxides; D010713:Phosphatidylcholines; D011759:Pyrrolidines; D017382:Reactive Oxygen Species; C057590:phosphatidylcholine hydroperoxide; C077426:3-carbamoyl-2,2,5,5-tetramethyl-1-pyrrolidinyl-N-oxyl; D003404:Creatinine