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Inhibition of Oxidative Stress in Renal Ischemia-Reperfusion Injury.
Anesth Analg. 2017 01; 124(1):204-213.A&A

Abstract

BACKGROUND

Superoxide, nitric oxide (NO), and peroxynitrite are important mediators in the pathogenesis of ischemia-reperfusion (I/R) injury. We tested the renoprotective effects of allopurinol (ALP), a xanthine oxidase inhibitor, N-nitro-L-arginine methyl ester (L-NAME), and 5,10,15,20-tetrakis (N-methyl-4-pyridyl) porphyrinato iron (III) (FeTMPyP) by selective inhibition of superoxide, NO, and peroxynitrite, respectively.

METHODS

Male Sprague-Dawley rats were randomly assigned to 5 groups (n = 6 per group). Group 1 was a sham-operated group. Group 2 was the renal I/R group (30-minute ischemia followed by 24-hour reperfusion). Rats in groups 3, 4, and 5 received ALP, L-NAME, or FeTMPyP, respectively, at 5 minutes before the reperfusion. Serum creatinine (Cr), blood urea nitrogen (BUN), renal tissue malondialdehyde, superoxide dismutase, histological changes, apoptosis, and monocyte infiltration were evaluated. In addition, the combined treatment with ALP and L-NAME was compared with FeTMPyP in a second independent experiment.

RESULTS

The administration of ALP, L-NAME, and FeTMPyP diminished the increase in Cr (P = .0066 for all) and BUN (P = .0066 for ALP; and P = .013 for L-NAME) induced by I/R injury and decreased the histological damage (P = .0066 for all). In addition, ALP, L-NAME, and FeTMPyP attenuated the oxidative stress response as determined by a decrease in malondialdehyde level (P = .0066 for all), apoptotic renal tubular cells (P = .0066 for all), and monocyte infiltration (P = .0066 for all). The combined treatment of ALP and L-NAME decreased Cr and BUN levels to a greater degree than FeTMPyP (P = .016 for Cr; P = .0079 for BUN).

CONCLUSIONS

Superoxide, NO, and peroxynitrite are involved in renal I/R injury. The reduction of peroxynitrite formation, via inhibition of superoxide or NO, or the induction of peroxynitrite decomposition may be beneficial in renal I/R injury.

Authors+Show Affiliations

From the *Department of Anesthesiology and Pain Medicine, School of Medicine, Kyungpook National University, Daegu, Korea; and †Department of Anesthesiology and Pain Medicine, Yeungnam University College of Medicine, Daegu, Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

27607480

Citation

Choi, Eun Kyung, et al. "Inhibition of Oxidative Stress in Renal Ischemia-Reperfusion Injury." Anesthesia and Analgesia, vol. 124, no. 1, 2017, pp. 204-213.
Choi EK, Jung H, Kwak KH, et al. Inhibition of Oxidative Stress in Renal Ischemia-Reperfusion Injury. Anesth Analg. 2017;124(1):204-213.
Choi, E. K., Jung, H., Kwak, K. H., Yi, S. J., Lim, J. A., Park, S. H., Park, J. M., Kim, S., Jee, D. L., & Lim, D. G. (2017). Inhibition of Oxidative Stress in Renal Ischemia-Reperfusion Injury. Anesthesia and Analgesia, 124(1), 204-213.
Choi EK, et al. Inhibition of Oxidative Stress in Renal Ischemia-Reperfusion Injury. Anesth Analg. 2017;124(1):204-213. PubMed PMID: 27607480.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Inhibition of Oxidative Stress in Renal Ischemia-Reperfusion Injury. AU - Choi,Eun Kyung, AU - Jung,Hoon, AU - Kwak,Kyung Hwa, AU - Yi,Soo Jin, AU - Lim,Jung A, AU - Park,Sol Hee, AU - Park,Jun-Mo, AU - Kim,Sioh, AU - Jee,Dae-Lim, AU - Lim,Dong Gun, PY - 2016/9/9/pubmed PY - 2017/7/14/medline PY - 2016/9/9/entrez SP - 204 EP - 213 JF - Anesthesia and analgesia JO - Anesth Analg VL - 124 IS - 1 N2 - BACKGROUND: Superoxide, nitric oxide (NO), and peroxynitrite are important mediators in the pathogenesis of ischemia-reperfusion (I/R) injury. We tested the renoprotective effects of allopurinol (ALP), a xanthine oxidase inhibitor, N-nitro-L-arginine methyl ester (L-NAME), and 5,10,15,20-tetrakis (N-methyl-4-pyridyl) porphyrinato iron (III) (FeTMPyP) by selective inhibition of superoxide, NO, and peroxynitrite, respectively. METHODS: Male Sprague-Dawley rats were randomly assigned to 5 groups (n = 6 per group). Group 1 was a sham-operated group. Group 2 was the renal I/R group (30-minute ischemia followed by 24-hour reperfusion). Rats in groups 3, 4, and 5 received ALP, L-NAME, or FeTMPyP, respectively, at 5 minutes before the reperfusion. Serum creatinine (Cr), blood urea nitrogen (BUN), renal tissue malondialdehyde, superoxide dismutase, histological changes, apoptosis, and monocyte infiltration were evaluated. In addition, the combined treatment with ALP and L-NAME was compared with FeTMPyP in a second independent experiment. RESULTS: The administration of ALP, L-NAME, and FeTMPyP diminished the increase in Cr (P = .0066 for all) and BUN (P = .0066 for ALP; and P = .013 for L-NAME) induced by I/R injury and decreased the histological damage (P = .0066 for all). In addition, ALP, L-NAME, and FeTMPyP attenuated the oxidative stress response as determined by a decrease in malondialdehyde level (P = .0066 for all), apoptotic renal tubular cells (P = .0066 for all), and monocyte infiltration (P = .0066 for all). The combined treatment of ALP and L-NAME decreased Cr and BUN levels to a greater degree than FeTMPyP (P = .016 for Cr; P = .0079 for BUN). CONCLUSIONS: Superoxide, NO, and peroxynitrite are involved in renal I/R injury. The reduction of peroxynitrite formation, via inhibition of superoxide or NO, or the induction of peroxynitrite decomposition may be beneficial in renal I/R injury. SN - 1526-7598 UR - https://www.unboundmedicine.com/medline/citation/27607480/Inhibition_of_Oxidative_Stress_in_Renal_Ischemia_Reperfusion_Injury_ L2 - https://doi.org/10.1213/ANE.0000000000001565 DB - PRIME DP - Unbound Medicine ER -