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Reactive oxygen species generated by renal ischemia and reperfusion trigger protection against subsequent renal ischemia and reperfusion injury in mice.
Am J Physiol Renal Physiol. 2010 Jan; 298(1):F158-66.AJ

Abstract

Ischemic preconditioning by a single event of ischemia and reperfusion (SIRPC) dramatically protects renal function against ischemia and reperfusion (I/R) induced several weeks later. We recently reported that reactive oxygen species (ROS) and oxidative stress were sustained in a kidney that had functionally recovered from I/R injury, thus suggesting an association between SIRPC and ROS and oxidative stress. However, the role of ROS in SIRPC remains to be clearly elucidated. To assess the involvement of ROS in SIRPC, mice were subjected to SIRPC (30 min of bilateral renal ischemia and 8 days of reperfusion) and then exposed to I/R injury. Thirty minutes of bilateral renal ischemia in the non-SIRPC mice resulted in a marked increase in plasma creatinine levels 4 and 24 h after reperfusion, which was not observed in the I/R in the SIRPC mice. SIRPC resulted in increases in the levels of kidney superoxide. Administrations of manganese(III) tetrakis(1-methyl-4-pyridyl) porphyrin [MnTMPyP; a cell-permeable superoxide dismutase (SOD) mimetic] and N-acetylcysteine (NAc; a ROS scavenger) to SIRPC mice blocked the SIRPC-induced increase in superoxide levels and removed approximately 48-64% of the functional protection of the SIRPC kidney. Additionally, these administrations significantly inhibited I/R-induced increases in superoxide formation, hydrogen peroxide production, and lipid peroxidation, along with the inhibition of I/R-induced reductions in the expression and activity of manganese SOD, copper-zinc SOD, and catalase. Furthermore, administrations of MnTMPyP or NAc inhibited the SIRPC-induced increase in inducible nitric oxide synthase expression but did not inhibit the SIRPC-induced increases in heat shock protein-25 expression. In conclusion, the renoprotection afforded by SIRPC was triggered by ROS generated by SIRPC.

Authors+Show Affiliations

Department of Anatomy, Kyungpook National University School of Medicine, Daegu, Republic of Korea.No affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

19864300

Citation

Kim, Jinu, et al. "Reactive Oxygen Species Generated By Renal Ischemia and Reperfusion Trigger Protection Against Subsequent Renal Ischemia and Reperfusion Injury in Mice." American Journal of Physiology. Renal Physiology, vol. 298, no. 1, 2010, pp. F158-66.
Kim J, Jang HS, Park KM. Reactive oxygen species generated by renal ischemia and reperfusion trigger protection against subsequent renal ischemia and reperfusion injury in mice. Am J Physiol Renal Physiol. 2010;298(1):F158-66.
Kim, J., Jang, H. S., & Park, K. M. (2010). Reactive oxygen species generated by renal ischemia and reperfusion trigger protection against subsequent renal ischemia and reperfusion injury in mice. American Journal of Physiology. Renal Physiology, 298(1), F158-66. https://doi.org/10.1152/ajprenal.00474.2009
Kim J, Jang HS, Park KM. Reactive Oxygen Species Generated By Renal Ischemia and Reperfusion Trigger Protection Against Subsequent Renal Ischemia and Reperfusion Injury in Mice. Am J Physiol Renal Physiol. 2010;298(1):F158-66. PubMed PMID: 19864300.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Reactive oxygen species generated by renal ischemia and reperfusion trigger protection against subsequent renal ischemia and reperfusion injury in mice. AU - Kim,Jinu, AU - Jang,Hee-Seong, AU - Park,Kwon Moo, Y1 - 2009/10/28/ PY - 2009/10/30/entrez PY - 2009/10/30/pubmed PY - 2010/1/12/medline SP - F158 EP - 66 JF - American journal of physiology. Renal physiology JO - Am J Physiol Renal Physiol VL - 298 IS - 1 N2 - Ischemic preconditioning by a single event of ischemia and reperfusion (SIRPC) dramatically protects renal function against ischemia and reperfusion (I/R) induced several weeks later. We recently reported that reactive oxygen species (ROS) and oxidative stress were sustained in a kidney that had functionally recovered from I/R injury, thus suggesting an association between SIRPC and ROS and oxidative stress. However, the role of ROS in SIRPC remains to be clearly elucidated. To assess the involvement of ROS in SIRPC, mice were subjected to SIRPC (30 min of bilateral renal ischemia and 8 days of reperfusion) and then exposed to I/R injury. Thirty minutes of bilateral renal ischemia in the non-SIRPC mice resulted in a marked increase in plasma creatinine levels 4 and 24 h after reperfusion, which was not observed in the I/R in the SIRPC mice. SIRPC resulted in increases in the levels of kidney superoxide. Administrations of manganese(III) tetrakis(1-methyl-4-pyridyl) porphyrin [MnTMPyP; a cell-permeable superoxide dismutase (SOD) mimetic] and N-acetylcysteine (NAc; a ROS scavenger) to SIRPC mice blocked the SIRPC-induced increase in superoxide levels and removed approximately 48-64% of the functional protection of the SIRPC kidney. Additionally, these administrations significantly inhibited I/R-induced increases in superoxide formation, hydrogen peroxide production, and lipid peroxidation, along with the inhibition of I/R-induced reductions in the expression and activity of manganese SOD, copper-zinc SOD, and catalase. Furthermore, administrations of MnTMPyP or NAc inhibited the SIRPC-induced increase in inducible nitric oxide synthase expression but did not inhibit the SIRPC-induced increases in heat shock protein-25 expression. In conclusion, the renoprotection afforded by SIRPC was triggered by ROS generated by SIRPC. SN - 1522-1466 UR - https://www.unboundmedicine.com/medline/citation/19864300/Reactive_oxygen_species_generated_by_renal_ischemia_and_reperfusion_trigger_protection_against_subsequent_renal_ischemia_and_reperfusion_injury_in_mice_ L2 - https://journals.physiology.org/doi/10.1152/ajprenal.00474.2009?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -