Renal Mitochondrial Lipid Peroxidation during Sepsis
Singh P, Parajuli N, Mayeux PR and MacMillan-Crow LA*
Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, USA
- *Corresponding Author:
- Lee Ann MacMillan-Crow, Ph.D.
Department of Pharmacology and Toxicology
University of Arkansas for Medical Sciences
325 Jack Stephens Drive
Biomedical Building I, 323D
Little Rock, AR 72205, USA
E-mail: [email protected]
Received Date: December 02, 2015; Accepted Date: February 18, 2016; Published Date: February 29, 2016
Citation: Singh P, Parajuli N, Mayeux PR, MacMillan-Crow LA (2016) Renal Mitochondrial Lipid Peroxidation during Sepsis. J Kidney 2:116. doi:10.4172/2472-1220.1000116
Copyright: © 2016 Singh P, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Sepsis can provoke kidney injury, which increases mortality. Human and animal studies have documented increased renal oxidative injury and mitochondrial damage during sepsis. However, few studies have attempted to dissect specific renal targets and/or types of oxidative injury using the cecal ligation and puncture (CLP) murine model of sepsis. The purpose of this short communication is to examine the extent of lipid peroxidation within renal mitochondria using CLP and blue native gel electrophoresis which separates intact mitochondrial respiratory complexes. Our results show that CLP induced increased 4-hydroxy-nonenal protein adduction (marker of lipid peroxidation) in renal homogenates and mitochondrial fractions. Blue native gel electrophoresis revealed that respiratory complex III was selectively targeted within mitochondrial fractions. This supports our prior report showing renal complex III inactivation following CLP. Future studies will identify specific renal proteins within complex III that are modified during sepsis to provide mechanistic insight on how mitochondrial respiration is inhibited during sepsis.