Postconditioning ameliorates mitochondrial DNA damage and deletion after renal ischemic injury.

ABSTRACT:

Background

Reactive oxygen species (ROS) play a major role in causing injury in ischemia-reperfusion (I/R). Mitochondrial DNA (mtDNA) is particularly vulnerable to oxidative damage. We propose that increased mitochondrial ROS production is likely to damage mtDNA, causing further injury to mitochondria, and postconditioning (POC) may ameliorate kidney I/R injury by mitigating mitochondrial damage.

Methods

Rats were divided into seven groups: (i) Sham-operated animals with an unconstricted renal artery; (ii) Sham + 5-hydroxydecanoate (5-HD); (iii) I/R; (iv) I/R + 5-HD; (v) POC; (vi) Sham POC and (vii) POC + 5-HD. Renal injury, oxidative DNA damage, mtDNA deletions, mitochondrial membrane potential (MMP) and expression of the ATP-sensitive K(+) (KATP) channel subunit Kir6.2 wer

SUBMITTER: Tan X 

PROVIDER: S-EPMC3811057 | biostudies-literature | 2013 Nov

REPOSITORIES: biostudies-literature