Altered mitochondrial functioning induced by preoperative fasting may underlie protection against renal ischemia/reperfusion injury. Issue 1 (14th November 2012)

• Record Type: Journal Article
• Authors: Verweij, Mariëlle; Sluiter, Wim; van den Engel, Sandra; Jansen, Eugène; IJzermans, Jan N.M.; de Bruin, Ron W.F.
• Is Part Of: Journal of cellular biochemistry. Volume 114:Issue 1(2013:Jan.)
• Page Start: 230
• Page End: 237
• Publication Date: 2012-11-14
• Subjects: Cytochemistry -- Periodicals; 572
• DOI: 10.1002/jcb.24360
• Languages: English
• ISSNs: 0730-2312

Abstract

<abstract abstract-type="main" xml:lang="en"> <title>Abstract</title> <p>We reported previously that the robust protection against renal ischemia/reperfusion (I/R) injury in mice by fasting was largely initiated before the induction of renal I/R. In addition, we found that preoperative fasting downregulated the gene expression levels of complexes I, IV, and V of the mitochondrial oxidative phosphorylation (OXPHOS) system, while it did not change those of complexes II and III. Hence, we now investigated the effect of 3 days of fasting on the functioning of renal mitochondria in order to better understand our previous findings. Fasting did not affect mitochondrial density. Surprisingly, fasting significantly <italic>increased</italic> the protein expression of complex II of the mitochondrial OXPHOS system by 19%. Complex II‐driven state 3 respiratory activity was significantly reduced by fasting (46%), which could be partially attributed to the significant decrease in the enzyme activity of complex II (16%). Fasting significantly inhibited Ca<sup>2+</sup>‐dependent mitochondrial permeability transition pore opening that is directly linked to protection against renal I/R injury. The inhibition of the mitochondrial permeability transition pore did not involve the expression of the voltage‐dependent anion channel by fasting. In conclusion, 3 days of fasting clearly induces the inhibition of complex II‐driven mitochondrial respiration state 3 in part by decreasing the amount of functional complex II, and inhibits mitochondrial permeability transition pore opening. This might be a relevant sequence of events that could contribute to the protection of the kidney against I/R injury. J. Cell. Biochem. 114: 230–237, 2012. © 2012 Wiley Periodicals, Inc.</p> </abstract>