C-phycocyanin confers protection against oxalate-mediated oxidative stress and mitochondrial dysfunctions in MDCK cells

PLoS One. 2014 Apr 1;9(4):e93056. doi: 10.1371/journal.pone.0093056. eCollection 2014.

Abstract

Oxalate toxicity is mediated through generation of reactive oxygen species (ROS) via a process that is partly dependent on mitochondrial dysfunction. Here, we investigated whether C-phycocyanin (CP) could protect against oxidative stress-mediated intracellular damage triggered by oxalate in MDCK cells. DCFDA, a fluorescence-based probe and hexanoyl-lysine adduct (HEL), an oxidative stress marker were used to investigate the effect of CP on oxalate-induced ROS production and membrane lipid peroxidation (LPO). The role of CP against oxalate-induced oxidative stress was studied by the evaluation of mitochondrial membrane potential by JC1 fluorescein staining, quantification of ATP synthesis and stress-induced MAP kinases (JNK/SAPK and ERK1/2). Our results revealed that oxalate-induced cells show markedly increased ROS levels and HEL protein expression that were significantly decreased following pre-treatment with CP. Further, JC1 staining showed that CP pre-treatment conferred significant protection from mitochondrial membrane permeability and increased ATP production in CP-treated cells than oxalate-alone-treated cells. In addition, CP treated cells significantly decreased the expression of phosphorylated JNK/SAPK and ERK1/2 as compared to oxalate-alone-treated cells. We concluded that CP could be used as a potential free radical-scavenging therapeutic strategy against oxidative stress-associated diseases including urolithiasis.

MeSH terms

  • Adenosine Triphosphate / metabolism
  • Animals
  • Cell Survival / drug effects
  • Cytoprotection / drug effects*
  • Dogs
  • Enzyme Activation / drug effects
  • Lipid Peroxidation / drug effects
  • Madin Darby Canine Kidney Cells
  • Membrane Potential, Mitochondrial / drug effects
  • Mitochondria / drug effects
  • Mitochondria / metabolism
  • Mitochondria / pathology*
  • Mitogen-Activated Protein Kinases / metabolism
  • Oxalates / toxicity*
  • Oxidative Stress / drug effects*
  • Phycocyanin / pharmacology*
  • Protective Agents / pharmacology
  • Reactive Oxygen Species / metabolism

Substances

  • Oxalates
  • Protective Agents
  • Reactive Oxygen Species
  • Phycocyanin
  • Adenosine Triphosphate
  • Mitogen-Activated Protein Kinases

Grant support

The authors have no support or funding to report.