C- Phycocyanin Confers Protection against Oxalate-Mediated Oxidative Stress and Mitochondrial Dysfunctions in MDCK Cells

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.