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

• Published in: PloS one 2014-04, Vol.9 (4), p.e93056
• Main Authors: Farooq, Shukkur M, Boppana, Nithin B, Devarajan, Asokan, Asokan, Devarajan, Sekaran, Shamala D, Shankar, Esaki M, Li, Chunying, Gopal, Kaliappan, Bakar, Sazaly A, Karthik, Harve S, Ebrahim, Abdul S
• Format: Article
• Language: English
• Subjects: Adenosine Triphosphate - metabolism; Analysis; Animals; Antioxidants; Apoptosis; ATP; Biology and Life Sciences; Cell Survival - drug effects; Cytoprotection - drug effects; Dogs; Drug dosages; Enzyme Activation - drug effects; Extracellular signal-regulated kinase; Fluorescein; Fluorescence; Free radicals; Health sciences; Hel protein; Infectious diseases; JNK protein; Kinases; Lipid peroxidation; Lipid Peroxidation - drug effects; Lipids; Lithiasis; Lysine; Madin Darby Canine Kidney Cells; Medicine; Medicine and Health Sciences; Membrane permeability; Membrane potential; Membrane Potential, Mitochondrial - drug effects; Mitochondria; Mitochondria - drug effects; Mitochondria - metabolism; Mitochondria - pathology; Mitogen-Activated Protein Kinases - metabolism; Orthopedics; Oxalates - toxicity; Oxalic acid; Oxidative stress; Oxidative Stress - drug effects; Oxygen; Pathogenesis; Permeability; Peroxidation; Pharmacy; Phycocyanin; Phycocyanin - pharmacology; Physiological aspects; Protective Agents - pharmacology; Reactive oxygen species; Reactive Oxygen Species - metabolism; Rodents; Staining; Toxicity; Urolithiasis
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0093056

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.