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

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

Author information

1
Department of Pharmacy Practice, Eugene Applebaum College of Pharmacy and Health Sciences, Wayne State University, Detroit, Michigan, United States of America.
2
Department of Pharmaceutical Sciences, Eugene Applebaum College of Pharmacy and Health Sciences, Wayne State University, Detroit, Michigan, United States of America.
3
Department of Medicine, University of California Los Angeles, Los Angeles, California, United States of America.
4
Department of Medical Microbiology, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia.
5
Tropical Infectious Diseases Research and Education Center (TIDREC), Department of Medical Microbiology, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia.
6
Department of Biochemistry and Molecular Biology, Wayne State University, School of Medicine, Detroit, Michigan, United States of America.
7
Department of Orthopedics, National Orthopedics Center for Excellence in Research and Learning (NOCERAL), Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia.
8
Department of Anatomy, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
9
Department of Internal Medicine, Wayne State University, Detroit, Michigan, United States of America.

Erratum in

  • PLoS One. 2014;9(7):e103361. Asokan, Devarajan [corrected to Devarajan, Asokan].

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.

PMID:
24691130
PMCID:
PMC3972226
DOI:
10.1371/journal.pone.0093056
[Indexed for MEDLINE]
Free PMC Article

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