Mitochondrial dysfunction is a primary event in renal cell oxalate toxicity.

@article{Cao2004MitochondrialDI,
  title={Mitochondrial dysfunction is a primary event in renal cell oxalate toxicity.},
  author={L. C. Cao and Thomas W. Honeyman and Rachel Cooney and Lori Kennington and Cheryl R. Scheid and Julie A. Jonassen},
  journal={Kidney international},
  year={2004},
  volume={66 5},
  pages={1890-900}
}
BACKGROUND In cultured renal epithelial cells, exposure to oxalate, a constituent of many kidney stones, elicits a cascade of responses that often leads to cell death. Oxalate toxicity is mediated via generation of reactive oxygen species (ROS) in a process that depends at least in part upon lipid signaling molecules that are generated through membrane events that culminate in phospholipase A2 (PLA2) activation. The present studies asked whether mitochondria, a major site of ROS production… CONTINUE READING

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