The role of endoplasmic reticulum Ca2+-independent phospholipase a2γ in oxidant-induced lipid peroxidation, Ca2+ release, and renal cell death.

Toxicological Sciences : an Official Journal of the Society of Toxicology
Andre C EaddyRick G Schnellmann

Abstract

Oxidant-induced lipid peroxidation and cell death are major components of ischemia/reperfusion and toxicant injury. Our previous studies showed that renal proximal tubular cells (RPTCs) express Ca(2+)-independent phospholipase A(2)γ (iPLA(2)γ) in endoplasmic reticulum (ER) and mitochondria and that iPLA(2)γ is cytoprotective. Our present studies reveal the role of ER-iPLA(2)γ in oxidant-induced ER lipid peroxidation, Ca(2+) release, and cell death. Oxidant tert-butyl hydroperoxide (TBHP) caused ER lipid peroxidation and Ca(2+) release in isolated rabbit kidney cortex microsomes. ER-iPLA(2)γ inhibition, using bromoenol lactone (BEL), potentiated both oxidant-induced ER lipid peroxidation and Ca(2+) release. Assessment of fatty acids using electrospray ionization-mass spectrometry revealed that ER-iPLA(2)γ mediates the TBHP-induced release of arachidonic acid (20:4), linoleic acid (18:2), and their oxidized forms (18:2-OH, 18:2-OOH, 20:4-OH, 20:4-OOH, 20:4-(OH)(3). iPLA(2)γ inhibition also accelerated oxidant-induced ER Ca(2+) release in RPTC. Depletion of ER Ca(2+) stores in RPTC with thapsigargin, an ER Ca(2+) pump inhibitor, prior to TBHP exposure reduced necrotic cell death and blocked the potentiation of TBHP-induced necroti...Continue Reading

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Citations

Sep 25, 2009·BMC Neuroscience·Arunmozhiarasi ArmugamKandiah Jeyaseelan
Sep 13, 2006·Journal of Neuroinflammation·Timothy J CunninghamJeffrey I Greenstein
Sep 13, 2006·Journal of Neuroinflammation·Timothy J CunninghamLihua Yao
Jan 31, 2006·Comparative Biochemistry and Physiology. Toxicology & Pharmacology : CBP·Rodrigo G StábeliAndreimar M Soares
Aug 11, 2016·Chemical Research in Toxicology·Lize DefermeJacco J Briedé
Oct 19, 2006·Neurotoxicology·Brianna PetersonBrian S Cummings

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