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Here, we report that NPC1\u2010deficient Chinese hamster ovary cells exhibit increased release of arachidonic acid (AA) and synthesis of prostaglandin E<jats:sub>2<\/jats:sub> compared with wild\u2010type cells. The enhanced release of AA was inhibited by both treatment with the selective inhibitor of cytosolic phospholipase A<jats:sub>2<\/jats:sub>\u03b1 (cPLA<jats:sub>2<\/jats:sub>\u03b1) and cultivation in lipoprotein\u2010deficient medium. There was no difference in the expression of both cyclooxygenase\u20101 and \u20102 between NPC cells and wild\u2010type cells. U18666A, a cholesterol transport\u2010inhibiting agent commonly used to mimic NPC, also increased the release of AA in L929 mouse fibrosarcoma cells. Furthermore, U18666A\u2010induced formation of reactive oxygen species (ROS) resulted in the induction of cell death and cell cycle delay\/arrest in L929 cells. Interestingly, these responses induced by U18666A were much weaker in cPLA<jats:sub>2<\/jats:sub>\u03b1 knockdown L929 cells. These results suggest that cPLA<jats:sub>2<\/jats:sub>\u03b1\u2010AA pathway plays important roles in the cytotoxicity and the ROS formation in NPC cells. J. Cell. Physiol. 227: 2847\u20132855, 2012. \u00a9 2011 Wiley Periodicals, Inc.<\/jats:p>","DOI":"10.1002\/jcp.23025","type":"journal-article","created":{"date-parts":[[2011,9,19]],"date-time":"2011-09-19T05:09:58Z","timestamp":1316408998000},"page":"2847-2855","source":"Crossref","is-referenced-by-count":6,"title":["Arachidonic acid metabolism via cytosolic phospholipase A<sub>2<\/sub>\u03b1 induces cytotoxicity in niemann\u2013pick disease type C 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