Phospholipid chlorohydrins cause ATP depletion and toxicity in human myeloid cells

Gary Dever, Laura-Jayne Stewart, Andrew Pitt, Corinne M. Spickett

Research output: Contribution to journalArticle

Abstract

Chlorohydrins of stearoyl-oleoyl phosphatidylcholine (SOPC), stearoyl-linoleoyl phosphatidylcholine, and stearoyl-arachidonyl phosphatidylcholine were incubated with cultured myeloid cells (111,60) for 24 h, and the cellular ATP level was measured using a bioluminescent assay. The chlorohydrins caused significant depletion of cellular ATP in the range 10100 muM. The ATP depletion by the phospholipid chlorohydrins was slightly less than that of 4-hydroxy-2-nonenal, but greater than that of hexanal, trans-2-nonenal, and autoxidised palmitoyl-arachidonoyl phosphatidylcholine. SOPC chlorohydrin was also found to cause loss of viability in U937 cells, and thus phospholipid chlorohydrins could contribute to the formation of a necrotic core in advanced atherosclerotic lesions.
Original languageEnglish
Pages (from-to)245-250
Number of pages6
JournalFEBS Letters
Volume540
Issue number1-3
DOIs
Publication statusPublished - 10 Apr 2003

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Keywords

  • phosphatidylcholine
  • HOCl
  • oxidative stress
  • chlorohydrin
  • HL60
  • atherosclerosis
  • Pharmacy and materia medica

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