Phospholipid chlorohydrins cause ATP depletion and toxicity in human myeloid cells

FEBS Letters

Pitt, Andrew R²  Stewart, Laura-Jayne¹  Dever, Gary¹  Spickett, Corinne M¹ 

[1] Department of Bioscience, University of Strathclyde, 204 George Street, Glasgow G1 1XW, UK;Department of Pure and Applied Chemistry, University of Strathclyde, 295 Cathedral Street, Glasgow G1 1XL, UK

关键词: Phosphatidylcholine;    HOCl;    Oxidative stress;    Chlorohydrin;    HL60;    Atherosclerosis;    DMSO;    dimethylsulfoxide;    ESMS;    electrospray mass spectrometry;    HBSS;    Hanks-buffered saline solution;    HNE;    4-hydroxy-2-trans-nonenal;    oxLDL;    oxidised low density lipoprotein;    PAPC;    palmitoyl-arachidonoyl phosphatidylcholine;    SAPC;    stearoyl-arachidonoyl phosphatidylcholine;    SLPC;    stearoyl-linoleoyl phosphatidylcholine;    SOPC;    stearoyl-oleoyl phosphatidylcholine;   

DOI  :  10.1016/S0014-5793(03)00271-0

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Chlorohydrins of stearoyl-oleoyl phosphatidylcholine (SOPC), stearoyl-linoleoyl phosphatidylcholine, and stearoyl-arachidonyl phosphatidylcholine were incubated with cultured myeloid cells (HL60) 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 10–100 μM. 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.

【 授权许可】

Unknown