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 language | English |
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Pages (from-to) | 245-250 |
Number of pages | 6 |
Journal | FEBS Letters |
Volume | 540 |
Issue number | 1-3 |
DOIs | |
Publication status | Published - 10 Apr 2003 |
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Keywords
- phosphatidylcholine
- HOCl
- oxidative stress
- chlorohydrin
- HL60
- atherosclerosis
- Pharmacy and materia medica