Phosphatidylserine peroxidation

Kawai, K., Tyurina, Y.Y, Tyurin, V.A., Kagan, V.E., and Fabisiak, J., 2000, Peroxidation and externalization of phosphatidylserine in plasma membrane of HL-60 ceUs during tert-butyl hydroperoxide-induced apoptosis Role of cytochrome c, The Toxicologist 54 SuppL 776. 

Studies carried out with complete cells in vivo, cell membranes and other cell fractions point to the selective oxidation of phosphatidylserine (26) to a hydroperoxide (PS-OOH) on oxidative stress caused by toxic agents such as H2O2, t-BuOOH and cumyl hydroperoxide (27). Formation of PS-OOH is observed during apoptosis. These phenomena are important because of the cytotoxic effects of various peroxides used in commercial products coming into direct contact with the human body, as is the case of epidermal keratinocytes in contact with cosmetic formulations" ". The toxic effects of f-BuOOH are associated with vasoconstriction and damage to the vascular smooth muscles ". Global determination methods for primary lipid oxidation products are discussed in Section IV.B. 

Phospholipids were extracted from erythrocyte membranes and were analyzed along with their lipoxygenase peroxide products using a 40°C aminopropyl column. Phospholipids (phosphatidylcholine [PC], phosphatidylethanolamine [PE], phospha-tidylinositol, phosphatidylserine [PS], and sphingomyelin) were separated using a 67/22/11 acetonitrile/methanol/water (0.2% TFA) mobile phase (A = 2I0nm). Elution was complete in 30 min and excellent resolution was achieved. The peroxide forms of PC, PE, and PS were separated at the same time but monitored at k — 234 nm. All samples were stabilized with 20mg/L BHT solutions [1185]. 

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