Secretion of lipid peroxides by the human placenta.

OBJECTIVE: We attempted to determine whether the human placenta secretes lipid peroxides. If it does, then it could be a source of lipid peroxides in maternal blood. STUDY
DESIGN: In study 1 isolated human placental cotyledons (n = 7) were perfused serially for 20-minute intervals with control Krebs-Ringer-bicarbonate buffer gassed with 95% oxygen and 5% carbon dioxide and Krebs-Ringer-bicarbonate buffer with progressively increasing concentrations of t-butyl hydroperoxide added (10, 25, 50, and 100 mumol/L) to stimulate endogenous lipid peroxide production. In study 2 placental cotyledons (n = 6) were perfused serially for 20-minute intervals with control Krebs-Ringer-bicarbonate buffer, t-butyl hydroperoxide (100 mumol/L), low-dose aspirin (5 x 10(-5) mol/L), and low-dose aspirin plus t-butyl hydroperoxide. Maternal and fetal effluent samples were analyzed for lipid peroxides by hydrogen peroxide equivalents.
RESULTS: In study 1, compared with control Krebs-Ringer-bicarbonate perfusion, peroxide perfusion significantly increased, in a dose-response manner, placental lipid peroxide secretion. In study 2, aspirin completely blocked the ability of peroxide to increase the secretion of lipid peroxides. In both studies placental secretion of lipid peroxides was significantly greater toward the maternal side of the placenta than toward the fetal side.
CONCLUSIONS: (1) The human placenta secretes lipid peroxides primarily into the maternal effluent. (2) Exogenous peroxide stimulates endogenous lipid peroxide production, which is blocked by aspirin, suggesting cyclooxygenase is involved in lipid peroxide production. (3) The placenta could be a source of circulating lipid peroxides in pregnant women.