Placenta · 2025
Determination of residue aspirin and its bioactive metabolites in human placenta: Application to high-risk to preeclampsia women received prophylactic low-dose aspirin.
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Tlaye Kenean Getaneh, Kin So Pui, Woldeamanuel Gashaw Garedew, Leung Bo Wah, Poon Liona C, Wang Chi Chiu
Аннотация
INTRODUCTION: The human placenta plays central role in preeclampsia (PE) pathogenesis and may modulate the effectiveness of prophylactic low-dose aspirin (LDA). In this study, we optimized and validated LC-MS/MS method to quantify the residual acetylsalicylic acid (ASA), salicylic acid (SA), and gentisic acid (GA) in the placenta of LDA exposed women.
METHODS: Analytes were extracted from the placenta using acetonitrile with 0.1 % formic acid (v/v). Stable deuterated isotopes i.e., ASA-d4, SA-d4, and GA-d3 were used as an internal standard (IS) for ASA, SA, and GA respectively. The multiple reaction monitoring (MRM) mode with ion transitions of m/z 178.9 → 93.2, 182.9 → 97, 136.9 → 92.9, 140.9 → 96.9, 152.9 → 108.9, and 154.9 → 110.9 were used for ASA, ASA-d4, SA, SA-d4, GA, and GA-d3, respectively.
RESULTS: The developed method was successfully applied to analyze ASA, SA, and GA residuals in the placenta of aspirin responder (R) and non-responder (NR) women who had been taking LDA for PE prevention. Slightly higher yet non-significant increment of ASA and SA was seen in R placenta. Following LDA, ASA and GA were found to be rarely detected and short-lived, while SA was the most abundant and retained in the placenta for an extended duration.
CONCLUSION: The method allows the determination of ASA, SA, and GA from human placenta. The difference in aspirin responsiveness among women at high risk for PE may be driven by other pharmacokinetic, pharmacodynamic, or pharmacogenomic variabilities, rather than by differences in the placental concentration of ASA.
METHODS: Analytes were extracted from the placenta using acetonitrile with 0.1 % formic acid (v/v). Stable deuterated isotopes i.e., ASA-d4, SA-d4, and GA-d3 were used as an internal standard (IS) for ASA, SA, and GA respectively. The multiple reaction monitoring (MRM) mode with ion transitions of m/z 178.9 → 93.2, 182.9 → 97, 136.9 → 92.9, 140.9 → 96.9, 152.9 → 108.9, and 154.9 → 110.9 were used for ASA, ASA-d4, SA, SA-d4, GA, and GA-d3, respectively.
RESULTS: The developed method was successfully applied to analyze ASA, SA, and GA residuals in the placenta of aspirin responder (R) and non-responder (NR) women who had been taking LDA for PE prevention. Slightly higher yet non-significant increment of ASA and SA was seen in R placenta. Following LDA, ASA and GA were found to be rarely detected and short-lived, while SA was the most abundant and retained in the placenta for an extended duration.
CONCLUSION: The method allows the determination of ASA, SA, and GA from human placenta. The difference in aspirin responsiveness among women at high risk for PE may be driven by other pharmacokinetic, pharmacodynamic, or pharmacogenomic variabilities, rather than by differences in the placental concentration of ASA.