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目的:检测血红蛋白与砷的结合,分析血红蛋白在三氧化二砷(ATO)抑制血小板聚集功能中发挥的作用。方法:电喷雾质谱(ESI-MS)检测血红蛋白与氨基氧化苯胂酸(PAPAO)的结合。在2 mg/L胶原或2μmol/L腺苷二磷酸(ADP)刺激下,比较经10μmol/L ATO处理后,富血小板血浆(PRP)和全血血小板聚集的差异。PRP中加入0、40、60、80、100、120 g/L的血红蛋白经10μmol/L的ATO处理后,检测血小板聚集。结果:血红蛋白β链可与一分子有机砷PAPAO结合,并脱去一分子水。ATO处理PRP以及全血,两者血小板聚集均受到显著抑制,但是对PRP血小板聚集的抑制更加明显。在刺激剂为2 mg/L胶原时,血红蛋白≥80 g/L可逆转ATO对血小板聚集的抑制,并且具有浓度依赖性(r=0.956,P=0.003);同样的,在刺激剂为2μmol/L ADP时,血红蛋白≥80 g/L可逆转ATO对血小板聚集的抑制(r=0.940,P=0.005)。结论:在体外血红蛋白通过与砷结合,能够削弱ATO对血小板聚集的抑制,并且具有浓度依赖性。血红蛋白在ATO抑制血小板聚集过程中发挥重要作用。
OBJECTIVE: To detect the binding of hemoglobin to arsenic, and to analyze the role of hemoglobin in the inhibition of platelet aggregation by arsenic trioxide (ATO). Methods: Electrospray ionization mass spectrometry (ESI-MS) was used to detect the binding of hemoglobin to phenylphthalocyanine (PAPAO). Differences in platelet-rich plasma (PRP) and whole blood platelet aggregation after 10 μmol / L ATO treatment were compared with either 2 mg / L collagen or 2 μmol / L adenosine diphosphate (ADP). PRP 0,40,60,80,100,120 g / L hemoglobin by 10μmol / L of ATO treatment, detection of platelet aggregation. Results: The hemoglobin β chain can be combined with a molecule of organic arsenic PAPAO, and take off one molecule of water. ATO treatment of PRP and whole blood, both platelet aggregation were significantly inhibited, but the inhibition of PRP platelet aggregation more pronounced. Hemoglobin> 80 g / L reversed the inhibition of platelet aggregation by ATO at a concentration of 2 mg / L collagen (r = 0.956, P = 0.003) and stimulated at 2 μmol / At ADP, hemoglobin ≥80 g / L reversed ATO inhibition of platelet aggregation (r = 0.940, P = 0.005). CONCLUSIONS: In vitro hemoglobin binding to arsenic attenuates the inhibition of platelet aggregation by ATO in a concentration-dependent manner. Hemoglobin plays an important role in ATO inhibiting platelet aggregation.