Dickinson R G, Baker P V, King A R
Department of Medicine, University of Queensland, Royal Brisbane Hospital, Australia.
Biochem Pharmacol. 1994 Feb 9;47(3):469-76. doi: 10.1016/0006-2952(94)90177-5.
Salicyl acyl glucuronide (SAG) is a significant metabolite of salicylic acid (SA) and aspirin. We have shown that, under physiological conditions in vitro, SAG undergoes rearrangement in a manner consistent with acyl migration to its 2-, 3- and 4-O-acyl positional isomers as the predominant pathway (T1/2 values were 1.4-1.7 hr in buffer at pH 7.4 and 37 degrees). Incubation of SAG or a mixture of its rearrangement isomers (iso-SAG) (each at approximately 50 micrograms SA equivalents/mL) with human serum albumin (HSA, at approximately 40 mg/mL) revealed the formation of covalent adducts with the protein, with peak concentrations of 1-2 micrograms SA equivalents/mL. The data support a role for the rearrangement/glycation mechanism of adduct formation. Covalent adducts of SA were also detected in the plasma of humans taking aspirin (at > or = 1200 mg/day), but the concentrations were low (<< 100 ng SA equivalents/mL). Reactivity of SAG thus provides a mechanism (though of uncertain quantitative importance) of covalent attachment of the salicyl moiety of aspirin to tissue macromolecules, which is in addition to its well-known acetylating capacity.
水杨酰葡糖醛酸(SAG)是水杨酸(SA)和阿司匹林的一种重要代谢产物。我们已经表明,在体外生理条件下,SAG以与酰基迁移至其2-、3-和4-O-酰基位置异构体一致的方式进行重排,这是主要途径(在pH 7.4和37摄氏度的缓冲液中,T1/2值为1.4 - 1.7小时)。将SAG或其重排异构体混合物(异-SAG)(每种浓度约为50微克SA当量/毫升)与人血清白蛋白(HSA,浓度约为40毫克/毫升)一起孵育,发现与该蛋白质形成了共价加合物,峰值浓度为1 - 2微克SA当量/毫升。这些数据支持了加合物形成的重排/糖基化机制的作用。在服用阿司匹林(≥1200毫克/天)的人的血浆中也检测到了SA的共价加合物,但浓度很低(<< 100纳克SA当量/毫升)。因此,SAG的反应性提供了一种机制(尽管其定量重要性尚不确定),使阿司匹林的水杨酰部分共价附着于组织大分子,这是除其众所周知的乙酰化能力之外的。