Tyapochkin Eduard, Cook Paul F, Chen Guangping
Department of Physiological Sciences, Center for Veterinary Health Sciences, Oklahoma State University, Stillwater, Oklahoma 74078, USA.
Biochemistry. 2008 Nov 11;47(45):11894-9. doi: 10.1021/bi801211t. Epub 2008 Oct 18.
Cytosolic sulfotransferase (SULT)-catalyzed sulfation regulates biosignaling molecular biological activities and detoxifies hydroxyl-containing xenobiotics. The universal sulfuryl group donor for SULTcatalyzed sulfation is adenosine 3'-phosphate 5'-phosphosulfate (PAPS). The reaction products are a sulfated product and adenosine 3',5'-diphosphate (PAP). Although the kinetics has been reported since the 1980s,SULT-catalyzed reaction mechanisms remain unclear. Human SULT1A1 catalyzes the sulfation of xenobiotic phenols and has very broad substrate specificity. It has been recognized as one of the most important phase II drug-metabolizing enzymes. Understanding the kinetic mechanism of this isoform is important in understanding drug metabolism and xenobiotic detoxification. In this report, we investigated the SULT1A1-catalyzed phenol sulfation mechanism. The SULT1A1-catalyzed reaction was brought to equilibrium by varying substrate (1-naphthol) and PAPS initial concentrations. Equilibrium constants were determined. Two isotopic exchanges at equilibrium ([14C]1-naphthol <=>[14C]1-naphthyl sulfate and[35S]PAPS<=>[35S]1-naphthyl sulfate) were conducted. First-order kinetics, observed for all the is otopic exchange reactions studied over the entire time scale that was monitored, indicates that the system was truly at equilibrium prior to addition of an isotopic pulse. Complete suppression of the 35S isotopic exchange rate was observed with an increase in the levels of 1-naphthol and 1-naphthyl sulfate in a constant ratio,while no suppression of the 14C exchange rate was observed with an increase in the levels of PAPS and PAP in a constant ratio. Data are consistent with a steady state ordered kinetic mechanism with PAPS and PAP binding to the free enzyme.
胞质磺基转移酶(SULT)催化的硫酸化作用可调节生物信号分子的生物学活性,并使含羟基的外源性物质解毒。SULT催化硫酸化作用的通用硫酰基供体是3'-磷酸腺苷5'-磷酸硫酸酯(PAPS)。反应产物是硫酸化产物和3',5'-二磷酸腺苷(PAP)。尽管自20世纪80年代以来就已报道了其动力学,但SULT催化的反应机制仍不清楚。人SULT1A1催化外源性酚类的硫酸化作用,具有非常广泛的底物特异性。它已被公认为最重要的II相药物代谢酶之一。了解该同工型的动力学机制对于理解药物代谢和外源性物质解毒很重要。在本报告中,我们研究了SULT1A1催化的酚硫酸化机制。通过改变底物(1-萘酚)和PAPS的初始浓度,使SULT1A1催化的反应达到平衡。测定了平衡常数。进行了两个平衡时的同位素交换([14C]1-萘酚⇌[14C]1-萘基硫酸酯和[35S]PAPS⇌[35S]1-萘基硫酸酯)。在整个监测的时间范围内,对所有研究的同位素交换反应均观察到一级动力学,这表明在添加同位素脉冲之前系统确实处于平衡状态。在1-萘酚和1-萘基硫酸酯水平以恒定比例增加时,观察到35S同位素交换速率完全受到抑制,而在PAPS和PAP水平以恒定比例增加时,未观察到14C交换速率受到抑制。数据与PAPS和PAP与游离酶结合的稳态有序动力学机制一致。