Medicinal Safety Research Laboratories, Daiichi Sankyo Co., Ltd., 717 Horikoshi, Fukuroi, Shizuoka 437-0065, Japan.
Drug Metab Dispos. 2012 Mar;40(3):497-503. doi: 10.1124/dmd.111.042911. Epub 2011 Dec 14.
We investigated the impact of glutathione transferases Mu 1 (GSTM1)- and glutathione transferase Theta 1 (GSTT1)-null genotypes on hepatic GST activities in humans and compared the results with those of Gstm1- and Gstt1-null mice. In liver with GSTM1/Gstm1-null genotype, GST activity toward p-nitrobenzyl chloride (NBC) was significantly decreased in both humans and mice. In addition, in liver with GSTT1/Gstt1-null genotype, GST activity toward dichloromethane (DCM) was significantly decreased in both humans and mice. Therefore, null genotypes of GSTM1/Gstm1 and GSTT1/Gstt1 are considered to decrease hepatic GST activities toward NBC and DCM, respectively, in both humans and mice. This observation shows the functional similarity between humans and mice for GSTM1 and GSTT1 toward some substrates. In the case of NBC and DCM, Gst-null mice would be relevant models for humans with GST-null genotype. In addition, decreases in GST activities toward 1,2-dichloro-4-nitrobenzene, trans-4-phenyl-3-buten-2-one, and 1-chloro-2,4,-dinitrobenzene were observed in Gstm1-null mice, and a decrease in GST activity toward 1,2-epoxy-3-(p-nitrophenoxy)propane was observed in Gstt1-null mice. However, an impact of GST-null genotypes on GST activities toward these substrates was not observed in humans. In the case of these mouse-specific substrates, Gst-null mice may be relevant models for humans regardless of GST genotype, because GST activities, which are higher in wild-type mice than in humans, were eliminated in Gst-null mice. This study shows that comparison of hepatic GST activities between humans and mice using genotype information would be valuable in using Gst-null mice as human models.
我们研究了谷胱甘肽转移酶 Mu 1(GSTM1)和谷胱甘肽转移酶 Theta 1(GSTT1)缺失基因型对人类肝脏 GST 活性的影响,并将结果与 Gstm1 和 Gstt1 缺失小鼠进行了比较。在 GSTM1/Gstm1 缺失基因型的肝脏中,人类和小鼠的对 p-硝基苄氯(NBC)的 GST 活性均显著降低。此外,在 GSTT1/Gstt1 缺失基因型的肝脏中,人类和小鼠的对二氯甲烷(DCM)的 GST 活性均显著降低。因此,GSTM1/Gstm1 和 GSTT1/Gstt1 的缺失基因型被认为分别降低了人类和小鼠肝脏中对 NBC 和 DCM 的 GST 活性。这一观察结果表明,人类和小鼠在某些底物方面的 GSTM1 和 GSTT1 具有功能相似性。在 NBC 和 DCM 的情况下,Gst 缺失小鼠将是 GST 缺失基因型人类的相关模型。此外,在 Gstm1 缺失小鼠中观察到对 1,2-二氯-4-硝基苯、反式-4-苯基-3-丁烯-2-酮和 1-氯-2,4-二硝基苯的 GST 活性降低,在 Gstt1 缺失小鼠中观察到对 1,2-环氧-3-(对硝基苯氧基)丙烷的 GST 活性降低。然而,在人类中没有观察到 GST 缺失基因型对这些底物的 GST 活性的影响。在这些小鼠特异性底物的情况下,无论 GST 基因型如何,Gst 缺失小鼠都可能是人类的相关模型,因为在 Gst 缺失小鼠中消除了野生型小鼠中比人类更高的 GST 活性。本研究表明,使用基因型信息比较人类和小鼠之间的肝脏 GST 活性,对于使用 Gst 缺失小鼠作为人类模型将是有价值的。