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含黄素单加氧酶3(FMO3)在白消安代谢途径中的作用。

Flavin-containing monooxygenase 3 (FMO3) role in busulphan metabolic pathway.

作者信息

El-Serafi Ibrahim, Terelius Ylva, Abedi-Valugerdi Manuchehr, Naughton Seán, Saghafian Maryam, Moshfegh Ali, Mattsson Jonas, Potácová Zuzana, Hassan Moustapha

机构信息

Experimental Cancer Medicine (ECM), Clinical Research Centre (KFC), Department of Laboratory Medicine, Karolinska Institutet, Huddinge, Stockholm, Sweden.

Cancer Center of Karolinska (CCK), Department of Oncology-Pathology, Karolinska Institutet, Solna, Stockholm, Sweden.

出版信息

PLoS One. 2017 Nov 9;12(11):e0187294. doi: 10.1371/journal.pone.0187294. eCollection 2017.

Abstract

Busulphan (Bu) is an alkylating agent used in the conditioning regimen prior to hematopoietic stem cell transplantation (HSCT). Bu is extensively metabolized in the liver via conjugations with glutathione to form the intermediate metabolite (sulfonium ion) which subsequently is degraded to tetrahydrothiophene (THT). THT was reported to be oxidized forming THT-1-oxide that is further oxidized to sulfolane and finally 3-hydroxysulfolane. However, the underlying mechanisms for the formation of these metabolites remain poorly understood. In the present study, we performed in vitro and in vivo investigations to elucidate the involvement of flavin-containing monooxygenase-3 (FMO3) and cytochrome P450 enzymes (CYPs) in Bu metabolic pathway. Rapid clearance of THT was observed when incubated with human liver microsomes. Furthermore, among different recombinant microsomal enzymes, the highest intrinsic clearance for THT was obtained via FMO3 followed by several CYPs including 2B6, 2C8, 2C9, 2C19, 2E1 and 3A4. In Bu- or THT-treated mice, inhibition of FMO3 by phenylthiourea significantly suppressed the clearance of both Bu and THT. Moreover, the simultaneous administration of a high dose of THT (200μmol/kg) to Bu-treated mice reduced the clearance of Bu. Consistently, in patients undergoing HSCT, repeated administration of Bu resulted in a significant up-regulation of FMO3 and glutathione-S-transfrase -1 (GSTA1) genes. Finally, in a Bu-treated patient, additional treatment with voriconazole (an antimycotic drug known as an FMO3-substrate) significantly altered the Bu clearance. In conclusion, we demonstrate for the first time that FMO3 along with CYPs contribute a major part in busulphan metabolic pathway and certainly can affect its kinetics. The present results have high clinical impact. Furthermore, these findings might be important for reducing the treatment-related toxicity of Bu, through avoiding interaction with other concomitant used drugs during conditioning and hence improving the clinical outcomes of HSCT.

摘要

白消安(Bu)是一种烷化剂,用于造血干细胞移植(HSCT)前的预处理方案。白消安在肝脏中通过与谷胱甘肽结合而被广泛代谢,形成中间代谢产物(锍离子),随后该产物降解为四氢噻吩(THT)。据报道,THT会被氧化形成THT - 1 - 氧化物,该氧化物会进一步氧化为环丁砜,最终生成3 - 羟基环丁砜。然而,这些代谢产物形成的潜在机制仍知之甚少。在本研究中,我们进行了体外和体内研究,以阐明含黄素单加氧酶 - 3(FMO3)和细胞色素P450酶(CYPs)在白消安代谢途径中的作用。将THT与人肝微粒体一起孵育时,观察到THT的快速清除。此外,在不同的重组微粒体酶中,通过FMO3获得的THT固有清除率最高,其次是几种CYPs,包括2B6、2C8、2C9、2C19、2E1和3A4。在接受白消安或THT治疗的小鼠中,苯硫脲对FMO3的抑制显著抑制了白消安和THT的清除。此外,向接受白消安治疗的小鼠同时给予高剂量的THT(200μmol/kg)会降低白消安的清除率。同样,在接受HSCT的患者中,重复给予白消安会导致FMO3和谷胱甘肽 - S - 转移酶 - 1(GSTA1)基因显著上调。最后,在一名接受白消安治疗的患者中,额外使用伏立康唑(一种已知为FMO3底物的抗真菌药物)进行治疗显著改变了白消安的清除率。总之,我们首次证明FMO3与CYPs在白消安代谢途径中起主要作用,并且肯定会影响其动力学。目前的结果具有很高的临床影响。此外,这些发现对于降低白消安的治疗相关毒性可能很重要,通过在预处理期间避免与其他同时使用的药物相互作用,从而改善HSCT的临床结果。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6599/5679629/86fd7c5bd1c5/pone.0187294.g001.jpg

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