Genetic Association of Single Nucleotide Polymorphisms with Acetaminophen-Induced Hepatotoxicity

被引：10

作者：

Heruth, Daniel P. ^{[1
]}

Shortt, Katherine ^{[1
,3
,4
]}

Zhang, Nini ^{[1
,2
,5
]}

Li, Ding-You ^{[2
]}

Zhang, Li Q. ^{[1
]}

Ye, Shui Qing ^{[1
,3
]}

机构：

[1] Childrens Mercy, Dept Pediat, Div Expt & Translat Genet, Kansas City, MO 64068 USA

[2] Childrens Mercy, Dept Pediat, Div Gastroenterol, Kansas City, MO 64068 USA

[3] Univ Missouri, Sch Med, Dept Biomed & Hlth Informat, Kansas City, MO 64108 USA

[4] Univ Missouri, Div Cell Biol & Biophys, Sch Biol Sci, Kansas City, MO 64110 USA

[5] Fourth Mil Med Univ, Tangdu Hosp, Dept Pediat, Xian, Shaanxi, Peoples R China

来源：

JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS | 2018年 / 367卷 / 01期

关键词：

INDUCED LIVER-INJURY; DRUG-INDUCED HEPATOTOXICITY; GENOME-WIDE ASSOCIATION; PARACETAMOL-INDUCED HEPATOTOXICITY; COVALENT BINDING; HEPATIC-NECROSIS; BENZOQUINONE IMINE; PROTEIN ADDUCTS; UNITED-STATES; IN-VIVO;

D O I：

10.1124/jpet.118.248583

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

Acetaminophen is commonly used to reduce pain and fever. Unfortunately, overdose of acetaminophen is a leading cause of acute liver injury and failure in many developed countries. The majority of acetaminophen is safely metabolized in the liver and excreted in the urine; however, a small percentage is converted to the highly reactive N-acetyl-p-benzoquinone imine (NAPQI). At therapeutic doses, NAPQI is inactivated by glutathione S-transferases, but at toxic levels, excess NAPQI forms reactive protein adducts that lead to hepatotoxicity. Individual variability in the response to both therapeutic and toxic levels of acetaminophen suggests a genetic component is involved in acetaminophen metabolism. In this review, we evaluate the genetic association studies that have identified 147 single nucleotide polymorphisms linked to acetaminophen-induced hepatotoxicity. The identification of novel genetic markers for acetaminophen-induced hepatotoxicity provides a rich resource for further evaluation and may lead to improved prognosis, prevention, and treatment.

引用

页码：95 / 100

页数：6

共 71 条

[1] Interindividual variability in acetaminophen sulfation by human fetal liver: Implications for pharmacogenetic investigations of drug-induced birth defects [J].

Adjei, Araba A. ;

Gaedigk, Andrea ;

Simon, Stephen D. ;

Weinshilboum, Richard M. ;

Leeder, J. Steven .

BIRTH DEFECTS RESEARCH PART A-CLINICAL AND MOLECULAR TERATOLOGY, 2008, 82 (03) :155-165

[2] Induction of Mrp3 and Mrp4 transporters during acetaminophen hepatotoxicity is dependent on Nrf2 [J].

Aleksunes, Lauren M. ;

Slitt, Angela L. ;

Maher, Jonathan M. ;

Augustine, Lisa M. ;

Goedken, Michael J. ;

Chan, Jefferson Y. ;

Cherrington, Nathan J. ;

Klaassen, Curtis D. ;

Manautou, Jose E. .

TOXICOLOGY AND APPLIED PHARMACOLOGY, 2008, 226 (01) :74-83

[3] Clinical Pharmacogenetics Implementation Consortium (CPIC) Guidelines for CYP3A5 Genotype and Tacrolimus Dosing [J].

Birdwell, K. A. ;

Decker, B. ;

Barbarino, J. M. ;

Peterson, J. F. ;

Stein, C. M. ;

Sadee, W. ;

Wang, D. ;

Vinks, A. A. ;

He, Y. ;

Swen, J. J. ;

Leeder, J. S. ;

van Schaik, R. H. N. ;

Thummel, K. E. ;

Klein, T. E. ;

Caudle, K. E. ;

MacPhee, I. A. M. .

CLINICAL PHARMACOLOGY & THERAPEUTICS, 2015, 98 (01) :19-24

[4] Role of IL-6 in an IL-10 and IL-4 double knockout mouse model uniquely susceptible to acetaminophen-induced liver injury [J].

Bourdi, Mohammed ;

Eiras, Daniel P. ;

Holt, Michael P. ;

Webster, Marie R. ;

Reilly, Timothy P. ;

Welch, Kevin D. ;

Pohl, Lance R. .

CHEMICAL RESEARCH IN TOXICOLOGY, 2007, 20 (02) :208-216

[5] Genome-wide association study identifies loci influencing concentrations of liver enzymes in plasma [J].

Chambers, John C. ;

Zhang, Weihua ;

Sehmi, Joban ;

Li, Xinzhong ;

Wass, Mark N. ;

Van der Harst, Pim ;

Holm, Hilma ;

Sanna, Serena ;

Kavousi, Maryam ;

Baumeister, Sebastian E. ;

Coin, Lachlan J. ;

Deng, Guohong ;

Gieger, Christian ;

Heard-Costa, Nancy L. ;

Hottenga, Jouke-Jan ;

Kuehnel, Brigitte ;

Kumar, Vinod ;

Lagou, Vasiliki ;

Liang, Liming ;

Luan, Jian'an ;

Vidal, Pedro Marques ;

Leach, Irene Mateo ;

O'Reilly, Paul F. ;

Peden, John F. ;

Rahmioglu, Nilufer ;

Soininen, Pasi ;

Speliotes, Elizabeth K. ;

Yuan, Xin ;

Thorleifsson, Gudmar ;

Alizadeh, Behrooz Z. ;

Atwood, Larry D. ;

Borecki, Ingrid B. ;

Brown, Morris J. ;

Charoen, Pimphen ;

Cucca, Francesco ;

Das, Debashish ;

de Geus, Eco J. C. ;

Dixon, Anna L. ;

Doering, Angela ;

Ehret, Georg ;

Eyjolfsson, Gudmundur I. ;

Farrall, Martin ;

Forouhi, Nita G. ;

Friedrich, Nele ;

Goessling, Wolfram ;

Gudbjartsson, Daniel F. ;

Harris, Tamara B. ;

Hartikainen, Anna-Liisa ;

Heath, Simon ;

Hirschfield, Gideon M. .

NATURE GENETICS, 2011, 43 (11) :1131-1138

[6] Key factors of susceptibility to anti-tuberculosis drug-induced hepatotoxicity [J].

Chen, Ru ;

Wang, Jing ;

Zhang, Yuan ;

Tang, Shaowen ;

Zhan, Siyan .

ARCHIVES OF TOXICOLOGY, 2015, 89 (06) :883-897

[7] Oxidation of acetaminophen to its toxic quinone imine and nontoxic catechol metabolites by baculovirus-expressed and purified human cytochromes P450 2E1 and 2A6 [J].

Chen, WQ ;

Koenigs, LL ;

Thompson, SJ ;

Peter, RM ;

Pettie, AE ;

Trager, WF ;

Nelson, SD .

CHEMICAL RESEARCH IN TOXICOLOGY, 1998, 11 (04) :295-301

[8] Selective protein covalent binding and target organ toxicity [J].

Cohen, SD ;

Pumford, NR ;

Khairallah, EA ;

Boekelheide, K ;

Pohl, LR ;

Amouzadeh, HR ;

Hinson, JA .

TOXICOLOGY AND APPLIED PHARMACOLOGY, 1997, 143 (01) :1-12

[9]

CORCORAN GB, 1985, J PHARMACOL EXP THER, V232, P864

[10]

CORCORAN GB, 1980, MOL PHARMACOL, V18, P536

← 1 2 3 4 5 6 7 8 →