参考文献/References:
[1] DAVERN T J. Drug-induced liver disease[J]. Clin Liver Dis, 2012, 16(2): 231-245.
[2]LEE K K, IMAIZUMI N, CHAMBERLAND S R, et al. Targeting mitochondria with methylene blue protects mice against acetaminophen-induced liver injury[J]. Hepatology, 2015, 61(1): 326-336.
[3]LANCASTER E M, HIATT J R, ZARRINPAR A. Acetaminophen hepatotoxicity: an updated review[J]. Arch Toxicol, 2015, 89(2): 193-199.
[4]SCHILLING A, COREY R, LEONARD M, et al. Acetaminophen: old drug, new warnings[J]. Cleve Clin J Med, 2010, 77(1): 19-27.
[5]BLIEDEN M, PARAMORE L C, SHAH D,et al. A perspective on the epidemiology of acetaminophen exposure and toxicity in the United States[J]. Expert Rev Clin Pharmacol, 2014, 7(3): 341-348.
[6]ANDERSON M E. Determination of glutathione and glutathione disulfide in biological samples[J]. Methods Enzymol, 1985,113:548-555.
[7]KJARTANSDOTTIR I, BERGMANN O M, ARNADOTTIR R S, et al. Paracetamol intoxications: a retrospective population-based study in Iceland[J]. Scand J Gastroenterol, 2012, 47(11): 1344-1352.
[8]MCGILL M R, SHARPE M R, WILLIAMS C D, et al. The mechanism underlying acetaminophen-induced hepatotoxicity in humans and mice involves mitochondrial damage and nuclear DNA fragmentation[J]. J Clin Invest, 2012, 122(4): 1574-1583.
[9]ROHRER P R, RUDRAIAH S, GOEDKEN M J, et al. Is nuclear factor erythroid 2-related factor 2 responsible for sex differences in susceptibility to acetaminophen-induced hepatotoxicity in mice? [J]. Drug Metab Dispos, 2014, 42(10): 1663-1674.
[10]SHENG Y, LIANG Q, DENG Z, et al. Acetaminophen induced gender-dependent liver injury and the involvement of GCL and GPX[J]. Drug Discov Ther, 2013, 7(2): 78-83.
[11]MASUBUCHI Y, NAKAYAMA J, WATANABE Y. Sex difference in susceptibility to acetaminophen hepatotoxicity is reversed by buthionine sulfoximine[J]. Toxicology, 2011, 287(1/2/3): 54-60.
[12]TARLOFF J B, KHAIRALLAH E A, COHEN S D, et al. Sex-and age-dependent acetaminophen hepato- and nephrotoxicity in Sprague-Dawley rats: role of tissue accumulation, nonprotein sulfhydryl depletion, and covalent binding[J]. Fundam Appl Toxicol, 1996, 30(1): 13-22.
[13]WAGNER E F, NEBREDA A R. Signal integration by JNK and p38 MAPK pathways in cancer development[J]. Nat Rev Cancer, 2009, 9(8): 537-549.
[14]DAVIS R J. Signal transduction by the JNK group of MAP kinases[J]. Cell, 2000, 103(2): 239-252.
[15]SEKI E, BRENNER D A, Karin M. A liver full of JNK: signaling in regulation of cell function and disease pathogenesis, and clinical approaches[J]. Gastroenterology, 2012, 143(2): 307-320.
[16]SAITO C, LEMASTERS J J, JAESCHKE H. C-Jun N-terminal kinase modulates oxidant stress and peroxynitrite formation independent of inducible nitric oxide synthase in acetaminophen hepatotoxicity[J]. Toxicol Appl Pharmacol, 2010, 246(1/2): 8-17.
[17]ZHANG Y F, HE W, XU D X, et al. Role of receptor interacting protein(RIP)1 on apoptosis-inducing factor-mediated necroptosis during acetaminophen-evoked acute liver failure in mice[J]. Toxicol Lett, 2014, 225(3): 445-453.
[18]SAITO C, ZWINGMANN C, JAESCHKE H. Novel mechanisms of protection against acetaminophen hepatotoxicity in mice by glutathione and N-acetylcysteine[J]. Hepatology, 2010, 51(1): 246-254.
[19]DAI G, HE L, CHOU N, et al. Acetaminophen metabolism does not contribute to gender difference in its hepatotoxicity in mouse[J]. Toxicol Sci, 2006, 92(1):33-41.
[20]DU K, WILLIAMS C D, MCGILL M R, et al. Lower susceptibility of female mice to acetaminophen hepatotoxicity: role of mitochondrial glutathione, oxidant stress and C-jun N-terminal kinase[J]. Toxicol Appl Pharmacol, 2014, 281(1): 58-66.