Mitochondrial bax translocation accelerates DNA fragmentation and cell necrosis in a murine model of acetaminophen hepatotoxicity.
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Mechanisms of acetaminophen-induced liver necrosisExperimental models of hepatotoxicity related to acute liver failureAcetaminophen-induced Liver Injury: from Animal Models to HumansXenobiotic and Endobiotic Mediated Interactions Between the Cytochrome P450 System and the Inflammatory Response in the LiverA liver full of JNK: signaling in regulation of cell function and disease pathogenesis, and clinical approachesIdentification of early biomarkers during acetaminophen-induced hepatotoxicity by fourier transform infrared microspectroscopySilencing glycogen synthase kinase-3beta inhibits acetaminophen hepatotoxicity and attenuates JNK activation and loss of glutamate cysteine ligase and myeloid cell leukemia sequence 1.The Impact of Sterile Inflammation in Acute Liver Injury.Mechanisms of acetaminophen hepatotoxicity and their translation to the human pathophysiology.c-Jun N-terminal kinase modulates oxidant stress and peroxynitrite formation independent of inducible nitric oxide synthase in acetaminophen hepatotoxicity.Pathologic role of stressed-induced glucocorticoids in drug-induced liver injury in mice.Temporal study of acetaminophen (APAP) and S-adenosyl-L-methionine (SAMe) effects on subcellular hepatic SAMe levels and methionine adenosyltransferase (MAT) expression and activityThe oxygen tension modulates acetaminophen-induced mitochondrial oxidant stress and cell injury in cultured hepatocytesSerum mitochondrial biomarkers and damage-associated molecular patterns are higher in acetaminophen overdose patients with poor outcome.Melatonin protects against apoptosis-inducing factor (AIF)-dependent cell death during acetaminophen-induced acute liver failureThe impact of partial manganese superoxide dismutase (SOD2)-deficiency on mitochondrial oxidant stress, DNA fragmentation and liver injury during acetaminophen hepatotoxicity.Role of the mitochondrion in programmed necrosisCurrent issues with acetaminophen hepatotoxicity--a clinically relevant model to test the efficacy of natural products.Hepatoprotective role of liver fatty acid binding protein in acetaminophen induced toxicity.The role of hypoxia-inducible factor-1α in acetaminophen hepatotoxicity.Apoptosis-inducing factor modulates mitochondrial oxidant stress in acetaminophen hepatotoxicity.Lower susceptibility of female mice to acetaminophen hepatotoxicity: Role of mitochondrial glutathione, oxidant stress and c-jun N-terminal kinase.Role of TRAIL and the pro-apoptotic Bcl-2 homolog Bim in acetaminophen-induced liver damage.Hepatitis C virus structural proteins can exacerbate or ameliorate acetaminophen-induced liver injury in mice.Mouse strain-dependent caspase activation during acetaminophen hepatotoxicity does not result in apoptosis or modulation of inflammation.Resveratrol prevents protein nitration and release of endonucleases from mitochondria during acetaminophen hepatotoxicity.The mechanism underlying acetaminophen-induced hepatotoxicity in humans and mice involves mitochondrial damage and nuclear DNA fragmentation.Liver-specific loss of Atg5 causes persistent activation of Nrf2 and protects against acetaminophen-induced liver injuryMitochondrial protein adducts formation and mitochondrial dysfunction during N-acetyl-m-aminophenol (AMAP)-induced hepatotoxicity in primary human hepatocytesBenzyl alcohol protects against acetaminophen hepatotoxicity by inhibiting cytochrome P450 enzymes but causes mitochondrial dysfunction and cell death at higher dosesLysosomal instability and cathepsin B release during acetaminophen hepatotoxicity.Critical review of resveratrol in xenobiotic-induced hepatotoxicity.TRAIL enhances paracetamol-induced liver sinusoidal endothelial cell death in a Bim- and Bid-dependent mannerAcetaminophen hepatotoxicity and repair: the role of sterile inflammation and innate immunity.Models of drug-induced liver injury for evaluation of phytotherapeutics and other natural products.Plasma and liver acetaminophen-protein adduct levels in mice after acetaminophen treatment: dose-response, mechanisms, and clinical implications.Fas receptor-deficient lpr mice are protected against acetaminophen hepatotoxicity due to higher glutathione synthesis and enhanced detoxification of oxidant stress.Metabolism and disposition of acetaminophen: recent advances in relation to hepatotoxicity and diagnosis.Recent advances in 2D and 3D in vitro systems using primary hepatocytes, alternative hepatocyte sources and non-parenchymal liver cells and their use in investigating mechanisms of hepatotoxicity, cell signaling and ADME.Receptor interacting protein kinase 3 is a critical early mediator of acetaminophen-induced hepatocyte necrosis in mice.
P2860
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P2860
Mitochondrial bax translocation accelerates DNA fragmentation and cell necrosis in a murine model of acetaminophen hepatotoxicity.
description
2007 nî lūn-bûn
@nan
2007年の論文
@ja
2007年学术文章
@wuu
2007年学术文章
@zh
2007年学术文章
@zh-cn
2007年学术文章
@zh-hans
2007年学术文章
@zh-my
2007年学术文章
@zh-sg
2007年學術文章
@yue
2007年學術文章
@zh-hant
name
Mitochondrial bax translocatio ...... acetaminophen hepatotoxicity.
@en
Mitochondrial bax translocatio ...... acetaminophen hepatotoxicity.
@nl
type
label
Mitochondrial bax translocatio ...... acetaminophen hepatotoxicity.
@en
Mitochondrial bax translocatio ...... acetaminophen hepatotoxicity.
@nl
prefLabel
Mitochondrial bax translocatio ...... acetaminophen hepatotoxicity.
@en
Mitochondrial bax translocatio ...... acetaminophen hepatotoxicity.
@nl
P2093
P356
P1476
Mitochondrial bax translocatio ...... acetaminophen hepatotoxicity.
@en
P2093
Anwar Farhood
Hartmut Jaeschke
John J Lemasters
Mary Lynn Bajt
P356
10.1124/JPET.107.129445
P407
P577
2007-09-28T00:00:00Z