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Toxicology and applied pharmacology, ISSN 0041-008X, 12/2015, Volume 289, Issue 2, pp. 213 - 222
...) with AMAP or APAP for up to 48h and measured several parameters to assess metabolism and injury... 
Protein adducts | Mitochondrial dysfunction | Acetaminophen | 3′-Hydroxyacetanilide (AMAP) | Hepatotoxicity | 3'-Hydroxyacetanilide (AMAP) | Pharmacology & Pharmacy | Toxicology | Life Sciences & Biomedicine | Science & Technology | L-Lactate Dehydrogenase - metabolism | Liver - pathology | Phosphorylation | Species Specificity | Glutathione - metabolism | Mitochondria, Liver - metabolism | Humans | Hepatocytes - pathology | JNK Mitogen-Activated Protein Kinases - metabolism | Hepatocytes - metabolism | Dose-Response Relationship, Drug | Liver - drug effects | Time Factors | Mitochondrial Proteins - metabolism | Cell Death - drug effects | Chemical and Drug Induced Liver Injury - pathology | Glutamate Dehydrogenase - metabolism | Chemical and Drug Induced Liver Injury - etiology | Hepatocytes - drug effects | Mitochondria, Liver - pathology | Liver - metabolism | Cells, Cultured | Mitochondria, Liver - drug effects | Animals | Signal Transduction - drug effects | Chemical and Drug Induced Liver Injury - metabolism | Acetanilides - toxicity | Protein Binding | Mice | Primary Cell Culture | Proteins | Mitochondrial DNA | Index Medicus | HUMAN POPULATIONS | APOPTOSIS | IMINES | LACTATES | MITOCHONDRIA | ADDUCTS | TOXICITY | BENZOQUINONES | 60 APPLIED LIFE SCIENCES | DISULFIDES | LACTATE DEHYDROGENASE | IODIDES | ALANINES | GLUTATHIONE | HAMSTERS | LIVER | LIVER CELLS | PHOSPHOTRANSFERASES | AMINOTRANSFERASES | TRANSGENIC MICE | protein adducts | acetaminophen | mitochondrial dysfunction | hepatotoxicity
Journal Article
Journal Article
Toxicology and applied pharmacology, ISSN 0041-008X, 11/2012, Volume 264, Issue 3, pp. 387 - 394
Acetaminophen (APAP) overdose is the most common cause of acute liver failure in the West. In mice, APAP hepatotoxicity can be rapidly induced with a single... 
Protein adducts | Mitochondria | Acetaminophen | Hepatotoxicity | Oxidant stress | c-Jun‐N-terminal kinase | C-Jun-N-terminal kinase | Pharmacology & Pharmacy | Toxicology | Life Sciences & Biomedicine | Science & Technology | Rats, Inbred F344 | Mitochondrial Proteins - genetics | MAP Kinase Kinase 4 - metabolism | Alanine Transaminase - genetics | Analgesics, Non-Narcotic - toxicity | Time Factors | Mitochondrial Proteins - metabolism | Glutamate Dehydrogenase - metabolism | Disease Models, Animal | Acetaminophen - toxicity | Mice, Inbred C57BL | Gene Expression Regulation | Antipyretics - toxicity | Rats | Mitochondria - metabolism | Mitochondria - drug effects | Glutamate Dehydrogenase - genetics | Rats, Sprague-Dawley | Animals | Chemical and Drug Induced Liver Injury - metabolism | MAP Kinase Kinase 4 - genetics | Protein Binding | Mice | Alanine Transaminase - metabolism | Oxidative Stress - drug effects | Oxidative stress | Liver diseases | Liver | Physiological aspects | Mitochondrial DNA | Comparative analysis | Index Medicus | Translocation | Oxidative metabolism | Toxicity | Data processing | Metabolism | Protein turnover | Necrosis | Proteins | c-Jun amino-terminal kinase | Models | Overdose | Intoxication | Injuries | OXIDATION | TRANSLOCATION | INJURIES | MITOCHONDRIA | RATS | TOXICITY | 60 APPLIED LIFE SCIENCES | NECROSIS | METABOLISM | OXIDIZERS | LIVER | MICE | PREFERRED SPECIES | protein adducts | oxidant stress | c-jun-N-terminal kinase | hepatotoxicity | mitochondria
Journal Article
Kidney international, ISSN 0085-2538, 03/2012, Volume 81, Issue 6, pp. 559 - 567
.... Following metabolic activation, aristolochic acid reacts with genomic DNA to form aristolactam-DNA adducts that generate a unique TP53 mutational spectrum in the urothelium... 
upper urinary tract cancer | endemic nephropathy | DNA adducts | Aristolochia | nephrotoxicity | aristolochic acid | Life Sciences & Biomedicine | Urology & Nephrology | Science & Technology | Urologic Neoplasms - epidemiology | Humans | Middle Aged | Balkan Nephropathy - chemically induced | Male | DNA Adducts - analysis | DNA Mutational Analysis | Croatia - epidemiology | Aged, 80 and over | Balkan Nephropathy - genetics | Genetic Predisposition to Disease | Risk Assessment | Balkan Nephropathy - metabolism | Risk Factors | Biomarkers - analysis | Environmental Monitoring - methods | Urologic Neoplasms - chemically induced | Environmental Exposure | Bosnia and Herzegovina - epidemiology | Aristolochic Acids - adverse effects | Diet | Epidemiological Monitoring | Molecular Epidemiology | Carcinoma - genetics | Mutation | Carcinogens, Environmental - metabolism | Balkan Nephropathy - epidemiology | Kidney Cortex - drug effects | Residence Characteristics | Urologic Neoplasms - diagnosis | Case-Control Studies | Tumor Suppressor Protein p53 - genetics | Urologic Neoplasms - genetics | Biotransformation | Carcinoma - epidemiology | Mass Spectrometry | Carcinogens, Environmental - adverse effects | Adult | Female | Urologic Neoplasms - metabolism | Carcinoma - chemically induced | Carcinoma - diagnosis | Kidney Cortex - pathology | Aristolochic Acids - metabolism | Kidney Cortex - chemistry | Aged | Balkan Nephropathy - diagnosis | Carcinoma - metabolism | Serbia - epidemiology | Urine | renal cortex | Carcinoma | biomarkers | Mass spectroscopy | Aristolochic acid | Urinary tract | urothelium | Kidney | p53 protein | Diets | Carcinogens | Nephropathy | urothelial carcinoma | DNA | Metabolic activation | genomics | Bioindicators | Mass spectrometry | Adducts | Tumors | Index Medicus
Journal Article
Chemical research in toxicology, ISSN 0893-228X, 12/2008, Volume 21, Issue 12, pp. 2361 - 2369
Journal Article
Journal Article