Research Topics
| Urs A BoelsterliSummaryAffiliation: HepaTox Consulting Country: Switzerland Publications
| Collaborators
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Detail Information
Publications
Mechanisms of NSAID-induced hepatotoxicity: focus on nimesulideUrs A Boelsterli
HepaTox Consulting, Pfeffingen, and Institute of Clinical Pharmacy, University of Basel, Basel, Switzerland
Drug Saf 25:633-48. 2002....
Toxicological consequences of altered peroxisome proliferator-activated receptor gamma (PPARgamma) expression in the liver: insights from models of obesity and type 2 diabetesUrs A Boelsterli
HepaTox Consulting, P O Box 14, CH 4148, Pfeffingen
Biochem Pharmacol 63:1-10. 2002..Therefore, receptor expression in human liver tissue of obese and T2DM patients should deserve increased consideration in the future...
Xenobiotic acyl glucuronides and acyl CoA thioesters as protein-reactive metabolites with the potential to cause idiosyncratic drug reactionsUrs A Boelsterli
HepaTox Consulting, CH 4148 Pfeffingen, and Institute of Clinical Pharmacy, University of Basel, Basel, CH 4031, Switzerland
Curr Drug Metab 3:439-50. 2002..More work is needed to provide a causal link between protein-reactive acyl glucuronides and acyl-CoA thioesters and the rare and unpredictable idiosyncratic drug reactions in humans...
Disease-related determinants of susceptibility to drug-induced idiosyncratic hepatotoxicityUrs A Boelsterli
HepaTox Consulting, PO Box 14, CH 4148 Pfeffingen, Switzerland
Curr Opin Drug Discov Devel 6:81-91. 2003..The need for an increased use of animal models of human disease in mechanistic investigations and drug candidate selection will also be emphasized...
Diclofenac-induced liver injury: a paradigm of idiosyncratic drug toxicityUrs A Boelsterli
HepaTox Consulting, CH 4148 Pfeffingen, and Institute of Clinical Pharmacy, University of Basel, CH 4031 Basel, Switzerland
Toxicol Appl Pharmacol 192:307-22. 2003..Increased efforts to identify both patient-specific risk factors and disease-related factors will help to define patient subsets at risk as well as increase the predictability of unexpected hepatotoxicity in drug development...
Animal models of human disease in drug safety assessmentUrs A Boelsterli
Institute of Clinical Pharmacy, University of Basel, Switzerland
J Toxicol Sci 28:109-21. 2003....
Troglitazone-induced hepatic necrosis in an animal model of silent genetic mitochondrial abnormalitiesMichie M K Ong
Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117 597
Toxicol Sci 97:205-13. 2007..These data are consistent with our hypothesis that inherited or acquired mitochondrial abnormalities may be one of the contributing determinants of susceptibility to troglitazone-induced idiosyncratic liver injury...
Troglitazone-induced hepatic mitochondrial proteome expression dynamics in heterozygous Sod2(+/-) mice: two-stage oxidative injuryYie Hou Lee
Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117597
Toxicol Appl Pharmacol 231:43-51. 2008....
Bioactivation and hepatotoxicity of nitroaromatic drugsUrs A Boelsterli
Molecular Toxicology Lab, Department of Pharmacology, Yong Loo Lin School of Medicine, Singapore
Curr Drug Metab 7:715-27. 2006..Most likely one of the next paradigm shifts will include the identification of determinants of susceptibility to nitroaromatic drug-induced hepatotoxicity...
Proteomics profiling of hepatic mitochondria in heterozygous Sod2+/- mice, an animal model of discreet mitochondrial oxidative stressYie Hou Lee
Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore
Proteomics 8:555-68. 2008..The results of this study are compatible with our hypothesis that the Sod2+/- mouse is a suitable animal model for studying clinically silent mitochondrial abnormalities...
Bax-mediated mitochondrial outer membrane permeabilization (MOMP), distinct from the mitochondrial permeability transition, is a key mechanism in diclofenac-induced hepatocyte injury: Multiple protective roles of cyclosporin AWoen Ping Siu
Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117 597
Toxicol Appl Pharmacol 227:451-61. 2008..These data support our concept that the Ca2+-Bid-Bax-MOMP axis is a critical pathway in diclofenac (metabolite)-induced hepatocyte injury...
The mitochondrial superoxide/thioredoxin-2/Ask1 signaling pathway is critically involved in troglitazone-induced cell injury to human hepatocytesPriscilla L K Lim
Department of Pharmacology, Yong Loo Lin School of Medicine National University of Singapore, Singapore 117595
Toxicol Sci 101:341-9. 2008..Furthermore, the data support our concept that targeted delivery of an antioxidant to mitochondria can inhibit upstream signaling and protect from troglitazone-induced lethal cell injury...
Molecular and functional characterization of drug-metabolizing enzymes and transporter expression in the novel spontaneously immortalized human hepatocyte line HC-04Priscilla L K Lim
Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117597, Singapore
Toxicol In Vitro 21:1390-401. 2007..Collectively, HC-04 cells provide a reliable, stable, and reproducible model for biomechanistic studies in drug toxicology...
Mitochondrial protection by the JNK inhibitor leflunomide rescues mice from acetaminophen-induced liver injuryCalivarathan Latchoumycandane
Department of Pharmacology, Yong Loo Lin School of Medicine, Singapore
Hepatology 45:412-21. 2007..Conclusion: Leflunomide afforded protection against APAP-induced hepatotoxicity in mice through inhibition of JNK-mediated activation of mitochondrial permeabilization...
Mitochondrial abnormalities--a link to idiosyncratic drug hepatotoxicity?Urs A Boelsterli
Molecular Toxicology Lab, Department of Pharmacology, Yong Loo Lin School of Medicine, Singapore
Toxicol Appl Pharmacol 220:92-107. 2007..New animal models (e.g., the Sod2(+/-) mouse) provide supporting evidence for this concept. However, genetic analyses of DILI patient samples are needed to ultimately provide the proof-of-concept...
Mitochondrial permeability transition as a source of superoxide anion induced by the nitroaromatic drug nimesulide in vitroVincent K S Tay
Department of Pharmacology, Faculty of Medicine, National University of Singapore, 18 Medical Drive, Singapore 117597
Free Radic Biol Med 39:949-59. 2005....
Nimesulide-induced hepatic mitochondrial injury in heterozygous Sod2(+/-) miceMichie M K Ong
Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore
Free Radic Biol Med 40:420-9. 2006..In conclusion, repeated administration of nimesulide can superimpose an oxidant stress, potentiate mitochondrial damage, and activate proapoptotic factors in mice with genetically compromised mitochondrial function...
Critical role of free cytosolic calcium, but not uncoupling, in mitochondrial permeability transition and cell death induced by diclofenac oxidative metabolites in immortalized human hepatocytesMiao Shan Lim
Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117597, Singapore
Toxicol Appl Pharmacol 217:322-31. 2006....
