NDLI: Apoptotic insults to human HepG2 cells induced by S-(+)-ketamine occurs through activation of a Bax-mitochondria-caspase protease pathway.

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Apoptotic insults to human HepG2 cells induced by S-(+)-ketamine occurs through activation of a Bax-mitochondria-caspase protease pathway.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Lee, S-T Wu, T-T Yu, P-Y Chen, R-M
Description	Country affiliation: China Author Affiliation: Lee ST ( Department of Pediatrics, Cathay General Hospital, Taipei, Taiwan, Republic of China.)
Abstract	BACKGROUND: Ketamine is widely used as an i.v. anaesthetic agent and as a drug of abuse. Hepatocytes contribute to the metabolism of endogenous and exogenous substances. This study evaluated the toxic effects of S-(+)-ketamine and possible mechanisms using human hepatoma HepG2 cells as the experimental model. METHODS: HepG2 cells were exposed to S-(+)-ketamine. Cell viability and the release of lactate dehydrogenase (LDH) and gamma-glutamyl transpeptidase (GPT) were measured to determine the toxicity of S-(+)-ketamine to HepG2 cells. Cell morphology, DNA fragmentation, and apoptotic cells were analysed to evaluate the mechanism of S-(+)-ketamine-induced cell death. Amounts of Bax, an apoptotic protein, and cytochrome c in the cytoplasm or mitochondria were quantified by immunoblotting. Cellular adenosine triphosphate levels were analysed using a bioluminescence assay. Caspases-3, -9, and -6 were measured fluorometrically. RESULTS: Exposure of HepG2 cells to S-(+)-ketamine increased the release of LDH and GPT, but decreased cell viability (all P<0.01). S-(+)-Ketamine time-dependently caused shrinkage of HepG2 cells. Exposure to S-(+)-ketamine led to significant DNA fragmentation and cell apoptosis (P=0.003 and 0.002). S-(+)-Ketamine increased translocation of Bax from the cytoplasm to mitochondria, but decreased the mitochondrial membrane potential and cellular adenosine triphosphate levels (all P<0.01). Sequentially, cytosolic cytochrome c levels and activities of caspases-9, -3, and -6 were augmented after S-(+)-ketamine administration (all P<0.001). Z-VEID-FMK, an inhibitor of caspase-6, alleviated the S-(+)-ketamine-induced augmentation of caspase-6 activity, DNA fragmentation, and cell apoptosis (all P<0.001). CONCLUSIONS: This study shows that S-(+)-ketamine can induce apoptotic insults to human HepG2 cells via a Bax-mitochondria-caspase protease pathway. Thus, we suggest that S-(+)-ketamine at a clinically relevant or an abused concentration may induce liver dysfunction possibly due to its toxicity to hepatocytes.
File Format	HTM / HTML
ISSN	00070912
e-ISSN	14716771
Journal	British Journal of Anaesthesia
Issue Number	1
Volume Number	102
Language	English
Publisher	Oxford University Press
Publisher Date	2009-01-01
Publisher Place	Great Britain (UK)
Access Restriction	Open
Subject Keyword	Discipline Anesthesiology Anesthetics, Dissociative Pharmacology Apoptosis Drug Effects Hepatocytes Ketamine Carcinoma, Hepatocellular Metabolism Pathology Caspases Dna Fragmentation Dose-response Relationship, Drug Membrane Potential, Mitochondrial Mitochondria Peptide Hydrolases Signal Transduction Tumor Cells, Cultured Bcl-2-associated X Protein Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Anesthesiology and Pain Medicine

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