Differential gene expression in rats following subacute exposure to the anticonvulsant sodium valproate

Toxicology and Applied Pharmacology

Volumn 183, Issue 2, 2002, Pages 127-134

  Plant, N ^a   Barber, P ^a   Horner, E ^a   Cockburn, C L ^a   Gibson, G ^a   Bugelski, P ^b   Lord, P ^b  

^a UNIVERSITY OF SURREY   (United Kingdom)

^b GLAXOSMITHKLINE   (United Kingdom)

Author keywords

Anticonvulsants; Gene expression; Hepatotoxicity; Subtractive suppression hybridization; Valproate

Indexed keywords

ANTICONVULSIVE AGENT; FRUCTOSE BISPHOSPHATE ALDOLASE; MESSENGER RNA; PROTEIN SUBUNIT; SUCCINATE DEHYDROGENASE; VALPROIC ACID;

ANIMAL CELL; ARTICLE; AUTOPSY; CELL ENERGY; DISORDERS OF MITOCHONDRIAL FUNCTIONS; DOSE TIME EFFECT RELATION; DOWN REGULATION; DRUG EFFECT; DRUG EXPOSURE; GENE EXPRESSION; GENETIC CODE; HOMEOSTASIS; HYBRIDIZATION; IN VITRO STUDY; IN VIVO STUDY; LIVER TOXICITY; MALE; NONHUMAN; NUCLEOTIDE SEQUENCE; POLYMERASE CHAIN REACTION; RAT; UPREGULATION;

EID: 0036408382     PISSN: 0041008X     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0041-008X(02)99463-9     Document Type: Article

References (19)

1. Altschul, S., et al. (1990). Basic local alignment search tool. J. Mol. Biol. 215, 403-410.
2. Bjorge, S. M., and Baillie, T. A. (1985). Inhibition of medium-chain fatty acid β-oxidation in vitro by valproic acid and its unsaturated metabolite, 2-n-propyl-4-pentenoic acid. Biochem. Biophys. Res. Commun. 132, 245-252.
3. Bowden, C. (1996). Role of newer medications for bipolar disorder. J. Clin. Psychopharmacol. 16, S48-S55.
4. Jagannathan, V., et al. (1956). Carbohydrate metabolism in citric acid fermentation. IV. Purification and properties of aldolase from Aspergillus niger. Biochem. J. 63, 94.
5. Jeavons, P. (1984). Non-dose related side effects of valproate. Epilepsia 25 (S1), S50-S55.
6. Keck, P., et al. (1993). Valproate oral loading in the treatment of acute mania. J. Clin. Psychiatry 54, 305-308.
7. Kesterson, J. W., et al. (1984). The hepatotoxicity of valproic acid and its metabolites in rats. I. Toxicologic, biochemical and histopathologic studies. Hepatology 4, 1143-1152.
8. Kolls, J., et al. (1993). cDNA equalisation for reverse transcription polymerase chain-reaction quantitiation. Anal. Biochem. 208, 264-269.
9. Loscher, W. (1999). Valproate: A reappraisal of its pharmacodynamic properties and mechanisms of action. Prog. Neurobiol. 58, 31-59.
10. Loscher, W., and Vetter, M. (1985). In vivo effects of aminooxyacetic acid and valproic acid on nerve terminal (synaptosomal) GABA levels in discrete brain areas of the rat. Biochem. Pharmacol. 34, 1747-1756.
11. McLaughlin, D. B., et al. (2000). Apparent autoinduction of valproate β-oxidation in humans. Br. J. Clin. Pharmacol. 49, 409-415.
12. McLean, M., and Macdonald, R. (1986). Sodium valproate, but not ethosuximide, produces use-and voltage-dependent limitation of high frequency repetitive firing of action potentials of mouse central neurons in cell culture. J. Pharmacol. Exp. Therapeut. 237, 1001-1011.
13. Neuman, M. G., et al. (2001). CYP2E1-mediated modulation of valproic acid-induced hepatocytoxicity. Clin. Biochem. 34, 211-218.
14. Penry, J., and Dean, J. (1989). The scope and use of valproate in epilepsy. J. Clin. Psychiatry 50, 17-22.
15. Serrano, B. B., et al. (1999). Valproate population pharmacokinetics in children. J. Clin. Pharmacy Therapeut. 24, 73-80.
16. Tang, W., et al. (1996). Conjugation of glutathione with a toxic metabolite of valproic acid, (E)-2-propyl-2, 4-pentadienoic acid, catalyzed by rat hepatic glutathione-S-transferases. Drug Metab. Dispos. 24, 436-446.
17. Vallee, B., and Hoch, F. (1955). Zinc, a component of yeast alcohol dehydrogenase. Proc. Natl. Acad. Sci. USA 41, 327.
18. Worthington Biochemical Corp. (1972). Worthington Enzyme Manual. Freehold, NJ.
19. Zeise, M., et al. (1991). Valproate suppresses N-methyl-D-asparate evoked, transient depolarizations in the rat neocortex in vitro. Brain Res. 544, 345-348.