Phenytoin-initiated hydroxyl radical formation: Characterization by enhanced salicylate hydroxylation

Molecular Pharmacology

Volumn 49, Issue 1, 1996, Pages 172-181

  Kim, Perry M ^a   Wells, Peter G ^a,b  

^a UNIVERSITY OF TORONTO   (Canada)

^b UNIVERSITY OF TORONTO   (Canada)

Author keywords

[No Author keywords available]

Indexed keywords

HYDROXYL RADICAL; PARAQUAT; PHENYTOIN; SALICYLIC ACID;

ANIMAL EXPERIMENT; ARTICLE; DOSE RESPONSE; DRUG HYDROXYLATION; DRUG OXIDATION; DRUG POTENTIATION; ENZYME ACTIVATION; ENZYME ACTIVITY; FEMALE; INTRAPERITONEAL DRUG ADMINISTRATION; MOUSE; NONHUMAN; OXIDATION REDUCTION REACTION; PRIORITY JOURNAL; TERATOGENICITY; TOXICITY TESTING;

ANIMALS; BIOTRANSFORMATION; FEMALE; GENTISATES; GLUCURONIDASE; HYDROLYSIS; HYDROXYBENZOIC ACIDS; HYDROXYL RADICAL; HYDROXYLATION; MICE; PARAQUAT; PHENYTOIN; SALICYLIC ACID; SALICYLIC ACIDS; TERATOGENS;

EID: 0030047170     PISSN: 0026895X     EISSN: None     Source Type: Journal    
DOI: None     Document Type: Article

References (40)

1. Winn, L. M. and P. G. Wells. Free radical-mediated mechanisms of anti-convulsant teratogenicity. Eur. J. Neurol. 2 (Suppl. 4):5-29 (1995).
2. Hanson, J. W., and D. W. Smith. The fetal hydantoin syndrome. Teratology 33:349-353 (1975).
3. Hansen, D. K. The embryotoxicity of phenytoin: an update on possible mechanisms. Proc. Soc. Exp. Biol. Med. 197:361-368 (1991).
4. Miranda, A. F., M J. Wiley, and P. G. Wells. Evidence for embryonic peroxidase-catalyzed bioactivation and glutathione-dependent cytoprotection in phenytoin teratogenicity: modulation by eicosatetraynoic acid and buthionine sulfoximine in murine embryo culture. Toxicol. Appl. Pharmacol. 124:230-241 (1994).
5. Yu, W. K., and P. G. Wells. Evidence for lipoxygenase-catalyzed bioactivation of phenytoin to a teratogenic reactive intermediate: in vitro studies using knoleic acid-dependent soybean lipoxygenase, and in vivo studies using pregnant CD-1 mice. Toxicol. Appl. Pharmacol. 131:1-12 (1995).
6. Parman, T., G. Chen, T. M. Bray, and P. G. Wells. Bioactivation of phenytoin, thalidomide and related teratogens to a free radical intermediate using prostaglandin H synthase (PHS) or hepatic microsomes: characterisation by electron spin resonance (ESR) spectrometry. Toxicologist 16, in press.
7. Liu, L., and P. G. Wells: In vivo phenytoin-initiated oxidative damage to proteins and lipids in murine hepatic and embryonic tissue organelles: potential molecular targets of chemical teratogenesis. Toxicol. Appl. Pharmacol. 125:247-255 (1994).
8. Liu, L., and P. G. Wells. DNA oxidation as a potential molecular mechanism mediating drug-induced birth defects: phenytoin and structurally related teratogens initiate the formation of 8-hydroxy-2′-deoxyguanosine in vitro and in vivo in murine maternal hepatic and embryonic tissues. Free Rad Biol. Med. 19:639-648 (1995).
9. Winn, L. M., and P. G. Wells. Phenytoin-initiated DNA oxidation in murine embryo culture, and embryoprotection by the antioxidative enzymes superoxide dismutase and catalase: evidence for reactive oxygen species-mediated DNA oxidation in the molecular mechanism of phenytoin teratogenicity. Mol. Pharmacol. 48:112-120 (1995).
10. Flower, R. J., S. Moncada, and J. R. Vane. Analgesic-antipyretics and anti-inflammatory agents: drugs employed in the treatment of gout, in The Pharmacological Basis of Therapeutics (A. G. Gilman, L. S. Goodman, T. W Rall, and F. Murad, eds.), Ed. 7. MacMillan Publishing Co., New York, 674-715 (1985).
11. Levy, G., T. Tsuchiya, and L. P. Amsel. Limited capacity for salicyl phenolic glucuronide formation and its effect on the kinetics of salicylate elimination in man. Clin. Pharmacol. Ther. 13:258-268 (1972).
12. Grootveld, M., and B. Halliwell. 2,3-Dihydroxybenzoic acid is a product of human aspirin metabolism. Biochem. Pharmacol. 37:271-280 (1988).
13. Halliwell, B., M. Grootveld, and J. M. C. Gutteridge. Methods for the measurement of hydroxyl radicals in biochemical systems: deoxyribose degradation and aromatic hydroxylation. Methods Biochem. Anal. 33: 59-90 (1988).
14. Floyd, R. A., J. J. Watson, and P. K. Wong. Sensitive assay of hydroxyl free radical formation utilizing high pressure liquid chromatography with electrochemical detection of phenol and salicylate hydroxylation products. J. Biochem. Biophys. Methods 10:221-235 (1984).
15. Udassin, R., I. Ariel, Y. Haskel, N. Kitrossky, and M. Chevion. Salicylate as an in vivo free radical trap: studies on ischemic insult to the rat intestine. Free Rad. Biol. Med. 10:1-6 (1991).
16. Halliwell, B., H. Kaur, and M. Ingelman-Sundberg. Hydroxylation of salicylate as an assay for hydroxyl radicals: a cautionary note. Free Rad. Biol. Med. 10:439-441 (1991).
17. Grootveld, M., and B. Halliwell. Aromatic hydroxylation as a potential measure of hydroxyl radical formation in vivo: identification of hydroxylated derivatives of salicylate in human body fluids. Biochem. J. 237:499-504 (1986).
18. Halliwell, B., and J. M. C. Gutteridge. Oxygen free radicals and iron in relation to biology and medicine: some problems and concepts. Arch. Biochem. Biophys. 246:501-514 (1986).
19. Ingelman-Sundberg, M., H. Kaur, Y. Terelius, J. Persson, and B. Halliwell. Hydroxylation of salicylate by microsomal fractions and cytochrome P-450: lack of production of 2,3-dihydroxybenzoate unless hydroxyl radical formation is permitted. Biochem. J. 276:753-757 (1991).
20. Dutton, G. J. Acceptor substrates of UDP-glucuronosyltransferase and their assay, in Glucuronidation of Drugs and Other Compounds (G. J. Dutton, ed.). CRC Press, Boca Raton, FL, 69-78 (1980).
21. Miyamoto, T, M. Ogino, S. Yamamoto, and O. Hayaishi. Purification of prostaglandin endoperoxide synthase from bovine vesicular gland microsomes. J. Biol. Chem. 251:2629-2636 (1976).
22. Yamazaki, I., L. H. Piette, and T. A. Grover. Kinetic studies on spin trapping of superoxide and hydroxyl radicals generated in NADPH-cytochrome P-450 reductase-paraquat systems. J. Biol. Chem. 265:652-659 (1990).
23. Bus, J. S., S. Z. Cagen, M. Olgaard, and J. E. Gibson. A mechanism of paraquat toxicity in mice and rats. Toxicol. Appl. Pharmacol. 35:501-513 (1976).
24. Kehrer, J. P. Free radicals as mediators of tissue injury and disease. Crit. Rev. Toxicol. 23:21-48 (1993).
25. Prescott, L. F. Kinetics and metabolism of paracetamol and phenacetin. Br. J. Clin. Pharmacol. 10:291S-298S (1980).
26. Nemoto, N. Glutathione, glucuronide and sulfate transferase in polycyclic aromatic hydrocarbon metabolism, in Polycyclic Hydrocarbons and Cancer (H. V. Gelboin and P. O. P. T'so, eds.), Vol. 3. Academic Press, New York, 213-258 (1981).
27. Kalabis, G. M., and P. G. Wells. Biphasic modulation of acetaminophen bioactivation and hepatotoxicity by pretreatment with the interferon inducer polyinosinic-polycytidylic acid. J. Pharmacol. Exp. Ther. 255:1408-1419 (1990).
28. de Morais, S. M., S. Y. M. Chow, and P. G. Wells. Biotransformation and toxicity of acetaminophen in congenic RHA rats with or without a hereditary deficiency in bilirubin UDP-glucuronosyltransferase. Toxicol. Appl. Pharmacol. 117:81-87 (1992).
29. Tomita, M., T. Okuyama, S. Watanabe, and H. Watanabe. Quantitation of the hydroxyl radical adducts of salicylic acid by micellar electrokinetic capillary chromatography: oxidising species formed by a Fenton reaction. Arch. Toxicol. 68:428-433 (1994).
30. Calderbank, A. The bipyridylium herbicides. Adv. Pest. Control Res. 8:127-235 (1968).
31. Coudray, C., M. Talla, S. Martin, M. Fatome, and A. Favier. High-performance liquid chromatography-electrochemical determination of salicylate hydroxylation products as an in vivo marker of oxidative stress. Anal. Biochem. 227:101-111 (1995).
32. Marnett, L. J. Prostaglandin synthase-mediated metabolism of carcinogens and a potential role for peroxyl radicals as reactive intermediates. Environ. Health Perspect. 88:5-12 (1990).
33. Halliwell, B., and J. M. C. Gutteridge. Free radicals and toxicology, in Free Radicals in Biology and Medicine (B. Halliwell and J. M. C. Gutteridge, eds.), Ed. 2. Oxford University Press, New York, 299-365 (1989).
34. Gutteridge, J. M. C., I. Zs.-Nagy, L. Maidt, and R. A. Floyd. ADP-iron as a Fenton reactant: radical reactions detected by spin trapping, hydrogen abstraction, and aromatic hydroxylation. Arch. Biochem. Biophys. 272: 422-428 (1990).
35. O'Connell, M., B. Halliwell, C. P. Moorhouse, O. I. Aruoma, H. Baum, and T. J. Peters. Formation of hydroxyl radicals in the presence of ferritin and haemosiderin: is haemosiderin formation a biological protective mechanism? Biochem. J. 234:727-731 (1986).
36. Puppo, A., and B. Halliwell. Formation of hydroxyl radicals from hydrogen peroxide in the presence of iron: is haemoglobin a biological Fenton reagent? Biochem. J. 249:185-190 (1988).
37. Aruoma, O. I., and B. Halliwell. Superoxide-dependent and ascorbate-dependent formation of hydroxyl radicals from hydrogen peroxide in the presence of iron: are lactoferrin and transferrin promoters of hydroxyl radical generation? Biochem. J. 241:273-278 (1987).
38. Arlen, R., and P. G. Wells. In vivo evidence for prostaglandin H synthase-catalyzed bioactivation of thalidomide to a teratogenic reactive intermediate in the New Zealand White rabbit. J. Pharmacol. Exp. Ther., in press.
39. Laposa, R. R., and P. G. Wells. Preliminary evaluation of phenytoin teratogenicity in transgenic mice deficient in the p53 tumor suppressor gene. Toxicologist 15:161 (1995).
40. Nicol, C. J., M. L. Harrison, R. R. Laposa, I. L. Gimelshtein, and P. G. Wells. A teratologic suppressor role for p53 in benzo[a]pyrene-treated transgenic p53-deficient mice. Nature Genet. 10:181-187 (1995).