DMD Large equally mixed donor pool

Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Conaway, C. C.
Right arrow Articles by Chung, F.-L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Conaway, C. C.
Right arrow Articles by Chung, F.-L.

Vol. 27, Issue 1, 13-20, January 1999

Disposition and Pharmacokinetics of Phenethyl Isothiocyanate and 6-Phenylhexyl Isothiocyanate in F344 Rats

C. Clifford Conaway, Ding Jiao, Toshiyuki Kohri,1 Leonard Liebes, and Fung-Lung Chung

Division of Carcinogenesis and Molecular Epidemiology, American Health Foundation, Valhalla, New York (C.C.C., D.J., T.K., F.-L.C.); and Department of Medicine, Kaplan Cancer Center, New York University Medical Center, New York, New York (L.L.)

Naturally occurring phenethyl isothiocyanate (PEITC) and its synthetic homolog 6-phenylhexyl isothiocyanate (PHITC) are both effective inhibitors of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone-induced lung tumor development in A/J mice and F344 rats. To help explain why PHITC is considerably more efficacious than PEITC in chemopreventive potency, comparative disposition and pharmacokinetics data for male F344 rats were obtained after a single gavage dose of 50 µmol/kg (3.71 µCi/µmol) [14C]PEITC or 50 µmol/kg (6.59 µCi/µmol) [14C]PHITC in corn oil. After [14C]PEITC dosing, whole blood 14C peaked at 2.9 h, with an elimination half-life (T1/2e) of 21.7 h; blood 14C from [14C]PHITC-treated rats peaked at 8.9 h, with an T1/2e of 20.5 h. In lungs, the target organ, the T1/2e for [14C]PHITC and its labeled metabolites were more than twice that for [14C]PEITC and its labeled metabolites. The effective dose (area under the concentration-time curve) for 14C from PHITC was greater than 2.5 times the area under the concentration-time curve of 14C from PEITC in liver, lungs, and several other tissues. During 48 h, approximately 16.5% of the administered dose of [14C]PHITC was expired as [14C]CO2, more than 100 times the [14C]CO2 expired by rats treated with [14C]PEITC. In rats given [14C]PEITC, 88.7 ± 2.2% and 9.9 ± 1.9% of the dose appeared in the urine and feces, respectively, during 48 h; however, rats given [14C]PHITC excreted 7.2 ± 0.8% of the dose of 14C in urine and 47.4 ± 14.0% in the feces. Higher effective doses of PHITC in the lungs and other organs may be the basis, in part, for its greater potency as a chemopreventive agent.


1   Present address: Mitsui Norin Co., Ltd., Food Research Laboratories, 233 Miyabara, Fujieda City, Shizouka 426-01, Japan.


Copyright © 1999 by The American Society for Pharmacology and Experimental Therapeutics



This article has been cited by other articles:


Home page
Am. J. Clin. Nutr.Home page
J. W Lampe
Interindividual differences in response to plant-based diets: implications for cancer risk
Am. J. Clinical Nutrition, May 1, 2009; 89(5): 1553S - 1557S.
[Abstract] [Full Text] [PDF]


Home page
Cancer Prevention ResearchHome page
F. Kassie, I. Matise, M. Negia, D. Lahti, Y. Pan, R. Scherber, P. Upadhyaya, and S. S. Hecht
Combinations of N-Acetyl-S-(N-2-Phenethylthiocarbamoyl)-L-Cysteine and myo-Inositol Inhibit Tobacco Carcinogen-Induced Lung Adenocarcinoma in Mice
Cancer Prevention Research, September 1, 2008; 1(4): 285 - 297.
[Abstract] [Full Text] [PDF]


Home page
aacrmtgHome page
J. W. Lampe
Interindividual differences in response to cruciferous vegetable diets: Implications for cancer risk.
AACR Meeting Abstracts, April 1, 2006; 2006(1): 1365 - 1366.
[Abstract]


Home page
Am. J. Clin. Nutr.Home page
A. V Gasper, A. Al-janobi, J. A Smith, J. R Bacon, P. Fortun, C. Atherton, M. A Taylor, C. J Hawkey, D. A Barrett, and R. F Mithen
Glutathione S-transferase M1 polymorphism and metabolism of sulforaphane from standard and high-glucosinolate broccoli
Am. J. Clinical Nutrition, December 1, 2005; 82(6): 1283 - 1291.
[Abstract] [Full Text] [PDF]


Home page
J. Pharmacol. Exp. Ther.Home page
R. Hu, V. Hebbar, B.-R. Kim, C. Chen, B. Winnik, B. Buckley, P. Soteropoulos, P. Tolias, R. P. Hart, and A.-N. T. Kong
In Vivo Pharmacokinetics and Regulation of Gene Expression Profiles by Isothiocyanate Sulforaphane in the Rat
J. Pharmacol. Exp. Ther., July 1, 2004; 310(1): 263 - 271.
[Abstract] [Full Text] [PDF]


Home page
Molecular Cancer TherapeuticsHome page
Y. Zhang, L. Tang, and V. Gonzalez
Selected isothiocyanates rapidly induce growth inhibition of cancer cells
Mol. Cancer Ther., October 1, 2003; 2(10): 1045 - 1052.
[Abstract] [Full Text]


Home page
J. Nutr.Home page
J. W. Lampe and S. Peterson
Brassica, Biotransformation and Cancer Risk: Genetic Polymorphisms Alter the Preventive Effects of Cruciferous Vegetables
J. Nutr., October 1, 2002; 132(10): 2991 - 2994.
[Abstract] [Full Text] [PDF]


Home page
CarcinogenesisHome page
L. Ye and Y. Zhang
Total intracellular accumulation levels of dietary isothiocyanates determine their activity in elevation of cellular glutathione and induction of Phase 2 detoxification enzymes
Carcinogenesis, December 1, 2001; 22(12): 1987 - 1992.
[Abstract] [Full Text] [PDF]


Home page
CarcinogenesisHome page
Y. Zhang
Molecular mechanism of rapid cellular accumulation of anticarcinogenic isothiocyanates
Carcinogenesis, March 1, 2001; 22(3): 425 - 431.
[Abstract] [Full Text] [PDF]




Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
All ASPET Journals Molecular Pharmacology Pharmacological Reviews
 Molecular Interventions Drug Metabolism and Disposition

Copyright © 1999 by the American Society for Pharmacology and Experimental Therapeutics.