Quantitative and statistical analysis of differences in sensitivity between Long-Evans and Han/Wistar rats following long-term exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin

Regulatory Toxicology and Pharmacology

Volumn 57, Issue 2-3, 2010, Pages 136-145

  Sand, Salomon ^a,b   Fletcher, Nicholas ^a   Rosen, Dietrich von ^c   Kalantari, Fereshteh ^a   Viluksela, Matti ^d   Tuomisto, Jouni T ^d   Tuomisto, Jouko ^d   Falk Filipsson, Agneta ^e   Håkansson, Helen ^a  

^a KAROLINSKA INSTITUTE   (Sweden)

^b NATIONAL FOOD ADMINISTRATION   (Sweden)

^c SWEDISH UNIVERSITY OF AGRICULTURAL SCIENCES   (Sweden)

^d NATIONAL PUBLIC HEALTH INSTITUTE   (Finland)

^e Swedish Chemicals Agency   (Sweden)

Author keywords

Benchmark dose; BMD; Dose response; Strain sensitivity; Strain variation; TCDD

Indexed keywords

2,3,7,8 TETRACHLORODIBENZO PARA DIOXIN; CYTOCHROME P450 1A1; RETINOID;

ANIMAL EXPERIMENT; ARTICLE; BODY WEIGHT; CONTROLLED STUDY; ENZYME INDUCTION; FEMALE; LIVER; LONG EVANS RAT; NONHUMAN; ORGAN WEIGHT; PRIORITY JOURNAL; QUANTITATIVE ANALYSIS; RAT; SENSITIVITY ANALYSIS; SPECIES DIFFERENCE; STATISTICAL ANALYSIS; STATISTICAL MODEL; STRAIN DIFFERENCE; TISSUE LEVEL; WISTAR HANNOVER RAT;

ANIMALS; BENCHMARKING; BODY WEIGHT; CYTOCHROME P-450 CYP1A1; CYTOCHROMES; DOSE-RESPONSE RELATIONSHIP, DRUG; FEMALE; LIVER; ORGAN SIZE; ORGAN SPECIFICITY; RATS; RATS, LONG-EVANS; RATS, WISTAR; SPECIES SPECIFICITY; TETRACHLORODIBENZODIOXIN; TIME FACTORS; TOXICITY TESTS, CHRONIC; VITAMIN A;

RATTUS;

EID: 77953363737     PISSN: 02732300     EISSN: 10960295     Source Type: Journal    
DOI: 10.1016/j.yrtph.2010.01.006     Document Type: Article

References (37)

1. Allen B.C., Strong P.L., Price C.J., Hubbard S.A., Daston G.P. Benchmark dose analysis of developmental toxicity in rats exposed to boric acid. Fundam. Appl. Toxicol. 1996, 32:194-204.
2. Allen B.C., Gentry R., Shipp A., Van Landingham C. Calculation of benchmark doses for reproductive and developmental toxicity observed after exposure to isopropanol. Regul. Toxicol. Pharmacol. 1998, 28:38-44.
3. Andreola F., Fernandez-Salguero P.M., Chiantore M.V., Petkovich M.P., Gonzalez F.J., De Luca L.M. Aryl hydrocarbon receptor knockout mice (AHR-/-) exhibit liver retinoid accumulation and reduced retinoic acid metabolism. Cancer Res. 1997, 57:2835-2838.
4. Barton H.A., Andersen M.E., Allen B.C. Dose-response characteristics of uterine responses in rats exposed to estrogen agonists. Regul. Toxicol. Pharmacol. 1998, 28:133-149.
5. Chen H., Howald W.N., Juchau M.R. Biosynthesis of all-trans-retinoic acid from all-trans-retinol: catalysis of all-trans-retinol oxidation by human P-450 cytochromes. Drug Metab. Dispos. 2000, 28:315-322.
6. Crump K. A new method for determining allowable daily intakes. Fundam. Appl. Toxicol. 1984, 4:854-871.
7. Guidance of the Scientific Committee on a request from EFSA on the use of the benchmark dose approach in risk assessment. EFSA J. 2009, 1150:1-72. EFSA.
8. Fletcher N., Giese N., Schmidt C., Stern N., Lind P.M., Viluksela M., Tuomisto J.T., Tuomisto J., Nau H., Håkansson H. Altered retinoid metabolism in female Long-Evans and Han/Wistar rats following long-term 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-treatment. Toxicol. Sci. 2005, 86:264-272.
9. Gaylor D.W., Aylward L.L. An evaluation of benchmark dose methodology for non-cancer continuous-data health effects in animals due to exposures to dioxin (TCDD). Regul. Toxicol. Pharmacol. 2004, 40:9-17.
10. Jämsä T., Viluksela M., Tuomisto J.T., Tuomisto J., Tuukkanen J. Effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin on bone in two rat strains with different aryl hydrocarbon receptor structures. J. Bone Miner. Res. 2001, 16:1812-1820.
11. Kavlock R.J., Allen B.C., Faustman E.M., Kimmel C.A. Dose-response assessments for developmental toxicity. IV. Benchmark doses for fetal weight changes. Fundam. Appl. Toxicol. 1995, 26:211-222.
12. Kim A.H., Kohn M.C., Portier C.J., Walker N.J. Impact of physiologically based pharmacokinetic modeling on benchmark dose calculations for TCDD-induced biochemical responses. Regul. Toxicol. Pharmacol. 2002, 36:287-296.
13. Marill J., Cresteil T., Lanotte M., Chabot G.G. Identification of human cytochrome P450s involved in the formation of all-trans-retinoic acid principal metabolites. Mol. Pharmacol. 2000, 58:1341-1348.
14. Murrell J.A., Portier C.J., Morris R.W. Characterizing dose-response I: critical assessment of the benchmark dose concept. Risk Anal. 1998, 18:13-26.
15. Nilsson C.B., Håkansson H. The retinoid signaling system - a target in dioxin toxicity. Crit. Rev. Toxicol. 2002, 32:211-232.
16. Nishimura N., Yonemoto J., Miyabara Y., Yokoi C., Takeuchi Y., Fujii-Kuriyama Y., Maeda S., Tohyama C. Lack of thyroxine and retinoid metabolic response to 2,3,7,8-tetrachlorodibenzo-p-dioxin in arylhydrocarbon receptor-null mice but not in transthyretin-null mice. Organohalogen Compd. 2002, 56:49-51.
17. Pohjanvirta R., Kulju T., Morselt A.F., Tuominen R., Juvonen R., Rozman K., Mannisto P., Collan Y., Sainio E.L., Tuomisto J. Target tissue morphology and serum biochemistry following 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure in a TCDD-susceptible and a TCDD-resistant rat strain. Fundam. Appl. Toxicol. 1989, 12:698-712.
18. Pohjanvirta R., Vartiainen T., Uusi-Rauva A., Mönkkönen J., Tuomisto J. Tissue distribution, metabolism, and excretion of 14C-TCDD in a TCDD-susceptible and a TCDD-resistant rat strain. Pharmacol. Toxicol. 1990, 66:93-100.
19. Pohjanvirta R., Unkila M., Tuomisto J. Comparative acute lethality of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), 1,2,3,7,8-pentachlorodibenzo-p-dioxin and 1,2,3,4,7,8-hexachlorodibenzo-p-dioxin in the most TCDD-susceptible and the most TCDD-resistant rat strain. Pharmacol. Toxicol. 1993, 73:52-56.
20. Pohjanvirta R., Tuomisto J. Short-term toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin in laboratory animals: effects, mechanisms, and animal models. Pharmacol. Rev. 1994, 46:483-549.
21. Pohjanvirta R., Wong J.M., Li W., Harper P.A., Tuomisto J., Okey A.B. Point mutation in intron sequence causes altered carboxyl-terminal structure in the aryl hydrocarbon receptor of the most 2,3,7,8-tetrachlorodibenzo-p-dioxin-resistant rat strain. Mol. Pharmacol. 1998, 54:86-93.
22. Pohjanvirta R., Viluksela M., Tuomisto J.T., Unkila M., Karasinska J., Franc M.A., Holowenko M., Giannone J.V., Harper P.A., Tuomisto J., Okey A.B. Physicochemical differences in the AH receptors of the most TCDD-susceptible and the most TCDD-resistant rat strains. Toxicol. Appl. Pharmacol. 1999, 155:82-95.
23. Raner G.M., Vaz A.D.M., Coon M.J. Metabolism of all-trans, 9-cis and 13-cis isomers of retinal by purified enzymes of microsomal cytochrome P450 and mechanism-based inhibition of retinoid oxidation by citral. Mol. Pharmacol. 1996, 49:515-522.
24. Sand S., von Rosen D., Eriksson P., Fredriksson A., Viberg H., Victorin K., Filipsson A.F. Dose-response modeling and benchmark calculations from spontaneous behavior data on mice neonatally exposed to 2,2',4,4',5-pentabromodiphenyl ether. Toxicol. Sci. 2004, 81:491-501.
25. Sand S., von Rosen D., Victorin K., Filipsson A.F. Identification of a critical dose level for risk assessment: developments in benchmark dose analysis of continuous endpoints. Toxicol. Sci. 2006, 90:241-251.
26. Sand S., Victorin K., Filipsson A.F. The current state of knowledge on the use of the benchmark dose concept in risk assessment. J. Appl. Toxicol. 2008, 28:405-421.
27. Schmidt C.K., Brouwer A., Nau H. Chromatographic analysis of endogenous retinoids in tissues and serum. Anal. Biochem. 2003, 315:36-48.
28. Simanainen U., Tuomisto J.T., Tuomisto J., Viluksela M. Structure-activity relationships and dose responses of polychlorinated dibenzo-p-dioxins for short-term effects in 2,3,7,8-tetrachlorodibenzo-p-dioxin-resistant and sensitive rat strains. Toxicol. Appl. Pharmacol. 2002, 181:38-47.
29. Simanainen U., Tuomisto J.T., Tuomisto J., Viluksela M. Dose-response analysis of short-term effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin in three differentially susceptible rat lines. Toxicol. Appl. Pharmacol. 2003, 187:128-136.
30. Slob W., Pieters M.N. A probabilistic approach for deriving acceptable human intake limits and human health risks from toxicological studies: general framework. Risk Anal. 1998, 18:787-798.
31. Slob W. Dose-response modeling of continuous endpoints. Toxicol. Sci. 2002, 66:298-312.
32. Toyoshiba H., Walker N.J., Bailer A.J., Portier C.J. Evaluation of toxic equivalency factors for induction of cytochromes P450 CYP1A1 and CYP1A2 enzyme activity by dioxin-like compounds. Toxicol. Appl. Pharmacol. 2004, 194:156-168.
33. Tuomisto J.T., Viluksela M., Pohjanvirta R., Tuomisto J. The AH receptor and a novel gene determine acute toxic responses to TCDD: segregation of the resistant alleles to different rat lines. Toxicol. Appl. Pharmacol. 1999, 155:71-81.
34. Unkila M., Pohjanvirta R., MacDonald E., Tuomisto J.T., Tuomisto J. Dose response and time course of alterations in tryptophan metabolism by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in the most TCDD-susceptible and the most TCDD-resistant rat strain: relationship with TCDD lethality. Toxicol. Appl. Pharmacol. 1994, 128:280-292.
35. Viluksela M., Bager Y., Tuomisto J.T., Scheu G., Unkila M., Pohjanvirta R., Flodström S., Kosma V., Mäki-Paakkanen J., Vartiainen T., Klimm C., Schramm K., Wärngård L., Tuomisto J. Liver tumor-promoting activity of 2,3,7,8-tetrachlodibenzo-p-dioxin (TCDD) in TCDD-sensitive and TCDD-resistant rat strains. Cancer Res. 2000, 60:6911-6920.
36. Woutersen R.A., Jonker D., Stevenson H., te Biesebeek J.D., Slob W. The benchmark approach applied to a 28-day toxicity study with Rhodorsil Silane in rats: the impact of increasing the number of dose groups. Food Chem. Toxicol 2001, 39:697-707.
37. Zhang Q.Y., Dunbar D., Kaminsky L. Human cytochrome p-450 metabolism of retinals to retinoic acids. Drug Metab. Dispos. 2000, 28:292-297.