2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) Increases Bilirubin Formation but Hampers Quantitative Hepatic Conversion of Biliverdin to Bilirubin in Rats with Wild-Type AH Receptor

Author:

Niittynen Marjo1,Simanainen Ulla1,Pohjanvirta Raimo2,Sankari Satu3,Tuomisto Jouni T.1

Affiliation:

1. Department of Environmental Health; National Institute for Health and Welfare; Kuopio; Finland

2. Department of Food Hygiene and Environmental Health; Faculty of Veterinary Medicine; University of Helsinki; Helsinki Finland

3. Department of Equine and Small Animal Medicine; Faculty of Veterinary Medicine; University of Helsinki; Helsinki Finland

Funder

Academy of Finland

Emil Aaltonen Foundation

Finnish Cultural Foundation

The Graduate School in Environmental Health

Publisher

Wiley

Subject

Pharmacology,Toxicology,General Medicine

Reference51 articles.

1. Enzymatic functions as targets of the toxicity of “Dioxin” (2,3,7,8-tetrachlorodibenzo-p-dioxin);Buu-Hoi;Naturwissenschaften,1972

2. Essential role of the AH receptor in the dysfunction of heme metabolism induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin;Davies;Chem Res Toxicol,2008

3. Short-term toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin in laboratory animals: effects, mechanisms, and animal models;Pohjanvirta;Pharmacol Rev,1994

4. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD)-induced accumulation of biliverdin and hepatic peliosis in rats;Niittynen;Toxicol Sci,2003

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