The persistent DDT metabolite, 1,1‐dichloro‐2,2‐bis( p ‐chlorophenyl)ethylene, alters thyroid hormone‐dependent genes, hepatic cytochrome P4503A, and pregnane × receptor gene expressions in atlantic salmon ( Salmo salar ) parr

• Published in: Environmental Toxicology and Chemistry
• Main Authors: Mortensen, Anne S., Arukwe, Augustine
• Format: Article in Journal/Newspaper
• Language: English
• Published: Wiley 2006
• Subjects: Health, Toxicology and Mutagenesis; Environmental Chemistry; Atlantic salmon; Salmo salar
• Online Access: http://dx.doi.org/10.1897/05-376r1.1; https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1897%2F05-376R1.1; https://setac.onlinelibrary.wiley.com/doi/pdf/10.1897/05-376R1.1

Abstract The present study investigated the effects of 1,1‐dichloro‐2,2‐bis( p ‐chlorophenyl)ethylene (DDE) on the thyroid and steroid‐metabolizing system in Atlantic salmon ( Salmo salar ) parr. Fish were exposed to waterborne DDE and thyroxine (T 4 ), both singly and in combination, for 5 d. Thyroid‐stimulating hormone (TSHβ), T 4 deiodinase (T 4 ORD), thyroid receptors (TRα and TRβ), and insulin‐like growth factor type 1 receptor (IGF‐1R) were analyzed using quantitative (real‐time) polymerase chain reaction in liver, brain, and kidney, whereas cytochrome P4503A (CYP3A) and pregnane × receptor (PXR) mRNA levels were analyzed only in the liver. Exposure to DDE and T 4 , both singly and in combination, inhibited TSHβ expression in the brain. The DDE induced TSHβ in the liver, and T 4 inhibited TSHβ in the liver and kidney, both singly and in combination with DDE. The DDT‐metabolite DDE induced T 4 ORD expression in the kidney and liver, and combined exposure with T 4 inhibited T 4 ORD expression in the brain, kidney, and liver. The IGF‐1R and TRα expressions were induced by DDE and T 4 singly in the brain, whereas combined exposure with both compounds did not affect IGF‐1R and TRd transcript levels. Whereas T 4 inhibited TRβ expression in the liver, exposure to DDE, both singly and in combination with T 4 , induced TRβ transcript levels in the liver. Exposure to T 4 and DDE, both singly and in combination, resulted in a parallel pattern of CYP3A and PXR mRNA induction in the liver. These results indicate that DDE alters thyroid hormone–dependent genes and hepatic CYP3A and PXR levels. The hepatic modulation of CYP3A and PXR transcript levels by DDE represents a novel aspect of DDE toxicity that, to our knowledge, has not been demonstrated previously in fish. Therefore, the present study demonstrates some possible physiological and endocrine consequences from exposure to endocrine‐disrupting chemicals for salmon parr during smoltification.