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XB-ART-6090
Environ Health Perspect December 1, 2002; 110 (12): 1199-205.

Exposure to the herbicide acetochlor alters thyroid hormone-dependent gene expression and metamorphosis in Xenopus Laevis.

Crump D , Werry K , Veldhoen N , Van Aggelen G , Helbing CC .


Abstract
A growing number of substances released into the environment disrupt normal endocrine mechanisms in a wide range of vertebrates. Little is known about the effects and identities of endocrine-disrupting chemicals (EDCs) that target thyroid hormone (TH) action, particularly at the cellular level. Frog tadpole metamorphosis depends completely on TH, which has led to the suggestion of a metamorphosis-based assay for screening potential EDCs. A major mechanism of TH action is the alteration of gene expression via hormone-bound nuclear receptors. To assess the gene expression profiles in the frog model, we designed a novel multispecies frog cDNA microarray. Recently, the preemergent herbicide acetochlor was shown to accelerate 3,5,3 -triiodothyronine (T3)-induced forelimb emergence and increase mRNA expression of thyroid hormone ss receptors in ranid tadpoles. Here we show that T3-induced metamorphosis of Xenopus laevis, a species commonly used in the laboratory, is accelerated upon acute exposure to an environmentally relevant level of acetochlor. The morphologic changes observed are preceded by alterations in gene expression profiles detected in the tadpole tail, and the nature of these profiles suggest a novel mechanism of action for acetochlor.

PubMed ID: 12460798
PMC ID: PMC1241106
Article link: Environ Health Perspect


Species referenced: Xenopus laevis
Genes referenced: bag6 casp9 cebpa dad1 dan4l dio3 dlx3 fap fmr1 fn1 fosl2 frat1 fzd7 gap43 gli2 glul id2 klf9 kras krt57 mapk14 max mbd3 mdm2 mmp13 mmp13l mmp2 myc nfic npr3 pkn2 ppara pten rara rpa1 smad2 tf tfam tfap2a thdl17 thdl18 thibz thra thrb vldlr

References [+] :
Adachi, Identification of nuclear pre-replication centers poised for DNA synthesis in Xenopus egg extracts: immunolocalization study of replication protein A. 1992, Pubmed, Xenbase