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This Article Accepted manuscript (PDF) All Versions of this Article: JOE-08-0123v1 198/2/301    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Jin, L. Articles by Van Sande, J. PubMed PubMed Citation Articles by Jin, L. Articles by Van Sande, J.

L Jin, Institut de Recherche Interdisciplinaire en Biologie Humaine et Moleculaire (IRIBHM), Universite Libre de Bruxelles, Brussels, Belgium
V Chico Galdo, Institut de Recherche Interdisciplinaire en Biologie Humaine et Moleculaire (IRIBHM), Universite Libre de Bruxelles, Brussels, Belgium
C Massart, Institut de Recherche Interdisciplinaire en Biologie Humaine et Moleculaire (IRIBHM), Universite Libre de Bruxelles, Brussels, Belgium
C Gervy, Clinical biochemistry department, Hôpital Erasme, Brussels, Belgium
V De Maertelaer, Institut de Recherche Interdisciplinaire en Biologie Humaine et Moleculaire (IRIBHM), Universite Libre de Bruxelles, Brussels, Belgium
M Friedman, Oviedo, United States
J Van Sande, Institut de Recherche Interdisciplinaire en Biologie Humaine et Moleculaire (IRIBHM), Universite Libre de Bruxelles, Brussels, Belgium

Correspondence: Vanessa Chico Galdo, Email: vchicoga{at}ulb.ac.be

Abstract

Chronic administration of acrylamide has been shown to induce thyroid tumors in rat.

In vitro acrylamide also causes DNA damage, as demonstrated by the comet assay, in various types of cells including human thyroid cells and lymphocytes, as well as rat thyroid cell lines. In this work, mice were administered acrylamide in their drinking water in doses comparable to those used in rats, i.e. around 3-4 mg/kg/day for mice treated 2, 6 and 8 months. Some of the mice were also treated with thyroxine to depress the activity of the thyroid. Others were treated with methimazole which inhibits thyroid hormone synthesis and consequently secretion and thus induces TSH secretion and thyroid activation. These moderate treatments were shown to have their known effect on the thyroid (e.g. thyroid hormone and thyrotropin serum levels, thyroid gland morphology...). Besides, thyroxine induced an important polydipsia and degenerative hypertrophy of adrenal medulla. Acrylamide exerted various discrete effects and at high doses caused peripheral neuropathy, as demonstrated by hind leg paralysis. However it did not induce thyroid tumorigenesis. These results show that the thyroid tumorigenic effects of acrylamide are not observed in another rodent species, the mouse and suggest the necessity of an epidemiological study in human to conclude on a public health policy.