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Faculté de Médecine, Institute of Interdisciplinary Research (IRIBHM), Universtité Libre de Bruxelles, Campus Erasme, Route de Lennik 808,  B 1070 Brussels, Belgium¹ Clinical Biochemistry Department, Hôpital Erasme, B 1070 Brussels, Belgium² University of Medicine and Dentistry of New Jersey, Oviedo, Newark, New Jersey, USA

(Correspondence should be addressed to V Chico-Galdo; Email: vchicoga{at}ulb.ac.be)

^* (L Jin and V Chico-Galdo contributed equally to this work)

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 with those used in rats, i.e., around 3–4 mg/kg per day for mice treated 2, 6, and 8 months. Some of the mice were also treated with thyroxine (T₄) to depress the activity of the thyroid. Others were treated with methimazole that 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, T₄ 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.