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Effect of dioxins on regulation of tyrosine hydroxylase gene expression by aryl hydrocarbon receptor a neurotoxicology study.doc

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Effect of dioxins on regulation of tyrosine hydroxylase gene expression by aryl hydrocarbon receptor a neurotoxicology study

Environmental Health BioMedCentral Research Open Access Effect of dioxins on regulation of tyrosine hydroxylase gene expression by aryl hydrocarbon receptor: a neurotoxicology study Eiichi Akahoshi, Seiko Yoshimura, Saeko Uruno and Mitsuko Ishihara- Sugano* Address: Functional Material Laboratory, Corporate Research Development Center, Toshiba Corporation, 1 Komukai-Toshiba cho, Saiwai-ku, Kawasaki 212-8582, Japan Email: Eiichi Akahoshi - eiichi.akahoshi@toshiba.co.jp; Seiko Yoshimura - seiko.yoshimura@toshiba.co.jp; Saeko Uruno - saeko.uruno@toshiba.co.jp; Mitsuko Ishihara-Sugano* - mitsuko.sugano@toshiba.co.jp * Corresponding author Published: 6 June 2009 Received: 2 March 2009 Accepted: 6 June 2009 Environmental Health 2009, 8:24 doi:10.1186/1476-069X-8-24 This article is available from: /content/8/1/24 ? 2009 Akahoshi et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Background: Dioxins and related compounds are suspected of causing neurological disruption. Epidemiological studies indicated that exposure to these compounds caused neurodevelopmental disturbances such as learning disability and attention deficit hyperactivity disorder, which are thought to be closely related to dopaminergic dysfunction. Although the molecular mechanism of their actions has not been fully investigated, a major participant in the process is aryl hydrocarbon receptor (AhR). This study focused on the effect of 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD) exposure on the regulation of TH, a rate-limiting enzyme of dopamine synthesis, gene expression by AhR. Methods: N2a-Rβ cells were established by transfecting murine neuroblastoma Neuro2a with the rat AhR cDNA. TH expression induced by TCDD was assessed