کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2590818 1131782 2015 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Selective damage to dopaminergic transporters following exposure to the brominated flame retardant, HBCDD
موضوعات مرتبط
علوم زیستی و بیوفناوری علوم محیط زیست بهداشت، سم شناسی و جهش زایی
پیش نمایش صفحه اول مقاله
Selective damage to dopaminergic transporters following exposure to the brominated flame retardant, HBCDD
چکیده انگلیسی


• Exposure to environmental toxicants is a risk factor for Parkinson disease (PD).
• Flame retardant chemicals, like PCBs and PBDEs alter the dopamine system, as in PD.
• Manufacture and use of HBCDD has increased as PCBs and PBDEs have been phased out.
• Our study found HBCDD damages dopamine neurons using in vitro and in vivo models.
• Future work will further identify HBCDD-mediated alterations to dopamine synapses.

Over the last several decades, the use of halogenated organic compounds has become the cause of environmental and human health concerns. Of particular notoriety has been the establishment of the neurotoxicity of polychlorinated biphenyls (PCBs) and polybrominated diphenyl ethers (PBDEs). The subsequent banning of PBDEs has led to greatly increased use of 1,2,5,6,9,10-hexabromocyclododecane (HBCDD, also known as HBCD) as a flame retardant in consumer products. The physiochemical similarities between HBCDD and PBDEs suggest that HBCDD may also be neurotoxic to the dopamine system, which is specifically damaged in Parkinson disease (PD). The purpose of this study was to assess the neurotoxicity of HBCDD on the nigrostriatal dopamine system using an in vitro and in vivo approach. We demonstrate that exposure to HBCDD (0–25 μM) for 24 h causes significant cell death in the SK-N-SH catecholaminergic cell line, as well as reductions in the growth and viability of TH + primary cultured neurons at lower concentrations (0–10 μM) after 72 h of treatment. Assessment of the in vivo neurotoxicity of HBCDD (25 mg/kg for 30 days) resulted in significant reductions in the expression of the striatal dopamine transporter and vesicular monoamine transporter 2, both of which are integral in mediating dopamine homeostasis and neurotransmission in the dopamine circuit. However, no changes were seen in the expression of tyrosine hydroxylase in the dopamine terminal, or striatal levels of dopamine. To date, these are the first data to demonstrate that exposure to HBCDD disrupts the nigrostriatal dopamine system. Given these results and the ubiquitous nature of HBCDD in the environment, its possible role as an environmental risk factor for PD should be further investigated.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neurotoxicology and Teratology - Volume 52, Part B, November–December 2015, Pages 162–169
نویسندگان
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