کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2589583 1562051 2014 9 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Vanadium exposure induces olfactory dysfunction in an animal model of metal neurotoxicity
ترجمه فارسی عنوان
قرار گرفتن وانادیوم اختلال بویایی را در یک مدل حیوانی از عصب نوکلئیک فلز ایجاد می کند
موضوعات مرتبط
علوم زیستی و بیوفناوری علوم محیط زیست بهداشت، سم شناسی و جهش زایی
چکیده انگلیسی


• Low dose intranasal vanadium exposure induces locomotor impairment.
• Intranasal vanadium exposure also causes profound olfactory deficits.
• Intranasal vanadium exposure decreases the levels of TH protein and dopamine in the olfactory bulb.
• Intranasal vanadium exposure also increases astroglial proliferation in the olfactory bulb.

Epidemiological evidence indicates chronic environmental exposure to transition metals may play a role in chronic neurodegenerative conditions such as Parkinson's disease (PD). Chronic inhalation exposure to welding fumes containing metal mixtures may be associated with development of PD. A significant amount of vanadium is present in welding fumes, as vanadium pentoxide (V2O5), and incorporation of vanadium in the production of high strength steel has become more common. Despite the increased vanadium use in recent years, the neurotoxicological effects of this metal are not well characterized. Recently, we demonstrated that V2O5 induces dopaminergic neurotoxicity via protein kinase C delta (PKCδ)-dependent oxidative signaling mechanisms in dopaminergic neuronal cells. Since anosmia (inability to perceive odors) and non-motor deficits are considered to be early symptoms of neurological diseases, in the present study, we examined the effect of V2O5 on the olfactory bulb in animal models. To mimic the inhalation exposure, we intranasally administered C57 black mice a low-dose of 182 μg of V2O5 three times a week for one month, and behavioral, neurochemical and biochemical studies were performed. Our results revealed a significant decrease in olfactory bulb weights, tyrosine hydroxylase (TH) levels, levels of dopamine (DA) and its metabolite, 3,4-dihydroxyphenylacetic acid (DOPAC) and increases in astroglia of the glomerular layer of the olfactory bulb in the treatment groups relative to vehicle controls. Neurochemical changes were accompanied by impaired olfaction and locomotion. These findings suggest that nasal exposure to V2O5 adversely affects olfactory bulbs, resulting in neurobehavioral and neurochemical impairments. These results expand our understanding of vanadium neurotoxicity in environmentally-linked neurological conditions.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: NeuroToxicology - Volume 43, July 2014, Pages 73–81
نویسندگان
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