Vanadium exposure induces olfactory dysfunction in an animal model of metal neurotoxicity.
Vanadium exposure induces olfactory dysfunction in an animal model of metal neurotoxicity.
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DOI：
10.1016/j.neuro.2013.12.004
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发表时间：
2014-07
期刊：
影响因子：
3.4
通讯作者：
Kanthasamy, Anumantha G.
中科院分区：
文献类型：
--
作者：
Ngwa, Hilary Afeseh;Kanthasamy, Arthi;Jin, Huajun;Anantharam, Vellareddy;Kanthasamy, Anumantha G.
流行病学证据表明，长期环境接触过渡金属可能与帕金森病 (PD) 等慢性神经退行性疾病有关。长期吸入含有金属混合物的焊接烟雾可能与局部放电的发生有关。焊接烟雾中含有大量的钒，如五氧化二钒 (V2O5)，并且在高强度钢的生产中掺入钒已变得越来越普遍。尽管近年来钒的使用量有所增加，但这种金属的神经毒理学作用尚未得到很好的表征。最近，我们证明 V2O5 通过多巴胺能神经元细胞中蛋白激酶 C δ (PKCδ) 依赖性氧化信号机制诱导多巴胺能神经毒性。由于嗅觉缺失（无法感知气味）和非运动障碍被认为是神经系统疾病的早期症状，因此在本研究中，我们在动物模型中研究了 V2O5 对嗅球的影响。为了模拟吸入暴露，我们向 C57 黑小鼠鼻内给予低剂量 182 µg V2O5，每周 3 次，持续一个月，并进行行为、神经化学和生化研究。我们的结果显示，与媒介物对照组相比，治疗组的嗅球重量、酪氨酸羟化酶（TH）水平、多巴胺（DA）及其代谢物3, 4-二羟基苯乙酸（DOPAC）水平显着下降，并且嗅球肾小球层星形胶质细胞增加。神经化学变化伴随着嗅觉和运动受损。这些发现表明，鼻腔接触 V2O5 会对嗅球产生不利影响，导致神经行为和神经化学损伤。这些结果拓展了我们对钒在与环境相关的神经系统疾病中的神经毒性的理解。
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.
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影响因子：
3.4
作者：
DOTY, RL;RISSER, JM
通讯作者：
RISSER, JM
DOI：
10.1196/annals.1306.009
发表时间：
2004-01-01
期刊：
REDOX-ACTIVE METALS IN NEUROLOGICAL DISORDERS
影响因子：
--
作者：
Dobson, AW;Erikson, KM;Aschner, M
通讯作者：
Aschner, M
影响因子：
2.5
作者：
Avila-Costa, MR;Colín-Barenque, L;Fortoul, TI
通讯作者：
Fortoul, TI
影响因子：
9.9
作者：
Antunes, Marcelo B.;Bowler, Rosemarie;Doty, Richard L.
通讯作者：
Doty, Richard L.
影响因子：
3.8
作者：
Dorman, DC;Struve, MF;Wong, BA
通讯作者：
Wong, BA