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Evaluation of the toxicity of zinc in the rat olfactory neuronal cell line, Odora

机译：锌对大鼠嗅觉神经元细胞Odora的毒性评估

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摘要

Zinc (Zn) has long been touted as a panacea for common cold. Recently, there has been some controversy over whether an intranasal (IN) zinc gluconate gel, purported to fight colds, causes anosmia, or loss of the sense of smell, in humans. Previous evidence has shown that IN zinc sulfate (ZnSO4) solutions can cause anosmia in humans as well as significant damage to the olfactory epithelium in rodents. Using an in vitro olfactory neuron model (the rat Odora cell line), we tested the hypothesis that Zn toxicity was caused by inhibition of the hydrogen voltage-gated channel 1 (HVCN1), leading to acidosis and apoptotic cell death. Following studies to characterize the toxicity of zinc gluconate and ZnSO4, Odora cells were grown on coverslips and loaded with 2',7'-bis-(2-carboxyethyl)-5-(and-6)-carboxyfluorescein acetoxymethyl ester to measure intracellular pH in the presence and absence of Zn salts. While we found that HVCN1 is not functional in Odora cells, we found that olfactory neurons in vitro maintain their intracellular pH through a sodium/proton exchanger, specifically the sodium proton antiporter I. ZnSO4, at nontoxic levels, had no impact on intracellular pH after acute exposure or after 24 h of incubation with the cells. In conclusion, Zn toxicity is not mediated through an acidification of intracellular pH in olfactory neurons in vitro.
机译：长期以来，人们一直认为锌（Zn）是普通感冒的万能药。最近，关于鼻内（IN）葡萄糖酸锌凝胶据称能抵抗感冒，引起人的失眠或嗅觉丧失，引起了一些争议。先前的证据表明，1N硫酸锌（ZnSO4）溶液可引起人体失眠，并对啮齿动物的嗅觉上皮造成严重损害。使用体外嗅觉神经元模型（大鼠Odora细胞系），我们测试了以下假设：锌毒性是由氢电压门控通道1（HVCN1）的抑制引起的，导致酸中毒和凋亡性细胞死亡。在研究了表征葡萄糖酸锌和ZnSO4毒性的研究之后，将Odora细胞生长在盖玻片上，并装载2'，7'-双-（2-羧乙基）-5-（和-6）-羧基荧光素乙酰氧基甲基酯以测量细胞内pH在存在和不存在锌盐的情况下。尽管我们发现HVCN1在Odora细胞中不起作用，但我们发现嗅觉神经元在体外通过钠/质子交换剂（特别是钠质子反转运蛋白I）维持其细胞内pH。ZnSO4在无毒水平下对细胞内pH没有影响急性暴露或与细胞孵育24小时后。总之，在体外，嗅觉神经元的细胞内pH值不能通过酸化来调节Zn的毒性。

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