Sawada Yosuke, Hosokawa Hiroshi, Matsumura Kiyoshi, Kobayashi Shigeo
Division of Biological Information, Department of Intelligence Science and Technology, Graduate School of Informatics, Kyoto University, Yoshidahonmachi, Kyoto 606-8501, Japan.
Eur J Neurosci. 2008 Mar;27(5):1131-42. doi: 10.1111/j.1460-9568.2008.06093.x.
Hydrogen peroxide (H(2)O(2)), which is contained in industrial products, is also generated within cells. H(2)O(2) causes pain but it has not been elucidated how it activates sensory neurons in the pain pathway. Here we show that transient receptor potential ankyrin 1 (TRPA1), expressed by sensory neurons in the pain pathway, is a receptor for H(2)O(2). H(2)O(2) activated mouse TRPA1 to induce Ca(2+) influx and elicit non-selective cation currents. These effects of H(2)O(2) were mimicked by both reactive oxygen species and reactive nitrogen species. Cysteine-reducing agents suppressed H(2)O(2)-induced TRPA1 activation, whereas cysteine-oxidizing agents activated TRPA1. H(2)O(2) caused Ca(2+) influx in a subset of dorsal root ganglia neurons, which responded to allyl isothiocyanate, a TRPA1 ligand. These results suggest that TRPA1 might be involved in the sensation of pain caused by H(2)O(2).
工业产品中含有的过氧化氢（H₂O₂）也在细胞内产生。H₂O₂会引发疼痛，但尚未阐明其如何激活疼痛通路中的感觉神经元。在此我们表明，疼痛通路中感觉神经元所表达的瞬时受体电位锚蛋白1（TRPA1）是H₂O₂的一种受体。H₂O₂激活小鼠TRPA1以诱导Ca²⁺内流并引发非选择性阳离子电流。活性氧和活性氮均可模拟H₂O₂的这些效应。半胱氨酸还原剂可抑制H₂O₂诱导的TRPA1激活，而半胱氨酸氧化剂则可激活TRPA1。H₂O₂在一部分对TRPA1配体异硫氰酸烯丙酯有反应的背根神经节神经元中引起Ca²⁺内流。这些结果表明，TRPA1可能参与了由H₂O₂引起的疼痛感觉。
