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首頁> 外文期刊>BioMetals >The dopamine metabolite aminochrome inhibits mitochondrial complex I and modifies the expression of iron transporters DMT1 and FPN1
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The dopamine metabolite aminochrome inhibits mitochondrial complex I and modifies the expression of iron transporters DMT1 and FPN1

機(jī)譯：多巴胺代謝產(chǎn)物氨基色素抑制線粒體復(fù)合體I并修飾鐵轉(zhuǎn)運(yùn)蛋白DMT1和FPN1的表達(dá)

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Hallmarks of idiopathic and some forms of familial Parkinson’s disease are mitochondrial dysfunction, iron accumulation and oxidative stress in dopaminergic neurons of the substantia nigra. There seems to be a causal link between these three conditions, since mitochondrial dysfunction can give rise to increased electron leak and reactive oxygen species production. In turn, recent evidence indicates that diminished activity of mitochondrial complex I results in decreased Fe–S cluster synthesis and anomalous activation of Iron Regulatory Protein 1. Thus, mitochondrial dysfunction could be a founding event in the process that leads to neuronal death. Here, we present evidence showing that at low micromolar concentrations, the dopamine metabolite aminochrome inhibits complex I and ATP production in SH-SY5Y neuroblastoma cells differentiated into a dopaminergic phenotype. This effect is apparently direct, since it is replicated in isolated mitochondria. Additionally, overnight treatment with aminochrome increased the expression of the iron import transporter divalent metal transporter 1 and decreased the expression of the iron export transporter ferroportin 1. In accordance with these findings, cells treated with aminochrome presented increased iron uptake. These results suggest that aminochrome is an endogenous toxin that inhibits by oxidative modifications mitochondrial complex I and modifies the levels of iron transporters in a way that leads to iron accumulation.
機(jī)譯：特發(fā)性和某些形式的家族性帕金森氏病的標(biāo)志是黑質(zhì)的多巴胺能神經(jīng)元的線粒體功能障礙，鐵蓄積和氧化應(yīng)激。這三種情況之間似乎存在因果關(guān)系，因?yàn)榫€粒體功能障礙會(huì)導(dǎo)致電子泄漏增加和活性氧產(chǎn)生增加。反過來，最近的證據(jù)表明，線粒體復(fù)合體I的活性降低導(dǎo)致Fe–S團(tuán)簇合成減少和鐵調(diào)節(jié)蛋白1的異常激活。因此，線粒體功能障礙可能是導(dǎo)致神經(jīng)元死亡的過程中的基礎(chǔ)事件。在這里，我們提供的證據(jù)表明，在低微摩爾濃度下，多巴胺代謝物氨基色素可抑制分化為多巴胺能表型的SH-SY5Y神經(jīng)母細(xì)胞瘤細(xì)胞中的復(fù)合物I和ATP產(chǎn)生。這種作用顯然是直接的，因?yàn)樗诠铝⒌木€粒體中復(fù)制。另外，用氨基染料過夜處理可增加鐵輸入轉(zhuǎn)運(yùn)蛋白二價(jià)金屬轉(zhuǎn)運(yùn)蛋白1的表達(dá)，并降低鐵輸出轉(zhuǎn)運(yùn)蛋白ferroportin 1的表達(dá)。根據(jù)這些發(fā)現(xiàn)，用氨基色素處理的細(xì)胞鐵吸收增加。這些結(jié)果表明，氨基色素是一種內(nèi)源性毒素，可通過氧化修飾線粒體復(fù)合體I抑制并以導(dǎo)致鐵蓄積的方式修飾鐵轉(zhuǎn)運(yùn)蛋白的水平。

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