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首页> 外文期刊>The European Journal of Neuroscience >The essential nutrient pyrroloquinoline quinone may act as a neuroprotectant by suppressing peroxynitrite formation.
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The essential nutrient pyrroloquinoline quinone may act as a neuroprotectant by suppressing peroxynitrite formation.

机译：必需营养素吡咯并喹啉醌可通过抑制过亚硝酸盐的形成而充当神经保护剂。

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Pyrroloquinoline quinone (PQQ) is a redox active essential nutrient that can generate or scavenge superoxide depending on its microenvironment. PQQ has been shown previously to be neuroprotective in a rodent stroke model. Here we test whether PQQ interacts with reactive nitrogen species, known to be involved in the pathogenesis of stroke. Using rat forebrain neurons in culture, we determined that the toxicity of SIN-1 was mediated by peroxynitrite and that PQQ could block this toxic action. However, PQQ could not block the toxicity of peroxynitrite itself. Both SIN-1 and peroxynitrite caused ATP depletion, but only SIN-1 evoked ATP depletion was blocked by PQQ. In a cell-free system, PQQ blocked nitration of bovine serum albumin produced by SIN-1, but potentiated peroxynitrite-induced nitration. PQQ was unable to block ATP depletion and cell death induced by NO. donors (DEA/NO, DPT/NO and DETA/NO), indicating that it does not directly interact with nitric oxide, and suggesting that it acts as a superoxide scavenger. PQQ significantly potentiated cGMP accumulation evoked by SIN-1, similar to the effect of superoxide dismutase (SOD). However, unlike SOD, which potentiated neurotoxicity induced by SIN-1, PQQ blocked its toxicity, arguing against the possibility that PQQ functions simply as a SOD mimetic. Indeed, substantially less H2O2 was produced by the incubation of SIN-1 with PQQ, when compared to SOD. These results suggest that PQQ scavenges superoxide without forming toxic levels of H2O2. Therefore, the protective effect of PQQ on stroke might be due, at least in part, to the suppression of peroxynitrite formation.
机译：吡咯并喹啉醌（PQQ）是一种氧化还原活性必需营养素，可根据其微环境产生或清除超氧化物。先前已证明PQQ在啮齿动物中风模型中具有神经保护作用。在这里，我们测试了PQQ是否与已知与中风发病有关的活性氮物质相互作用。使用培养的大鼠前脑神经元，我们确定SIN-1的毒性是由过亚硝酸盐介导的，而PQQ可以阻止这种毒性作用。但是，PQQ无法阻止过氧亚硝酸盐本身的毒性。 SIN-1和过亚硝酸盐都引起ATP耗竭，但是只有SIN-1引起的ATP耗竭被PQQ阻止。在无细胞系统中，PQQ阻断了SIN-1产生的牛血清白蛋白的硝化作用，但增强了过氧亚硝酸盐诱导的硝化作用。 PQQ无法阻止NO诱导的ATP耗竭和细胞死亡。供体（DEA / NO，DPT / NO和DETA / NO），表明它不与一氧化氮直接相互作用，并暗示它起着超氧化物清除剂的作用。 PQQ显着增强了SIN-1引起的cGMP积累，类似于超氧化物歧化酶（SOD）的作用。然而，与SOD增强SIN-1诱导的神经毒性不同，PQQ阻止了它的毒性，从而争论了PQQ只是作为SOD模拟物起作用的可能性。实际上，与SOD相比，通过SIN-1与PQQ孵育产生的H2O2少得多。这些结果表明，PQQ可清除超氧化物而不形成有毒的H2O2。因此，PQQ对中风的保护作用可能至少部分是由于过氧亚硝酸盐形成的抑制。

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