论文标题
老年,应力或用抗氧化剂处理时,量子监测各个酵母突变体应变细胞的代谢
Quantum monitoring the metabolism of individual yeast mutant strain cells when aged, stressed or treated with antioxidant
论文作者
论文摘要
自由基在衰老过程中起关键作用。衰老的强烈争论的自由基理论甚至指出,自由基造成的损害是细胞水平上衰老的主要原因。但是,自由基很小,反应性和短暂寿命,因此挑战衡量。为此,我们利用一种称为钻石磁力测定法的新技术。我们利用纳米原子座中的氮空位中心。通过量子效应,这些缺陷将磁共振信号转换为光学信号。尽管这种方法越来越流行于其在物理学上的前所未有的敏感性,但我们首次在这里使用该技术来测量活细胞中的自由基。我们的信号等同于常规MRI中的T1信号,但来自具有亚细胞分辨率的单个细胞的纳米级体素。使用这种强大的工具,我们能够在化学诱导应力后遵循自由基的生成。此外,我们可以观察到存在抗氧化剂的自由基减少。我们能够清楚地区分新陈代谢改变的突变菌株。最后,我们的钻石颗粒的出色稳定性使我们能够遵循衰老过程并区分年轻细胞。我们可以确认旧野生型和SOD1δ突变体中的自由基载荷的预期增加。我们进一步应用了这项新技术来研究TOR1δ和PEX19δ细胞。对于这些突变体,已经报道了寿命增加,但确切的机制尚不清楚。我们发现自由基负载减少,这可能为这些细胞中寿命增加提供了解释。
Free radicals play a key role in the ageing process. The strongly debated free radical theory of ageing even states that damage caused by free radicals is the main cause of aging on a cellular level. However, free radicals are small, reactive and short lived and thus challenging to measure. We utilize a new technique called diamond magnetometry for this purpose. We make use of nitrogen vacancy centers in nanodiamonds. Via a quantum effect these defects convert a magnetic resonance signal into an optical signal. While this method is increasingly popular for its unprecedented sensitivity in physics, we use this technique here for the first time to measure free radicals in living cells. Our signals are equivalent to T1 signals in conventional MRI but from nanoscale voxels from single cells with sub-cellular resolution. With this powerful tool we are able to follow free radical generation after chemically inducing stress. In addition, we can observe free radical reduction in presence of an antioxidant. We were able to clearly differentiate between mutant strains with altered metabolism. Finally, the excellent stability of our diamond particles allowed us to follow the ageing process and differentiate between young and old cells. We could confirm the expected increase of free radical load in old wild type and sod1Δ mutants. We further applied this new technique to investigate tor1Δ and pex19Δ cells. For these mutants an increased lifespan has been reported but the exact mechanism is unclear. We find a decreased free radical load in, which might offer an explanation for the increased lifespan in these cells.