SIMULATION OF FCS CURVES FROM ARBITRARY SIMULATED COLLECTION PROFILES

在此之前，我们已经证明了细胞自发荧光 当被700-800 nm光激发的多光子主要是由于 NAD(P)H.在细胞内，该信号主要起源于 预计NADH集中的线粒体。研究 在过去的一年中进行了多次调查，试图确定 可归因于正常的自体荧光信号 线粒体功能。两个啮齿动物细胞系(EMT6、RBL)和一个 到目前为止，人类细胞系(HeLa)已经被检测过。在所有三行中 细胞的自发荧光是动态的，根据状态而变化 线粒体的。当线粒体解偶联或 同样地，当底物被移除时，自体荧光通常 从基础水平下降约20%。相比之下，投毒 线粒体与氰化物导致2.5倍增加 信号。在确定自发荧光信号是一种 代谢状态的动态指标，最近的项目 利用这种内源信号作为线粒体健康的报告。

Previously we have demonstrated that cellular autofluorescence when multiphoton excited by 700-800 nm light is primarily due to NAD(P)H. Within the cell, this signal primarily originates from mitochondria where NADH is expected to be concentrated. Studies conducted within the last year have sought to identify the magnitude of the autofluorescence signal which can be attributed to normal mitochondrial function. Two rodent cell lines (EMT6, RBL) and one human cell line (HeLa) have been examined to date. In all three lines cellular autofluorescence is dynamic, changing according to the status of the mitochondria. When the mitochondria are uncoupled or equivalently when substrate is removed, autofluorescence typically drops by approximately 20% from basal levels. In contrast, poisoning the mitochondria with cyanide results in a 2.5 fold increase in signal. Having established that the autofluorescence signal is a dynamic indicator of metabolic state, more recent projects have utilized this endogenous signal as a reporter of mitochondrial health.