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缺氧和 KCl 去极化对海马 CA3 区自发荧光和 ROS 变化的影响。

Effect of hypoxia and KCl depolarization in autofluorescence and ROS changes at the hippocampal CA3 area.

机构信息

CIEPQPF - Chemical Engineering Processes and Forest Products Research Center, Department of Chemical Engineering, University of Coimbra, Coimbra, Portugal.

Federal University of Rio de Janeiro, COPPE - Chemical Engineering Program, Technology Center - University City, Rio de Janeiro, Brazil.

出版信息

Gen Physiol Biophys. 2024 Nov;43(6):585-592. doi: 10.4149/gpb_2024005.

DOI:10.4149/gpb_2024005
PMID:39584302
Abstract

The increasing incidence of neurodegenerative and other diseases is considered to involve an excessive production of reactive oxygen species (ROS). Water supplies are often characterized by excessive organic waste that is decomposed by bacteria, using dissolved oxygen, leading to oxygen depletion. The potassium content of these waters may also affect negatively the mitochondrial metabolism and cellular ROS formation. This work focused on characterizing mitochondrial autofluorescence changes, with flavoprotein origin, and fluorescence ROS signals measured using the 2',7'-dichlorodihydrofluorescein diacetate indicator H2DCFDA. All signals were evoked by hypoxia or by the depolarizing agent KCl (20 mM), at the hippocampal mossy fiber synapses of CA3 area. It was observed that both hypoxia and KCl-induced depolarization elicited a small rise in the autofluorescence and ROS changes. The hypoxia-induced signals were maintained upon normal reoxygenation, but of those evoked by KCl, the autofluorescence signals recovered during washout, while the ROS changes were irreversible.

摘要

神经退行性疾病和其他疾病的发病率不断上升被认为与活性氧(ROS)的过度产生有关。供水中通常存在大量有机废物,这些有机废物被细菌分解,消耗溶解氧,导致缺氧。这些水中的钾含量也可能对线粒体代谢和细胞 ROS 形成产生负面影响。本工作重点研究了线粒体自发荧光变化的特征,其起源为黄素蛋白,并使用 2',7'-二氯二氢荧光素二乙酸酯指示剂 H2DCFDA 测量了荧光 ROS 信号。所有信号均由缺氧或去极化剂 KCl(20mM)在 CA3 区的海马苔藓纤维突触处诱发。观察到缺氧和 KCl 诱导的去极化均引起自发荧光和 ROS 变化的轻微升高。缺氧诱导的信号在正常复氧时保持不变,但 KCl 诱导的信号中,自发荧光信号在洗脱过程中恢复,而 ROS 变化则是不可逆的。

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