Acute hypermethioninemia impairs redox homeostasis and acetylcholinesterase activity in the hippocampus, striatum, and cerebellum of young rats,International Journal of Developmental Neuroscience

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Acute hypermethioninemia impairs redox homeostasis and acetylcholinesterase activity in the hippocampus, striatum, and cerebellum of young rats
International Journal of Developmental Neuroscience ( IF 1.7 ) Pub Date : 2021-02-19 , DOI: 10.1002/jdn.10098
Bernardo de Moraes Meine ₁ , Natália Pontes Bona ₁ , Karina Pereira Luduvico ₁ , Luiza Spohr ₂ , Nathalia Stark Pedra ₂ , Roselia Maria Spanevello ₂ , Francieli Moro Stefanello ₁ , Mayara Sandrielly Pereira Soares ₂

Affiliation

Hypermethioninemia is characterized by high plasma concentrations of methionine (Met) and its metabolites, such as methionine sulfoxide (MetO), and neurological changes, such as cerebral edema and cognitive deficits. The aim of this study was to analyze the redox status and acetylcholinesterase (AChE) activity in the hippocampus, striatum, and cerebellum of young Wistar rats subjected to an acute hypermethioninemia protocol. The animals received, by subcutaneous injection, a single dose of Met (0.4 g/kg), MetO (0.1 g/kg), and Met + MetO, and 1 or 3 hr after administration, the animals were euthanatized for brain structure obtaining. In the hippocampus, an increase in lipid peroxidation and glutathione peroxidase (GPx) activity was observed at 1 hr in the MetO and Met + MetO groups, and a reduction in the superoxide dismutase activity was found in the Met + MetO group. Met and/or MetO induced a decrease in the thiol content and GPx activity and enhanced the lipid peroxidation at 3 hr. In the striatum, a reduction in the thiol content and GPx activity, an increase in lipid peroxidation, and AChE activity were induced by Met and/or MetO at 1 or 3 hr. Additionally, in the cerebellum, an increase in the AChE in the MetO and Met + MetO groups 1 hr after administration was observed. These data help to better understand the pathophysiological mechanisms that underlie the neurological changes found in hypermethioninemia patients.

中文翻译：

急性高甲硫氨酸血症损害幼鼠海马、纹状体和小脑的氧化还原稳态和乙酰胆碱酯酶活性

高甲硫氨酸血症的特点是血浆中甲硫氨酸 (Met) 及其代谢物如甲硫氨酸亚砜 (MetO) 的血浆浓度高，以及神经系统变化，如脑水肿和认知缺陷。本研究的目的是分析接受急性高甲硫氨酸血症方案的年轻 Wistar 大鼠的海马、纹状体和小脑的氧化还原状态和乙酰胆碱酯酶 (AChE) 活性。通过皮下注射，动物接受单剂量的 Met (0.4 g/kg)、MetO (0.1 g/kg) 和 Met + MetO，给药后 1 或 3 小时，对动物实施安乐死以获得脑结构。在海马中，MetO 和 Met + MetO 组在 1 小时时观察到脂质过氧化和谷胱甘肽过氧化物酶 (GPx) 活性增加，在 Met + MetO 组中发现超氧化物歧化酶活性降低。Met 和/或 MetO 诱导硫醇含量和 GPx 活性降低，并在 3 小时时增强脂质过氧化。在纹状体中，在 1 或 3 小时时，Met 和/或 MetO 会诱导硫醇含量和 GPx 活性降低、脂质过氧化增加和 AChE 活性。此外，在小脑中，观察到给药 1 小时后 MetO 和 Met + MetO 组的 AChE 增加。这些数据有助于更好地了解导致高甲硫氨酸血症患者神经系统变化的病理生理机制。在 1 小时或 3 小时时，Met 和/或 MetO 诱导脂质过氧化增加和 AChE 活性。此外，在小脑中，观察到给药 1 小时后 MetO 和 Met + MetO 组的 AChE 增加。这些数据有助于更好地了解导致高甲硫氨酸血症患者神经系统变化的病理生理机制。在 1 小时或 3 小时时，Met 和/或 MetO 诱导脂质过氧化增加和 AChE 活性。此外，在小脑中，观察到给药 1 小时后 MetO 和 Met + MetO 组的 AChE 增加。这些数据有助于更好地了解导致高甲硫氨酸血症患者神经系统变化的病理生理机制。

更新日期：2021-02-19

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