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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Effects of 4-hydroxynonenal, a lipid peroxidation product, on dopamine transport and Na+/K+ ATPase in rat striatal synaptosomes.
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Effects of 4-hydroxynonenal, a lipid peroxidation product, on dopamine transport and Na+/K+ ATPase in rat striatal synaptosomes.

机译：脂质过氧化产物4-羟基壬烯醛对大鼠纹状体突触小体中多巴胺转运和Na + / K + ATPase的影响。

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摘要

Incubation of rat striatal synaptosomes in ascorbic acid induced the production of thiobarbituric acid reactive substances, a marker of lipid peroxidation, and 4-hydroxynonenal (4-HNE), a lipid peroxidation aldehydic product. Incubations with 4-HNE, used at a range of concentrations comparable to those obtained during peroxidation, induced a simultaneous, dose-dependent decrease of dopamine (DA) uptake and Na+/K+ ATPase activity and a loss of sulfhydryl (SH) groups. Similar results were observed in a previous study when lipid peroxidation was induced after incubation of synaptosomes in ascorbic acid. Taken together, these data suggest that 4-HNE is an important mediator of oxidative stress and may alter DA uptake after binding to SH groups of the DA transporter and to Na+/K+ ATPase. These toxic events may contribute to the onset and progression of Parkinson's disease.
机译：将大鼠纹状体突触小体在抗坏血酸中孵育可诱导产生硫代巴比妥酸反应性物质（脂质过氧化的标志物）和脂质过氧化醛化的4-羟基壬烯醛（4-HNE）。 4-HNE孵育的浓度范围与过氧化过程中获得的浓度相当，可同时引起剂量依赖性的多巴胺（DA）吸收和Na + / K + ATPase活性下降，以及巯基（SH）的丢失。在抗坏血酸中孵育突触体后诱导脂质过氧化的先前研究中，观察到了相似的结果。综上所述，这些数据表明4-HNE是氧化应激的重要介质，并且在与DA转运蛋白的SH基团和Na + / K + ATP酶结合后可能会改变DA的吸收。这些中毒事件可能有助于帕金森氏病的发作和发展。

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