Dabrowiecki Z, Gordon-Majszak W, Lazarewicz J
Pol J Pharmacol Pharm. 1985 May-Jun;37(3):325-31.
This paper described the effect of in vitro peroxidation achieved by 60 s or 5 min exposure to 60 microM Fe2+ with 200 microM ascorbic acid, on selected properties of rat brain synaptosomes reflecting some steps of chemical neurotransmission. The studies have revealed dramatic differences between dopamine, GABA and choline high affinity uptake systems in response to peroxidation. The uptake of calcium by synaptosomes submitted to free radical oxidation, mostly its K+-depolarization-dependent portion, was significantly suppressed. In contrast, peroxidation appeared not to influence the transmembrane synaptosomal potential. It is concluded, that peroxidation of synaptic endings modifies the lipid content of synaptoplasmatic membranes and consequently leads to severe disturbances in the function of neurotransmitter uptake systems and depolarization-dependent calcium channels.
本文描述了通过将大鼠脑突触体暴露于含有200微摩尔抗坏血酸的60微摩尔亚铁离子中60秒或5分钟所实现的体外过氧化作用,对反映化学神经传递某些步骤的大鼠脑突触体特定性质的影响。研究揭示了多巴胺、γ-氨基丁酸(GABA)和胆碱高亲和力摄取系统在应对过氧化作用时存在显著差异。遭受自由基氧化的突触体对钙的摄取,主要是其钾离子去极化依赖性部分,受到显著抑制。相比之下,过氧化作用似乎不影响跨膜突触体电位。得出的结论是,突触末梢的过氧化作用改变了突触质膜的脂质含量,从而导致神经递质摄取系统和去极化依赖性钙通道功能的严重紊乱。