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Perturbations in the thiol homeostasis following neonatal cerebral hypoxia-ischemia in rats.

机译:新生大鼠脑缺氧缺血后硫醇稳态的扰动。

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摘要

Changes in the thiol/disulphide status in the neonatal rat brain were evaluated after an episode of neonatal hypoxia-ischemia (HI) in 7-day-old rats. The glutathione level decreased in the post-HI period. The lowest values (43-68%) were obtained 24 h post-HI. A statistically significant difference first appeared in hippocampus, immediately after the HI event, and only 12 h later in striatum and cortex. On the 7th day post-HI the glutathione content was completely recovered in the hippocampus and the striatum, and partially in the cortex. The glutathione loss could not be explained through its conversion to glutathione disulphide or to protein mixed disulphide (S-thiolation), whose values remained constant. Furthermore, we found a consistent decrease (20-30%) in protein thiols, which were not recovered after 7 days post-HI. Perturbations in protein thiols, along with the glutathione loss, may represent a valuable marker of immature rat brain damage.
机译:在7天大的大鼠发生新生儿缺氧缺血(HI)后,评估了新生大鼠大脑中硫醇/二硫化物状态的变化。 HI后谷胱甘肽水平下降。 HI后24小时获得最低值(43-68%)。 HI事件后立即在海马中出现统计学上的显着差异,纹状体和皮质仅在12小时后才出现。 HI后第7天,海马和纹状体中的谷胱甘肽含量完全恢复,皮质中部分恢复。谷胱甘肽的损失不能通过将其转化为谷胱甘肽二硫化物或蛋白质混合二硫化物(S-硫醇化)来解释,其值保持恒定。此外,我们发现蛋白质硫醇含量持续下降(20-30%),在HI后7天未恢复。蛋白硫醇的扰动以及谷胱甘肽的损失可能代表了未成熟大鼠脑损伤的重要标志。

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