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聚硫化物在血清白蛋白中对氧化应激的独特反应

Mayumi Ikeda-Imafuku¹, Maki Sakai², Keitaro Umezawa³

¹Department of Physical Pharmaceutics, Wakayama Medical University, 25-1 Shichibancho, Wakayama, 640-8156, Japan. imayu@wakayama-med.ac.jp.

Scientific reports

|November 27, 2025

概括

细胞外聚硫化物,对氧化应激反应至关重要,在氧化和减少形式之间转换. 它们的水平在糖尿病脏病和功能衰竭中下降,影响血清.

科学领域:

生物化学生物化学
氧化压力是一种氧化压力.
脏生理学脏生理学

背景情况:

超硫化物 (超硫化物和多硫化物) 是硫链 (R-SSH,R-SSn-H).
细胞内超硫化物作用已知,但细胞外功能尚不清楚.
糖尿病病包括显著的氧化应激和损伤.

研究的目的:

为了研究降解和氧化聚硫化物在血中的作用.
分析糖尿病病患者的病理变化和氧化应激.
了解多硫化物对血清抗氧化活性的调节.

主要方法:

通过使用dithiothreitol (DDT) 和ascorbic acid/alkali.用量化减少和氧化多硫化物.
对人血清白蛋白 (HSA) 和其氨酸残留物的分析.
在小鼠模型中评估因拉布多解诱导的急性损伤 (AKI).
在患有糖尿病脏病,慢性功能衰竭和健康对照患者中比较聚硫化物水平.

主要成果:

氧化HSA降低了氧化多硫化物,增加了抗氧化活性.
在HSA中发现了七种半氨酸残留物,在氧化后减少了多硫化物.
进一步的氧化减少了多硫化物和HSA的抗氧化作用.
在AKI模型中,血降低的多硫化物随着增强的抗氧化活性而暂时增加.
与对照组相比,糖尿病脏病和慢性功能衰竭患者的多硫化物水平较低.
在早期的损伤阶段 (1-3),dithiothreitol释放的多硫化物增加,但在第5阶段下降.

结论:

血清抗氧化活性,包括HSA,是由多硫化物的氧化还原状态调节的.
氧化和减少的多硫化物之间的切换是对氧化应激的关键反应.
改变的多硫化物水平与病进展有关.

关键词:

脏疾病是一种脏疾病.氧化应激是一种氧化应激.聚硫化物多硫化物血清中白蛋白的使用.这是一种超硫化物.

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