通过降低细胞内谷氨水平,CHAC1加剧了矿的细胞毒性
Daigo Sumi1, Hiroki Taguchi1, Kumiko Takeuchi1
1Faculty of Pharmaceutical Sciences, Tokushima Bunri University.
The Journal of toxicological sciences
|September 4, 2023
概括
CHAC1调节细胞内谷氨 (GSH) 水平,影响 HaCaT 细胞对酸盐 (As(III)) 的敏感性. 降低CHAC1的调节减少了As(III) 诱导的亡,突出显示了CHAC1.
科学领域:
- 细胞生物学 细胞生物学
- 毒理学 毒理学 毒理学
- 生物化学 生物化学
背景情况:
- 化物 (As(III)) 是一种有毒的金属化物,已知可在各种细胞类型中诱导细胞毒性和细胞亡.
- 谷氨 (GSH) 在抵抗氧化应激和毒性侮辱的细胞防御中起着至关重要的作用.
- CHAC1 (也称为AIG1) 是由内质网膜压力诱导的基因,与亡有关.
研究的目的:
- 调查CHAC1在化 (As(III)) 诱导的细胞毒性和HaCaT细胞的亡中的作用.
- 确定CHAC1表达,细胞内GSH水平和As (III) 敏感度之间的关系.
主要方法:
- 用CHAC1siRNA感染HaCaT细胞以减少CHAC1的表达.
- 细胞被用化物 (As(III)) 和/或布氨酸硫胺 (BSO) 治疗,这是GSH生物合成的抑制剂.
- 评估了细胞内GSH水平,细胞活力和亡 (caspase-3裂变).
主要成果:
- 降低CHAC1的调节导致对As (III) 诱导的细胞毒性敏感性降低.
- 在CHAC1-贫乏细胞中细胞内GSH水平升高与降低的As (III) 敏感性相关.
- 由于III) 暴露增加了CHAC1的表达和诱导的亡,这在CHAC1 siRNA转移的细胞中被废除.
结论:
- CHAC1参与调节细胞内GSH水平,从而调节HaCaT细胞对酸盐的敏感性.
- 在HaCaT细胞中,CHAC1在As(III) 诱导的亡中起着重要作用.
- 向CHAC1可能提供一种减轻矿毒性的策略.
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