• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

小鼠烯丙醇中毒时的铁释放与红细胞损伤

Iron release and erythrocyte damage in allyl alcohol intoxication in mice.

作者信息

Ferrali M, Ciccoli L, Signorini C, Comporti M

机构信息

Istituto di Patologia Generale dell'Università di Siena, Italy.

出版信息

Biochem Pharmacol. 1990 Oct 1;40(7):1485-90. doi: 10.1016/0006-2952(90)90444-p.

DOI:10.1016/0006-2952(90)90444-p
PMID:2222504
Abstract

Allyl alcohol administration in a toxic dose (1.5 mmol/kg) to starved mice causes the development of hemolysis in nearly 50% of the animals. Malonic dialdehyde (MDA) appears in plasma of the animals showing hemolysis. The treatment of mice with desferrioxamine after allyl alcohol intoxication completely prevents lipid peroxidation and hemolysis, suggesting the involvement of iron in the allyl alcohol-induced erythrocyte damage. Erythrocytes obtained from intoxicated mice before the development of hemolysis show, upon incubation, release of iron, lipid peroxidation and lysis. Studies carried out with reconstituted systems of erythrocyte lysates, containing ghosts and different fractions of erythrocyte cytosol and incubated in the presence of acrolein (the major metabolite of allyl alcohol), strongly suggest that iron is released from hemoglobin. This iron appears to promote lipid peroxidation which is accompanied by erythrocyte lysis. Thus, the allyl alcohol-induced hemolysis appears to be a model for iron delocalization from iron stores.

摘要

给饥饿小鼠给予中毒剂量(1.5 mmol/kg)的烯丙醇,会导致近50%的动物发生溶血。丙二醛(MDA)出现在发生溶血的动物血浆中。烯丙醇中毒后用去铁胺治疗小鼠可完全预防脂质过氧化和溶血,这表明铁参与了烯丙醇诱导的红细胞损伤。在溶血发生前从中毒小鼠获得的红细胞,在孵育时会出现铁释放、脂质过氧化和裂解。用含有红细胞膜泡和不同红细胞胞质组分的红细胞裂解物重组系统进行的研究,在丙烯醛(烯丙醇的主要代谢产物)存在下孵育,强烈提示铁从血红蛋白中释放。这种铁似乎会促进脂质过氧化,进而伴随红细胞裂解。因此,烯丙醇诱导的溶血似乎是铁从铁储存中游离的一个模型。

相似文献

1
Iron release and erythrocyte damage in allyl alcohol intoxication in mice.小鼠烯丙醇中毒时的铁释放与红细胞损伤
Biochem Pharmacol. 1990 Oct 1;40(7):1485-90. doi: 10.1016/0006-2952(90)90444-p.
2
Allyl alcohol-induced hemolysis and its relation to iron release and lipid peroxidation.
Biochem Pharmacol. 1989 Jun 1;38(11):1819-25. doi: 10.1016/0006-2952(89)90417-6.
3
Iron release, lipid peroxidation, and morphological alterations of erythrocytes exposed to acrolein and phenylhydrazine.
Exp Mol Pathol. 1994 Apr;60(2):108-18. doi: 10.1006/exmp.1994.1010.
4
NADH-dependent reductive stress and ferritin-bound iron in allyl alcohol-induced lipid peroxidation in vivo: the protective effect of vitamin E.
Chem Biol Interact. 1992 Jan;81(1-2):57-68. doi: 10.1016/0009-2797(92)90026-h.
5
The role of acrolein in allyl alcohol-induced lipid peroxidation and liver cell damage in mice.
Biochem Pharmacol. 1987 Jan 1;36(1):51-7. doi: 10.1016/0006-2952(87)90381-9.
6
Methoxyflurane enhances allyl alcohol hepatotoxicity in rats. Possible involvement of increased acrolein formation.甲氧氟烷增强大鼠烯丙醇的肝毒性。可能与丙烯醛生成增加有关。
Drug Metab Dispos. 1989 Mar-Apr;17(2):117-22.
7
Activation of the microsomal glutathione-S-transferase and reduction of the glutathione dependent protection against lipid peroxidation by acrolein.微粒体谷胱甘肽-S-转移酶的激活以及丙烯醛对谷胱甘肽依赖性脂质过氧化保护作用的降低。
Biochem Pharmacol. 1988 May 15;37(10):1933-8. doi: 10.1016/0006-2952(88)90539-4.
8
Oxidative cell injury in the killing of cultured hepatocytes by allyl alcohol.烯丙醇对培养肝细胞杀伤过程中的氧化细胞损伤
Arch Biochem Biophys. 1988 Sep;265(2):302-10. doi: 10.1016/0003-9861(88)90132-4.
9
Protection against oxidative damage of erythrocyte membrane by the flavonoid quercetin and its relation to iron chelating activity.
FEBS Lett. 1997 Oct 20;416(2):123-9. doi: 10.1016/s0014-5793(97)01182-4.
10
Iron release and membrane damage in erythrocytes exposed to oxidizing agents, phenylhydrazine, divicine and isouramil.暴露于氧化剂、苯肼、豆科嘧啶和异豆科嘧啶的红细胞中的铁释放和膜损伤。
Biochem J. 1992 Jul 1;285 ( Pt 1)(Pt 1):295-301. doi: 10.1042/bj2850295.

引用本文的文献

1
The effects of hypoxia/reoxygenation on the physiological behaviour of U373-MG astrocytes.缺氧/复氧对 U373-MG 星形胶质细胞生理行为的影响。
Neurochem Res. 2010 Jan;35(1):42-9. doi: 10.1007/s11064-009-0028-3. Epub 2009 Jul 7.
2
Iron-induced oxidant stress in nonparenchymal liver cells: mitochondrial derangement and fibrosis in acutely iron-dosed gerbils and its prevention by silybin.铁诱导的非实质肝细胞氧化应激:急性铁剂量沙鼠的线粒体紊乱和纤维化以及水飞蓟宾对其的预防作用
J Bioenerg Biomembr. 2002 Feb;34(1):67-79. doi: 10.1023/a:1013874804911.
3
Iron-induced oxidant stress leads to irreversible mitochondrial dysfunctions and fibrosis in the liver of chronic iron-dosed gerbils. The effect of silybin.
铁诱导的氧化应激导致慢性铁给药沙鼠肝脏中不可逆的线粒体功能障碍和纤维化。水飞蓟宾的作用。
J Bioenerg Biomembr. 2000 Apr;32(2):175-82. doi: 10.1023/a:1005512014280.
4
Effect of gamma-irradiated carbohydrates on isolated synaptic membranes.γ射线辐照碳水化合物对离体突触膜的影响。
Radiat Environ Biophys. 1993;32(4):345-55. doi: 10.1007/BF01225922.
5
Iron release and membrane damage in erythrocytes exposed to oxidizing agents, phenylhydrazine, divicine and isouramil.暴露于氧化剂、苯肼、豆科嘧啶和异豆科嘧啶的红细胞中的铁释放和膜损伤。
Biochem J. 1992 Jul 1;285 ( Pt 1)(Pt 1):295-301. doi: 10.1042/bj2850295.