• 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

不同品系小鼠的四氯化碳活化、脂质过氧化和肝坏死

Carbon tetrachloride activation, lipid peroxidation and liver necrosis in different strains of mice.

作者信息

de Toranzo E G, Gómez M I, Castro J A

出版信息

Res Commun Chem Pathol Pharmacol. 1978 Feb;19(2):347-52.

PMID:644126
Abstract

Males from three different strains of mice (GXF; CF1, and Swiss) were compared in their liver response to CCl4 effects. They were capable to intensively activate CCl4 to .CCl3. No CCl4 induced lipid peroxidation was detected in the liver microsomes from any of them. All the strains remakably responded to the CCl4 induced liver damage. Results further strengthen our previous hypothesis that covalent binding of CCl4 reactive metabolites to cellular constituents is more important in relation to liver cell injury than early changes in lipid peroxidation.

摘要

对三种不同品系的雄性小鼠(GXF、CF1和瑞士小鼠)的肝脏对四氯化碳作用的反应进行了比较。它们能够将四氯化碳强烈激活为三氯甲烷。在它们任何一种的肝脏微粒体中均未检测到四氯化碳诱导的脂质过氧化。所有品系对四氯化碳诱导的肝损伤均有显著反应。结果进一步强化了我们之前的假设,即四氯化碳反应性代谢产物与细胞成分的共价结合相对于脂质过氧化的早期变化在肝细胞损伤方面更为重要。

相似文献

1
Carbon tetrachloride activation, lipid peroxidation and liver necrosis in different strains of mice.不同品系小鼠的四氯化碳活化、脂质过氧化和肝坏死
Res Commun Chem Pathol Pharmacol. 1978 Feb;19(2):347-52.
2
Species differences in carbon tetrachloride-induced hepatotoxicity: the role of CCl4 activation and of lipid peroxidation.四氯化碳诱导的肝毒性中的种属差异:CCl4激活及脂质过氧化的作用
Toxicol Appl Pharmacol. 1975 Oct;34(1):102-14. doi: 10.1016/0041-008x(75)90179-9.
3
Lipid peroxidation in purified plasma membrane fractions of rat liver in relation to the hepatoxicity of carbon tetrachloride.大鼠肝脏纯化质膜组分中的脂质过氧化与四氯化碳肝毒性的关系。
Cell Biochem Funct. 1988 Apr;6(2):87-99. doi: 10.1002/cbf.290060203.
4
Relationship of oxygen and glutathione in protection against carbon tetrachloride-induced hepatic microsomal lipid peroxidation and covalent binding in the rat. Rationale for the use of hyperbaric oxygen to treat carbon tetrachloride ingestion.氧气与谷胱甘肽在保护大鼠免受四氯化碳诱导的肝微粒体脂质过氧化及共价结合中的关系。使用高压氧治疗四氯化碳摄入的理论依据。
J Clin Invest. 1984 Dec;74(6):1996-2001. doi: 10.1172/JCI111621.
5
Carbon tetrachloride-induced liver injury in the rabbit.四氯化碳诱导的家兔肝损伤
Br J Exp Pathol. 1983 Jun;64(3):261-7.
6
Evidence for carbon tetrachloride- and ethanol-induced lipid peroxidation in vivo demonstrated by ethane production in mice and rats.通过小鼠和大鼠体内乙烷生成证明四氯化碳和乙醇诱导体内脂质过氧化的证据。
Toxicol Appl Pharmacol. 1977 Sep;41(3):639-48. doi: 10.1016/s0041-008x(77)80017-3.
7
Prevention of carbon tetrachloride-induced liver necrosis by several amino acids.几种氨基酸对四氯化碳诱导的肝坏死的预防作用。
Br J Exp Pathol. 1983 Apr;64(2):166-71.
8
Evidence for carbon tetrachloride-induced lipid peroxidation in mouse liver.四氯化碳诱导小鼠肝脏脂质过氧化的证据。
Biochem Pharmacol. 1982 Feb 1;31(3):405-9. doi: 10.1016/0006-2952(82)90189-7.
9
Mechanism of carbon tetrachloride-induced hepatotoxicity. Hepatocellular damage by reactive carbon tetrachloride metabolites.四氯化碳诱导肝毒性的机制。活性四氯化碳代谢产物对肝细胞的损伤。
Z Naturforsch C J Biosci. 2001 Jul-Aug;56(7-8):649-59. doi: 10.1515/znc-2001-7-826.
10
Studies on the mechanism of glutathione prevention of carbon tetrachloride-induced liver injury.谷胱甘肽预防四氯化碳诱导肝损伤的机制研究。
Br J Exp Pathol. 1983 Aug;64(4):388-95.

引用本文的文献

1
Signals and cells involved in regulating liver regeneration.参与调控肝脏再生的信号和细胞。
Cells. 2012 Dec 13;1(4):1261-92. doi: 10.3390/cells1041261.
2
Genetics of carbon tetrachloride-induced liver injury in mice. II. Multigenic regulation.小鼠四氯化碳诱导肝损伤的遗传学。II. 多基因调控。
Br J Exp Pathol. 1984 Feb;65(1):125-31.