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四氯化碳诱导肝损伤大鼠体内64铜、65锌和203汞的胆汁排泄

Biliary excretion of 64Cu, 65Zn and 203Hg in the rat with liver injury induced by CCl4.

作者信息

Cikrt M, Tichý M, Holusa R

出版信息

Arch Toxicol. 1975 Nov 20;34(3):227-36. doi: 10.1007/BF00353285.

DOI:10.1007/BF00353285
PMID:1243622
Abstract

In rats the effect of a chronic administration of CCl4 on the excretion and disstribution of 64Cu, 65Zn, and 203Hg was investigated. The bilary excretion of these metals was studied with particular attention. It was found that total excretion of 64Cu, 65Zn, or 203Hg from the organism did not change significantly in comparison with the control groupp, but the ratio of individual excretion pathways did change. The course of excretion curves regarding the bile in exposed animals is prolonged. The histologic examination of the livers revealed a large interindividual variability in the response of the liver tissue to the same CCl4 exposure. Differences in distribution in the kidneys and livers in exposed and control animals was also found.

摘要

在大鼠中,研究了长期给予四氯化碳对64Cu、65Zn和203Hg排泄及分布的影响。特别关注了这些金属的胆汁排泄情况。结果发现,与对照组相比,机体对64Cu、65Zn或203Hg的总排泄量没有显著变化,但个体排泄途径的比例发生了改变。暴露动物胆汁排泄曲线的过程延长。肝脏的组织学检查显示,肝组织对相同四氯化碳暴露的反应存在很大的个体差异。还发现了暴露动物与对照动物在肾脏和肝脏中的分布差异。

相似文献

1
Biliary excretion of 64Cu, 65Zn and 203Hg in the rat with liver injury induced by CCl4.四氯化碳诱导肝损伤大鼠体内64铜、65锌和203汞的胆汁排泄
Arch Toxicol. 1975 Nov 20;34(3):227-36. doi: 10.1007/BF00353285.
2
Effect of chronic administration of carbon tetrachloride on copper, zinc, and mercury binding in bile in rats.长期给予四氯化碳对大鼠胆汁中铜、锌和汞结合的影响。
Toxicol Appl Pharmacol. 1976 Apr;36(1):163-72. doi: 10.1016/0041-008x(76)90036-3.
3
Bile formation in rats with acute liver damage from carbon tetrachloride.四氯化碳所致急性肝损伤大鼠的胆汁生成
Indian J Physiol Pharmacol. 1977 Oct-Dec;21(4):311-22.
4
[Excretion of 131I-labeled bromsulphalein in rats with experimental liver injury].
Sb Lek. 1986 Feb;88(2):33-41.
5
Uptake of Zn65 by rat liver damaged by CCl4.四氯化碳损伤的大鼠肝脏对锌-65的摄取
Frankf Z Pathol. 1967;77(1):61-6.
6
The effect of carbon tetrachloride on hepatic accumulation, metabolism, and biliary excretion of sulfobromophthalein in rainbow trout.四氯化碳对虹鳟鱼肝脏中磺溴酞的蓄积、代谢及胆汁排泄的影响。
Toxicol Appl Pharmacol. 1978 Jan;43(1):159-67. doi: 10.1016/s0041-008x(78)80040-4.
7
Hepato-biliary transport of amaranth by single pass liver perfusion in normal and carbon tetrachloride or alpha-naphthylisothiocyanate treated rats.在正常大鼠以及经四氯化碳或α-萘基异硫氰酸盐处理的大鼠中,通过单次肝脏灌注研究苋菜的肝胆转运。
J Pharmacobiodyn. 1986 Jul;9(7):570-7. doi: 10.1248/bpb1978.9.570.
8
Changes in 65Zn and 59Fe metabolism, and carbonic anhydrase and catalase activity in animals with liver-damaged by carbon tetrachloride or ethionine.四氯化碳或乙硫氨酸致肝损伤动物体内65锌和59铁代谢以及碳酸酐酶和过氧化氢酶活性的变化
Jpn J Pharmacol. 1967 Sep;17(3):393-408. doi: 10.1254/jjp.17.393.
9
[Metabolism of rifampicin. I. Biliary and urinary excretion in normal rats and with experimental liver injury].[利福平的代谢。I. 正常大鼠及实验性肝损伤大鼠的胆汁和尿液排泄]
Farmaco Prat. 1973;28(9):481-8.
10
Effect of some chelating agents on the biliary excretion of mercury. 2. Relationship between the excretion of mercury and its binding to bile fractions.
J Hyg Epidemiol Microbiol Immunol. 1980;24(3):309-23.

引用本文的文献

1
Copper and zinc in CCl4 treated rats.四氯化碳处理大鼠体内的铜和锌
Bull Environ Contam Toxicol. 1984 Apr;32(4):405-9. doi: 10.1007/BF01607516.
2
Trace elements (Cu, Fe, Zn) in several tissues of CCl4-induced chronic hepatitis rats.四氯化碳诱导的慢性肝炎大鼠几种组织中的微量元素(铜、铁、锌)
Bull Environ Contam Toxicol. 1986 Feb;36(2):306-10. doi: 10.1007/BF01623512.
3
Blood pressure reduction by CCl4 in the spontaneously hypertensive rat.四氯化碳对自发性高血压大鼠血压的降低作用。

本文引用的文献

1
The effect of chronic administration of carbon tetrachloride and alpha-napthylisothiocyanate on tissue copper levels in the rat.长期给予四氯化碳和α-萘基异硫氰酸酯对大鼠组织铜水平的影响。
Biochem Med. 1970 Nov;4(3):260-76. doi: 10.1016/0006-2944(70)90053-0.
2
Biliary excretion of 203 Hg, 64 Cu, 52 Mn, and 210 Pb in the rat.大鼠体内203汞、64铜、52锰和210铅的胆汁排泄
Br J Ind Med. 1972;29(1):74-80.
3
The effects of various drugs and toxic agents on bile flow rate and composition in the rat.各种药物和有毒制剂对大鼠胆汁流速及成分的影响。
Bull Environ Contam Toxicol. 1988 Jul;41(1):56-62. doi: 10.1007/BF01689059.
Toxicol Appl Pharmacol. 1971 Oct;20(2):157-74. doi: 10.1016/0041-008x(71)90042-1.