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镉对体外激活的人外周血单个核细胞中白细胞介素-1β和肿瘤坏死因子-α生物合成的抑制作用

Suppression of interleukin-1 beta and tumour necrosis factor-alpha biosynthesis by cadmium in in vitro activated human peripheral blood mononuclear cells.

作者信息

Theocharis S E, Souliotis V L, Panayiotidis P G

机构信息

Department of Experimental Pharmacology, School of Medicine, University of Athens, Greece.

出版信息

Arch Toxicol. 1994;69(2):132-6. doi: 10.1007/s002040050148.

Abstract

Cadmium is a highly toxic element responsible for acute and chronic toxicity in man. There is evidence that cadmium induces pathophysiological effects by modulating components of the immune system. Cytokines are being increasingly recognized as essential mediators of normal and pathologic immune responses. Cadmium at concentrations varying from 1.0 x 10(-4) to 3.3 x 10(-6) M inhibited the phytohemagglutinin induced production of interleukin-1 beta and tumour necrosis factor-alpha, in in vitro activated human peripheral blood mononuclear cells. The messenger RNA levels of interleukin-1 beta and tumour necrosis factor-alpha were examined during a 24-h culture period, at different time points. The decreased messenger RNA levels at the time points of the maximum expression of interleukin-1 beta and tumour necrosis factor-alpha indicate that cadmium suppresses their production at the transcriptional level.

摘要

镉是一种剧毒元素,可导致人类急性和慢性中毒。有证据表明,镉通过调节免疫系统的组成部分诱导病理生理效应。细胞因子越来越被认为是正常和病理免疫反应的重要介质。在体外激活的人外周血单核细胞中,浓度从1.0×10⁻⁴到3.3×10⁻⁶ M的镉抑制了植物血凝素诱导的白细胞介素-1β和肿瘤坏死因子-α的产生。在24小时培养期的不同时间点检测白细胞介素-1β和肿瘤坏死因子-α的信使核糖核酸水平。在白细胞介素-1β和肿瘤坏死因子-α最大表达的时间点,信使核糖核酸水平降低,表明镉在转录水平上抑制了它们的产生。

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