Association between oxidative stress and cytokine production in nickel-treated rats

被引：84

作者：

Chen, CY

Huang, YL

Lin, TH ^{[1
]}

机构：

[1] Kaohsiung Med Coll, Grad Inst Med, Kaohsiung, Taiwan

[2] Foo Yin Inst Technol, Dept Med Technol, Kaohsiung, Taiwan

[3] Kaohsiung Med Coll, Sch Technol Med Sci, Kaohsiung, Taiwan

来源：

ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS | 1998年 / 356卷 / 02期

关键词：

nickel chloride; lipid peroxidation; malondialdehyde; interleukin-1; tumor necrosis factor; transforming growth factor; hepatotoxicity;

D O I：

10.1006/abbi.1998.0761

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The aim of this study was to evaluate a possible relationship between lipid peroxidation, cytokine production, such as interleukin-1 (IL-1), tumor necrosis factor alpha (TNF-alpha), and transforming growth factor beta (TGF-beta), and hepatotoxicity of rats after nickel chloride (NiCl2) acute poisoning. Administration of NiCl2 significantly elevated the levels of malondialdehyde (MDA), IL-1, TNF-alpha, and TGF-beta in the serum of rats. The dose-effect relationship for the increase of serum MDA, as observed in the present study, corresponds closely to the increase of IL-1, TNF-alpha, and TGF-beta in serum. Treatment with ascorbic acid (Vit C) significantly lowered the levels of lipid peroxidation, cytokine production, and the activities of alanine transaminase and aspartate transaminase in the serum of the rats given NiCl2. The hepatic toxicity was increased in a dose-dependent manner and corresponds to the increase of serum IL-1, TNF-alpha, and TGF-beta. There was an association between lipid peroxidation and the levels of cytokines in serum of rats after NiCl2 administration. Reactive oxygen species may serve as a mediator of lipid peroxidation and production of cytokines in NiCl2 injection. (C) 1998 Academic Press.

引用

页码：127 / 132

页数：6

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