Wu Xiaonan, Lu Zufu, Chen Jie, Wang Jiali, Huang Fang
Public Health School, Fujian Medical University, Fuzhou, PR China.
Ann Nutr Metab. 2007;51(3):258-63. doi: 10.1159/000105446. Epub 2007 Jul 9.
To investigate the relationships between c-fos expression and oxidative stress or inflammation in the liver induced by acute cadmium (Cd) exposure.
Sixty male Sprague-Dawley rats were randomly assigned to 1 of 6 groups, 10 rats in each group. They were intragastrically pretreated with distilled water, distilled water, vitamin E (50 mg/100 g body weight), 25, 50 and 75% Sagittaria sagittifolia (SS) extract (2 ml/100 g weight) once a day for 10 consecutive days. Twenty-four hours after the last feeding, all animals were intraperitoneally administered CdCl(2) (20 micromol/kg body weight) except for the control group which was given distilled water. Twenty-four hours after intoxication, the glutathione (GSH) and malondialdehyde (MDA) contents and gene expression of tumor necrosis factor-alpha (TNF-alpha) and c-fos were measured in the livers.
Acute Cd exposure significantly increased MDA levels, decreased GSH levels and upregulated the gene expression of TNF-alpha and c-fos in the liver. Vitamin E and middle and high doses of SS were able to inhibit the MDA level, but only middle and high doses of SS enhanced the GSH level and inhibited the upregulation of TNF-alpha gene expression. However, neither vitamin E nor SSwas able to inhibit the upregulation of c-fos gene expression in the liver.
Our data suggested that c-fos induction is independent of oxidative stress or inflammation in the liver during the process of acute Cd exposure in rats.
探讨急性镉(Cd)暴露诱导的肝脏中c-fos表达与氧化应激或炎症之间的关系。
将60只雄性Sprague-Dawley大鼠随机分为6组,每组10只。连续10天每天经口给予蒸馏水、蒸馏水、维生素E(50毫克/100克体重)、25%、50%和75%的慈姑提取物(2毫升/100克体重)。末次给药24小时后,除对照组给予蒸馏水外,其余动物均腹腔注射CdCl₂(20微摩尔/千克体重)。染毒24小时后,检测肝脏中谷胱甘肽(GSH)、丙二醛(MDA)含量以及肿瘤坏死因子-α(TNF-α)和c-fos的基因表达。
急性镉暴露显著增加肝脏中MDA水平,降低GSH水平,并上调TNF-α和c-fos的基因表达。维生素E以及中、高剂量的慈姑提取物能够抑制MDA水平,但只有中、高剂量的慈姑提取物能提高GSH水平并抑制TNF-α基因表达的上调。然而,维生素E和慈姑提取物均不能抑制肝脏中c-fos基因表达的上调。
我们的数据表明,在大鼠急性镉暴露过程中,c-fos的诱导与肝脏中的氧化应激或炎症无关。