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饮食中维生素 E 的限制增强了二氯乙酸和三氯乙酸对小鼠的吞噬激活作用。

Vitamin E restriction in the diet enhances phagocytic activation by dichloroacetate and trichloroacetate in mice.

机构信息

The University of Toledo, College of Pharmacy and Pharmaceutical Sciences, HSC, 3000 Arlington Avenue, Toledo, OH 43614-2598, USA.

出版信息

Food Chem Toxicol. 2012 Mar;50(3-4):701-6. doi: 10.1016/j.fct.2011.11.055. Epub 2011 Dec 9.

Abstract

The effects of a vitamin E-restricted diet on the induction of phagocytic activation by dichloroacetate (DCA) and trichloroacetate (TCA) was investigated. Groups of B6C3F1 male mice were either kept on standard diet (Std diet group) or diet that had the vitamin provided only by its natural ingredients (Low-E diet group). The animals in each diet group were administered 77 mg of DCA or TCA/ kg/day, or 5 ml/kg water (controls), by gavage, for 13 weeks. Thereafter, peritoneal lavage cells (PLC) were assayed for superoxide anion (SA), tumor necrosis factor (TNF)-α, and myeloperoxidase (MPO), as well as for the activities of the anti-oxidant enzymes superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px). SA and TNFα production, as well as MPO, SOD, CAT and GSH-Px activities were significantly increased in the cells from the Low-E diet group treated with the compounds as compared with cells from hosts in the Std-diet group that received the corresponding treatments. The results indicate that consumption of a Vitamin E-restricted diet enhances the induction of phagocytic activation by DCA and TCA, a mechanism that was previously suggested to be an initial adaptive/protective response against the compounds long-term effects.

摘要

研究了维生素 E 限制饮食对二氯乙酸(DCA)和三氯乙酸(TCA)诱导吞噬细胞活化的影响。将 B6C3F1 雄性小鼠分为两组,一组给予标准饮食(Std 饮食组),另一组给予仅由天然成分提供维生素的饮食(Low-E 饮食组)。每组动物通过灌胃给予 77mg/kg/d DCA 或 TCA,或 5ml/kg 水(对照),共 13 周。然后,检测腹腔灌洗细胞(PLC)中超氧化物阴离子(SA)、肿瘤坏死因子(TNF)-α和髓过氧化物酶(MPO)的活性,以及抗氧化酶超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GSH-Px)的活性。与接受相应处理的 Std 饮食组宿主的细胞相比,用化合物处理的 Low-E 饮食组的细胞中 SA 和 TNFα 的产生以及 MPO、SOD、CAT 和 GSH-Px 活性显著增加。结果表明,摄入维生素 E 限制饮食增强了 DCA 和 TCA 诱导的吞噬细胞活化,这一机制先前被认为是对化合物长期作用的初始适应性/保护反应。

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