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牛乳铁蛋白对鼠巨噬细胞中弓形虫速殖子的生长抑制作用:活性氧和无机氮氧化物在弓形虫生长抑制活性中的作用

Growth inhibitory effect of bovine lactoferrin on Toxoplasma gondii tachyzoites in murine macrophages: role of radical oxygen and inorganic nitrogen oxide in Toxoplasma growth-inhibitory activity.

作者信息

Tanaka T, Omata Y, Narisawa M, Saito A, Shimazaki K, Igarashi I, Hirumi H, Suzuki N

机构信息

Department of Veterinary Physiology, Obihiro University of Agriculture and Veterinary Medicine, Japan.

出版信息

Vet Parasitol. 1997 Jan;68(1-2):27-33. doi: 10.1016/s0304-4017(96)01069-2.

DOI:10.1016/s0304-4017(96)01069-2
PMID:9066048
Abstract

To study the effector pathway of Toxoplasma growth-inhibitory activity induced by lactoferrin in murine macrophage, the role of reactive oxygen intermediates (O2-) and inorganic nitric oxide (NO) was examined. Production of O2- was diminished in cultures of macrophages supplemented with lactoferrin and the effect of lactoferrin was dose and time dependent. Production of NO was enhanced in cultures of macrophages supplemented with interferon-gamma, but not with lactoferrin. These findings suggest that this Toxoplasma growth-inhibitory activity induced by lactoferrin in macrophages is not mediated by O2- or NO molecules. A competitive inhibitor of the L-arginine dependent effector pathway, NG-monomethyl-L-arginine (NG MMA), virtually abolished the inhibitory effects induced by interferon-gamma. Similarly, the inhibitory activity induced by lactoferrin was also diminished in cultures supplemented with NG MMA. From these findings, it appears that the Toxoplasma growth-inhibitory activity induced by lactoferrin in macrophages may be mediated by an L-arginine-dependent effector pathway that does not involve NO production.

摘要

为研究乳铁蛋白在小鼠巨噬细胞中诱导的弓形虫生长抑制活性的效应途径,检测了活性氧中间体(O2-)和无机一氧化氮(NO)的作用。在添加乳铁蛋白的巨噬细胞培养物中,O2-的产生减少,且乳铁蛋白的作用呈剂量和时间依赖性。在添加γ干扰素的巨噬细胞培养物中,NO的产生增加,但添加乳铁蛋白时则不然。这些发现表明,乳铁蛋白在巨噬细胞中诱导的这种弓形虫生长抑制活性不是由O2-或NO分子介导的。L-精氨酸依赖性效应途径的竞争性抑制剂NG-单甲基-L-精氨酸(NG-MMA)几乎消除了γ干扰素诱导的抑制作用。同样,在添加NG-MMA的培养物中,乳铁蛋白诱导的抑制活性也降低。从这些发现来看,乳铁蛋白在巨噬细胞中诱导的弓形虫生长抑制活性可能由不涉及NO产生的L-精氨酸依赖性效应途径介导。

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