Effects of gallium on immune stimulation and apoptosis induction in human peripheral blood mononuclear cells

被引：30

作者：

Chang, KL

Liao, WT

Yu, CL

Lan, CCE

Chang, LW

Yu, HS

机构：

[1] Natl Taiwan Univ, Coll Med, Dept Dermatol, Taipei 100, Taiwan

[2] Kaohsiung Med Univ, Dept & Inst Biochem, Kaohsiung, Taiwan

[3] Natl Taiwan Univ, Coll Med, Dept Internal Med, Taipei, Taiwan

[4] Natl Taiwan Univ, Coll Med, Inst Mol Med, Taipei, Taiwan

[5] Kaohsiung Med Univ, Dept Dermatol, Kaohsiung, Taiwan

[6] Natl Hlth Res Inst, Div Environm Hlth & Occupat Med, Kaohsiung, Taiwan

来源：

TOXICOLOGY AND APPLIED PHARMACOLOGY | 2003年 / 193卷 / 02期

关键词：

gallium; lymphocytes; cytokine; cytotoxicity;

D O I：

10.1016/j.taap.2003.07.004

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

Gallium is commonly used in the semiconductor industry and medical field. Biologically, gallium is able to interrupt iron metabolism. Exposure to gallium has been shown to affect the human immune system. The purpose of this study was to investigate the in vitro biological effects of different gallium concentrations on cultured human peripheral blood mononuclear cells (PBMCs) in terms of cell growth, cytokine release, and apoptosis induction. In addition, the in vivo effects of gallium were analyzed by Wistar rat model. Our results revealed that low concentrations (1-10 mug/ml) of gallium promoted cells to enter the S phase of cell cycle and enhanced cellular release of tumor necrosis factor-alpha, interleukin-1beta, and interferon-gamma, both in vitro and in vivo. In contrast, high concentrations of gallium (50-100 mug/ml) induced apoptosis. Furthermore, gallium-induced cytokine release and apoptosis could be inhibited by iron-saturated transferrin (Tf-Fe). These results suggest that the concentration-dependent effects of gallium on PBMCs are related to iron metabolism. (C) 2003 Elsevier Inc. All rights reserved.

引用

页码：209 / 217

页数：9

共 31 条

[1] EFFECTS OF DIFFERENT TRANSFERRIN FORMS ON TRANSFERRIN RECEPTOR EXPRESSION, IRON UPTAKE, AND CELLULAR PROLIFERATION OF HUMAN-LEUKEMIC HL60 CELLS - MECHANISMS RESPONSIBLE FOR THE SPECIFIC CYTOTOXICITY OF TRANSFERRIN-GALLIUM [J].