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Cardiovascular Research 2002 53(4):1035-1042; doi:10.1016/S0008-6363(01)00541-7
© 2002 by European Society of Cardiology
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Copyright © 2002, European Society of Cardiology

Oxidant stress mechanism of homocysteine potentiating Con A-induced proliferation in murine splenic T lymphocytes

Qin Zhanga,1, Xiaokun Zenga,1, Jingxuan Guoa and Xian Wanga,b,*

aInstitute of Vascular Medicine, Third Hospital, Beijing, PR China
bDepartment of Physiology, Health Science Center, Peking University, Beijing 100083, PR China

zqcua{at}yahoo.com

xkzeng1013{at}yahoo.com

* Corresponding author. Present address: Department of Physiology, Health Science Center, Peking University, 38 Xue Yuan Road, Beijing 100083, PR China. Tel.: +86-10-6209-1443; fax: +86-10-6201-7700 xwang{at}mail.bjmu.edu.cn

Objective: An elevated plasma homocysteine (Hcy) level is considered an independent risk factor for atherosclerosis. However, the mechanisms by which hyperhomocysteinemia induces atherosclerosis are only partially understood. The effect of Hcy on T lymphocyte proliferation and its mechanisms were examined in normal and hyperhomocysteinemia ApoE-knockout mice. Methods: The mouse splenic T-cells were treated with Hcy, related compounds and/or antioxidants in the presence or absence of Concanavalin A (Con A). DNA synthesis, cell apoptosis, interleukin-2 level and production of reactive oxygen species (ROS) were measured. Results: Hcy (0.3–3.0 mM) and related compounds with thiol (–SH), such as cysteine and glutathione significantly potentiated Con A-induced proliferation and partially inhibited apoptosis in T lymphocytes, but it had no direct effect on resting T lymphocyte. ApoE-knockout mice with hyperhomocysteinemia (the level of plasma Hcy was 20.3±2.9 vs. 2.6±0.6 µM in control group, P<0.05) had a significant promotion of T-cell proliferation in response to Con A. Hcy (0.3–3.0 mM) also increased the intracellular ROS. Radical scavengers reduced Hcy effect. Conclusions: These data indicate that ROS generated by thiol (–SH) of Hcy auto-oxidation are involved in Hcy effect on Con A-induced T lymphocyte proliferation. These findings suggest a novel mechanism may be involved in chronic inflammatory progression of atherosclerosis with hyperhomocysteinemia.

KEYWORDS Apoptosis; Atherosclerosis; Free radicals; Immunology; Infection/Inflammation; Leukocytes

1 Qin Zhang and Xiaokun Zeng contributed equally to this work.


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