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硒与免疫细胞功能。II. 对淋巴细胞介导的细胞毒性的影响。

Selenium and immune cell functions. II. Effect on lymphocyte-mediated cytotoxicity.

作者信息

Roy M, Kiremidjian-Schumacher L, Wishe H I, Cohen M W, Stotzky G

机构信息

Department of Histology and Cell Biology, New York University Dental Center, New York 10010.

出版信息

Proc Soc Exp Biol Med. 1990 Feb;193(2):143-8. doi: 10.3181/00379727-193-43015.

Abstract

Selenium (Se) is an essential nutritional factor with a chemopreventive potential. This study examined the ability of C57BL/6J mice, maintained for 8 weeks on Se-deficient (0.02 ppm Se), normal (0.20 ppm Se), or Se-supplemented (2.00 ppm Se) Torula yeast-based diets, to generate cytotoxic lymphocytes (CTL) and to destroy tumor cells. CTL were generated in vivo by intraperitoneal immunization with P815 cells and in vitro by allogeneic stimulation of cells from animals maintained on a normal diet in media supplemented with 1 x 10(-9) to 1 x 10(-6) M Se (as selenite). Lymphocytes from animals maintained on the Se-supplemented diet had a greater ability to destroy tumor cells than lymphocytes from animals maintained on the normal diet, whereas Se deficiency reduced the cytotoxicity. The effects on cytotoxicity were accompanied by parallel changes in the levels of lymphotoxin produced. The greatest enhancement of tumor cytodestruction occurred with supplementation of 1 x 10(-7) M Se, whereas with 1 x 10(-6) M there was inhibition of the cytotoxic responses. The stimulatory effect of Se occurred during the phase of CTL generation rather than during the lytic phase of cytotoxicity. These results indicated that Se supplementation enhances CTL generation and the ability of a host to destroy malignant cells, whereas Se deficiency has the opposite effect.

摘要

硒(Se)是一种具有化学预防潜力的必需营养因子。本研究检测了在缺硒(0.02 ppm硒)、正常(0.20 ppm硒)或补硒(2.00 ppm硒)的基于圆酵母的饮食上维持8周的C57BL/6J小鼠产生细胞毒性淋巴细胞(CTL)并破坏肿瘤细胞的能力。CTL通过腹腔注射P815细胞在体内产生,并通过在补充有1×10⁻⁹至1×10⁻⁶ M硒(亚硒酸盐形式)的培养基中对正常饮食饲养动物的细胞进行同种异体刺激在体外产生。与正常饮食饲养动物的淋巴细胞相比,补硒饮食饲养动物的淋巴细胞具有更强的破坏肿瘤细胞的能力,而缺硒则降低了细胞毒性。对细胞毒性的影响伴随着所产生淋巴毒素水平的平行变化。补充1×10⁻⁷ M硒时肿瘤细胞破坏的增强最为显著,而补充1×10⁻⁶ M硒时则抑制了细胞毒性反应。硒的刺激作用发生在CTL产生阶段而非细胞毒性的裂解阶段。这些结果表明,补硒增强了CTL的产生以及宿主破坏恶性细胞的能力,而缺硒则具有相反的作用。

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