荷瘤小鼠体内辐照诱导浸润性白细胞产生一氧化氮。

Y Vodovotz, D Coffin, A M DeLuca, L McKinney, J A Cook, D Wink, J B Mitchell
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引用次数: 7

摘要

一氧化氮(NO)由于其在肿瘤细胞和浸润性白细胞中产生,在肿瘤的消退和进展中都有牵连。电离辐射可引起肿瘤的消退,并可增加巨噬细胞体外NO的产生。我们检测了小鼠体内抗辐射的RIF-1纤维肉瘤细胞皮下植入,然后在肿瘤部位进行辐照或假治疗后,细胞和全身NO的产生。植入肿瘤10天后,在60 Gy的照射后立即从切除的肿瘤中获得CD45-肿瘤细胞和CD45+白细胞,先前报道的剂量可减少肿瘤生长。来自受辐射宿主肿瘤的白细胞自发产生的NO比来自未受辐射小鼠的白细胞或来自未受辐射或受辐射小鼠的CD45-肿瘤细胞多四倍。在肿瘤植入后10-14天,放疗和未放疗小鼠血清NO2-/NO3-均有相同程度的升高,最终水平高于非荷瘤小鼠。尽管在体外接受1-10 Gy辐射处理的巨噬细胞产生一氧化氮增加,但体内肿瘤浸润性巨噬细胞可能需要更高的剂量,因此可能表明肿瘤浸润性巨噬细胞失活。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Induction of nitric oxide production in infiltrating leukocytes following in vivo irradiation of tumor-bearing mice.

Nitric oxide (NO) has been implicated both in regression and progression of tumors due to its production by both tumor cells and infiltrating leukocytes. Ionizing radiation causes the regression of tumors, and can augment the production of NO by macrophages in vitro. We examined the cellular and systemic production of NO in mice in which radiation-resistant RIF-1 fibrosarcoma cells were implanted subcutaneously and were then either irradiated or sham-treated at the tumor site. Ten days following implantation of the tumors, CD45- tumor cells and CD45+ leukocytes were derived from resected tumors immediately after irradiation with 60 Gy, a dose previously reported to reduce tumor growth. Leukocytes from tumors of irradiated hosts produced spontaneously up to four-fold more NO than did either leukocytes from unirradiated mice or CD45- tumor cells from either unirradiated or irradiated mice. Between days 10-14 following tumor implantation, serum NO2-/NO3- increased in both irradiated and unirradiated mice to an equal extent, culminating in levels higher than those of non-tumor-bearing mice. Though NO production is elevated in macrophages treated with 1-10 Gy of radiation in vitro, higher doses may be required by tumor-infiltrating macrophages in vivo and thus may indicate that tumor-infiltrating macrophages are deactivated.

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