Fischer Barbara, Coelho David, Valenti Lionel, Florentin Irene, Denis Jean-Marc, Gueulette John, Dufour Patrick, Bischoff Pierre
LCER, IRCAD, Hôpitaux Universitaires, 1 place de l'Hôpital, F-67091 Strasbourg, France.
Anticancer Res. 2003 Nov-Dec;23(6C):4601-6.
The purpose of this study was to assess apoptosis in hematopoietic tumor cells irradiated with carbon ions, in order to define its contribution to the cytotoxicity of these high-LET radiations.
RDM4 (murine T lymphoma), MOLT-4, TK6 and WTK1 (human lymphoblastoid) cells were irradiated with 12C or 13C. Apoptosis was assessed by flow cytometry. Cell growth and activities of caspases were determined during the same periods.
The ability of carbon ions to induce apoptosis markedly varied according to the cell line. MOLT-4 and TK6 cells underwent apoptosis at 1 Gy within 12 hours post-irradiation, whereas RDM4 and WTK1 showed little apoptosis under the same conditions.
These results indicate that apoptosis contributes to the overall cytotoxicity of carbon ions towards hematopoietic tumor cells although other death mechanisms must also account for this cytotoxicity.
本研究旨在评估碳离子辐照造血肿瘤细胞后的凋亡情况,以确定其对这些高传能线密度辐射细胞毒性的作用。
用12C或13C辐照RDM4(小鼠T淋巴瘤)、MOLT-4、TK6和WTK1(人淋巴母细胞样)细胞。通过流式细胞术评估凋亡情况。在同一时期测定细胞生长和半胱天冬酶活性。
碳离子诱导凋亡的能力因细胞系而异。MOLT-4和TK6细胞在辐照后12小时内接受1 Gy照射时发生凋亡,而RDM4和WTK1在相同条件下几乎未出现凋亡。
这些结果表明,尽管其他死亡机制也必定导致这种细胞毒性,但凋亡对碳离子对造血肿瘤细胞的总体细胞毒性有作用。