首页> 外文期刊>Mutation Research: International Journal on Mutagenesis, Chromosome Breakage and Related Subjects >Effect of ex vivo hyperthermia on radiation-induced micronuclei in lymphocytes of cancer patients before and during radiotherapy.
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Effect of ex vivo hyperthermia on radiation-induced micronuclei in lymphocytes of cancer patients before and during radiotherapy.

机译:离体热疗对放疗前后癌症患者淋巴细胞辐射诱导的微核的影响。

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To investigate the effect of ex vivo hyperthermia (HT) and 137Cs-irradiation on micronucleus (MN) production in cytokinesis-blocked lymphocytes, we obtained the peripheral blood samples from the same cancer patients (n=6) before and during fractionated partial-body radiotherapy (xRT). The whole blood cultures were heated at 43.5 degrees C for 60 min, followed by 137Cs irradiation (0-4 Gy). The control cultures from the same patients were incubated at 37 degreesC after being exposed to radiation. The lymphocytes were then stimulated with PHA. Cytochalasin B was applied at 44 h, and lymphocytes were harvested at 72 h. MN frequency was determined on Giemsa-stained slides. We found that in patients before xRT, HT (43.5 degrees C) significantly increased the MN yield (mean+/-SEM) in unirradiated lymphocytes from 15.6+/-2.8 (37 degrees C) to 39.7+/-10.9. Further, in patients either before or during xRT, when the lymphocytes were treated with HT (43.5 degrees C) and combined with ex vivo irradiation, the MN yield (Y) could be estimated by a linear equation Y=C+alphaD. Our findings indicate that as measured by the MN production in cytokinesis-blocked lymphocytes, HT alone at 43.5 degrees C++ induced DNA damage. Moreover, it enhanced the radiation-induced cytogenetic damage. Therefore, the application of HT may impair the T-cell function in cancer patients who are receiving radiotherapy. 1998 Elsevier Science B.V.
机译:为了研究离体高热(HT)和137Cs辐照对胞质分裂阻滞的淋巴细胞中微核(MN)产生的影响,我们从相同癌症患者(n = 6)的分次分体前后进行了外周血采集放疗(xRT)。将全血培养物在43.5摄氏度下加热60分钟,然后进行137Cs辐射(0-4 Gy)。来自相同患者的对照培养物在暴露于辐射后在37℃下孵育。然后用PHA刺激淋巴细胞。在第44小时施用细胞松弛素B,并在第72小时收获淋巴细胞。在吉姆萨染色的载玻片上确定MN频率。我们发现在xRT之前的患者中,HT(43.5摄氏度)显着增加了未照射淋巴细胞的MN产量(平均值+/- SEM)从15.6 +/- 2.8(37摄氏度)增加到39.7 +/- 10.9。此外,对于在xRT之前或期间的患者,当用HT(43.5摄氏度)处理淋巴细胞并结合离体照射后,可以通过线性方程Y = C + alphaD估算MN产量(Y)。我们的发现表明,如通过胞质分裂阻滞的淋巴细胞中的MN产生所测量的,单独的HT在43.5摄氏度时会诱导DNA损伤。而且,它增强了辐射诱导的细胞遗传学损害。因此,HT的应用可能会损害正在接受放射治疗的癌症患者的T细胞功能。 1998年Elsevier Science B.V.

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