Wojewódzka M, Kruszewski M, Szumiel I
Department of Radiobiology and Health Protection, Institute of Nuclear Chemistry and Technology, Warsaw, Poland.
Mutagenesis. 1996 Nov;11(6):593-6. doi: 10.1093/mutage/11.6.593.
Irradiation of human lymphocytes (1 cGy X-rays, 37 degrees C) evoked an approximately 30% decrease in the frequency of micronuclei upon subsequent X-irradiation (1.5 Gy). The response was reflected in a lower micronucleus frequency but not in the DNA repair rate measured by the comet assay directly after the challenge dose. Treatment of lymphocytes with anti-CD38 antibody 1 h before irradiation with the adaptive dose prevented the development of the adaptive response measured as micronuclei frequency, but adaptation was not reflected in a lower rate of DNA repair, measured by the alkaline version of the 'comet' assay. In lymphocytes that were anti-CD38-treated and irradiated and or irradiated with the adaptive dose the rate of DNA repair was not changed. However, the mean DNA damage level in adapted anti-CD38-treated lymphocytes was significantly lower than that in the control lymphocytes at all time points. We conclude that ligation of CD38 by antibody initiates signalling that prevents the development of the adaptive response induced by X-rays. Lower chromosome damage revealed by the cytokinesis block-micronucleus test in the adapted lymphocytes is unrelated to DNA repair rate.
对人淋巴细胞进行照射(1厘戈瑞X射线,37摄氏度)后,在随后进行1.5戈瑞的X射线照射时,微核频率降低了约30%。这种反应表现为微核频率降低,但在激发剂量后立即通过彗星试验测量的DNA修复率中并未体现。在用适应性剂量照射前1小时用抗CD38抗体处理淋巴细胞,可阻止以微核频率衡量的适应性反应的产生,但适应性反应并未体现在通过碱性彗星试验测量的较低DNA修复率上。在用抗CD38抗体处理并照射或用适应性剂量照射的淋巴细胞中,DNA修复率没有变化。然而,在所有时间点,适应性抗CD38处理的淋巴细胞中的平均DNA损伤水平均显著低于对照淋巴细胞。我们得出结论,抗体对CD38的连接引发了信号传导,从而阻止了X射线诱导的适应性反应的产生。在适应性淋巴细胞中,胞质分裂阻滞微核试验显示的较低染色体损伤与DNA修复率无关。