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Research on carcinogenesis modifying factor by static magnetic field exposure

静磁场暴露致癌调节因子的研究

基本信息

批准号：
16590486
负责人：
SUZUKI Yuji
金额：
$ 2.24万
依托单位：
Jikei University School of Medicine
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2004
资助国家：
日本
起止时间：
2004 至 2006
项目状态：
已结题

项目摘要

We have previously found that exposure to static magnetic fields (SMFs) increase the frequency of micronuclei. In this experiment, it became clear that co-exposure to SMFs increases the frequency of micronuclei induction by several mutagens including active oxygen radical inducible chemicals (doxorubicin (DOX), mitomycin C (MMC)). Therefore, the increase in micronucleus formation by SMFs might be related to active oxygen radical inducibility. In the present study, we used the mouse bone marrow micronucleus test to investigate whether antioxidant (ascorbic acid (AS)) can control the effects of SMF co-exposure on the frequency of micronuclei produced by radical-inducing chemicals. As a result, the following were clarified.1)As itself did not induce any micronuclei.2)Frequency of micronuclei by DOX or MMC increased by exposure to 5 T SMFs.3)Frequency of micronuclei induced by both DOX and MMC was increased by co-exposure to SMFs, but these increases were blocked by pretreatment with ascorbic acid.4)Frequency of micronuclei induced by co-exposure to MMC and SMFs decreased strongly at 20 min interval of ascorbic acid pre-treatment.5)Effect of ascorbic acid on the micronucleus frequency was maintained for at least 72 hours.6)Increased levels of 8-hydroxy-2'-deoxyguanosine (8-OHdG) in bone marrow cells was observed after exposure to SMFs.These results suggest that SMFs exposure triggers the induction of mutagen-related radicals. This effect might increase the micronucleus frequency.

我们以前发现，暴露于静磁场（SMF）增加微核的频率。在该实验中，很明显，共同暴露于SMF会增加几种诱变剂（包括活性氧自由基诱导化学品（多柔比星（DOX）、丝裂霉素C（MMC）的微核诱导频率。因此，SMFs引起的微核形成增加可能与活性氧自由基诱导有关。在本研究中，我们使用小鼠骨髓微核试验，以探讨抗氧化剂（抗坏血酸（AS））是否可以控制SMF的共同暴露的自由基诱导化学品产生的微核频率的影响。结果表明：1）As本身不诱导任何微核; 2）5 T SMF暴露增加DOX或MMC的微核率; 3）SMF联合暴露增加DOX和MMC诱导的微核率，但这种增加被抗坏血酸预处理所阻断。抗坏血酸预处理20 min后，MMC和SMF的微核率显著降低。5）抗坏血酸对微核率的影响可维持至少72 h。6）8-羟基脱氧鸟苷（8-OHdG）水平升高。这些结果表明，SMFs的暴露触发了诱变剂相关自由基的诱导。这种效应可能会增加微核率。