INFLUENCE OF EMF ON FREE RADICAL MEDIATED TOXOCOLOGICAL PROCESSES

尽管流行病学研究表明， 电磁场暴露与癌症的关系 目前几乎没有合理的分子机制来解释这一点 效果 已知自由基参与癌症的病因学 和其他疾病的可能性，电磁场可能会以某种方式发挥作用， 增加自由基的寿命和/或浓度。 它有 多年来已知在有组织的介质（例如洗涤剂）中 胶束）施加的磁场引起平均游离 自由基浓度和延长自由基的寿命。 如果 这些效应发生在体内，那么这可以解释一些报道的 EMF的生物效应 我们最初的研究集中在 完整的红细胞作为一个测试系统，可用于研究 MF对自由基过程的影响。我们发现酮洛芬， 一种具有光毒性的非甾体抗炎药（结构相关 二苯甲酮），导致完全溶血的人红细胞后， 紫外线照射20分钟。光致溶血依赖于 还原型谷胱甘肽和丁基化谷胱甘肽 羟基甲苯（BHT），表明机制涉及脂质 过氧化作用 当紫外线照射在磁场中进行时， （3500 G）50%细胞发生溶血所需的时间（t+） 显著缩短（78 min vs. 96 min）。 显著降低 在低至250 G的磁场下可以观察到t1/2的变化， 在100 G时消失。这些观测结果可以归因于一个磁场 场诱导的系统间穿越率的降低， 酮洛芬还原生成的成对三重态自由基对 在红细胞膜成分的三重激发态， 脂质。 据我们所知，这是第一次证明一种效应， MF对毒理学过程的影响，已知该过程通过游离 自由基机制

Although epidemiological studies suggest that there is a weak relationship between exposure to electromagnetic fields (EMF) and cancer there are at present few plausible molecular mechanisms to explain this effect. The known involvement of free radicals in the etiology of cancer and other diseases raises the possibility that EMF may somehow act by increasing the lifetime and/or concentration of free radicals. It has been known for many years that in organized media (e.g. detergent micelles) applied magnetic fields cause an increase in average free radical concentration and lengthen the lifetime of free radicals. If these effects occur in vivo then this may explain some of the reported biological effects of EMF. Our initial studies have focused on the intact erythrocyte as a test system that could be used to study the effects of MF on free radical processes. We have found that ketoprofen, a phototoxic, non-steroidal anti-inflammatory drug (structurally related to benzophenone), caused complete hemolysis of human erythrocytes after only 20 min UV irradiation. Photohemolysis was dependent on the presence of oxygen and was inhibited by reduced glutathione and butylated hydroxytoluene (BHT) suggesting that the mechanism involved lipid peroxidation. When UV irradiation was carried out in a magnetic field (3500G) the time taken for hemolysis to occur in 50% of the cells (t+) was significantly shortened (78 min vs. 96 min). A significant decrease in t1/2 could be observed at fields as low as 250G but the effect disappeared at 100G. These observations can be attributed to a magnetic field induced decrease in the rate of intersystem crossing of the geminate triplet radical pair generated by the reduction of ketoprofen in its triplet excited state by erythrocyte membrane components, probably lipids. To our knowledge this is the first demonstration of an effect of MF on a toxicological process that is known to occur via a free radical mechanism.