Wang Lei, Du Hua, Guo Xiaoying, Wang Xinan, Wang Meimei, Wang Yichen, Wang Min, Chen Shaopeng, Wu Lijun, Xu An
Key Laboratory of Ion Beam Bioengineering, Institute of Technical Biology and Agricultural Engineering, Hefei Institutes of Physical Science, Chinese Academy of Science, Hefei, Anhui, People's Republic of China.
Bioelectromagnetics. 2015 Apr;36(3):178-89. doi: 10.1002/bem.21906. Epub 2015 Mar 9.
Understanding the effects of strong static magnetic fields (SMFs) on living organisms is significant in health risk assessment, but underlying mechanisms are largely unknown. In the present study, we determined developmental abnormalities induced by 8.5Tesla (T) SMFs in a well-established in vivo model organism, Caenorhabditis elegans (C. elegans). Exposure of C. elegans eggs to 8.5 T SMF resulted in a time-dependent lifespan decrease, whereas only slight changes were observed upon exposure to 5 T SMF. Although SMF exposure did not alter brood size, development rate and stages were significantly modified by 8.5 T SMF. Germ cell apoptosis dramatically increased upon exposure to 8.5 T SMF in adult worms, as confirmed by ced-3 and ced-4 mutants, and could be prevented by concurrent treatment with a free radical scavenger, dimethyl sulfoxide. Compared to wild-type worms, shorter lifespan and greater numbers of apoptotic cells were observed in abnormal methyl viologen sensitivity-1 (mev-1(kn1)) nematodes with increased sensitivity to oxidative damage. Furthermore, exposure to 8.5 T SMF increased expression of superoxide dismutase-3 (sod-3), which is thought to protect against oxidative stress. However, 8.5 T SMF had minimal effects on lifespans of daf-2 and daf-16 mutants, which have compromised insulin/IGF-1 (insulin-like growth factors-1) mediated signaling pathways; this finding was consistent with the expression of these genes in wild-type worms. Our results indicate that developmental toxicity induced by strong SMF in C. elegans is mediated by oxidative stress and may be regulated by the insulin-like receptor pathway.
了解强静磁场（SMFs）对生物体的影响在健康风险评估中具有重要意义，但其潜在机制在很大程度上尚不清楚。在本研究中，我们在一种成熟的体内模式生物秀丽隐杆线虫（C. elegans）中确定了8.5特斯拉（T）静磁场诱导的发育异常。将秀丽隐杆线虫卵暴露于8.5 T静磁场会导致寿命随时间减少，而暴露于5 T静磁场时仅观察到轻微变化。虽然静磁场暴露不会改变产卵量，但8.5 T静磁场显著改变了发育速率和发育阶段。成年蠕虫暴露于8.5 T静磁场后生殖细胞凋亡显著增加，ced-3和ced-4突变体证实了这一点，并且可以通过同时用自由基清除剂二甲基亚砜处理来预防。与野生型蠕虫相比，对氧化损伤敏感性增加的异常甲基紫精敏感性-1（mev-1(kn1)）线虫寿命更短，凋亡细胞数量更多。此外，暴露于8.5 T静磁场会增加超氧化物歧化酶-3（sod-3）的表达，该酶被认为可以抵御氧化应激。然而，8.5 T静磁场对daf-2和daf-16突变体的寿命影响最小，这两种突变体的胰岛素/IGF-1（胰岛素样生长因子-1）介导的信号通路受损；这一发现与这些基因在野生型蠕虫中的表达一致。我们的结果表明，强静磁场在秀丽隐杆线虫中诱导的发育毒性是由氧化应激介导的，并且可能受胰岛素样受体途径调节。
