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Modulation of oxidative phosphorylation (OXPHOS) by radiation- induced biophotons
Environmental Research ( IF 7.7 ) Pub Date : 2018-02-22 , DOI: 10.1016/j.envres.2018.01.027
Michelle Le , Fiona E. McNeill , Colin B. Seymour , Andrej Rusin , Kevin Diamond , Andrew J. Rainbow , James Murphy , Carmel E. Mothersill

Radiation-induced biophotons are an electromagnetic form of bystander signalling. In human cells, biophoton signalling is capable of eliciting effects in non-irradiated bystander cells. However, the mechanisms by which the biophotons interact and act upon the bystander cells are not clearly understood. Mitochondrial energy production and ROS are known to be involved but the precise interactions are not known. To address this question, we have investigated the effect of biophoton emission upon the function of the complexes of oxidative phosphorylation (OXPHOS). The exposure of bystander HCT116 p53 +/+ cells to biophoton signals emitted from β-irradiated HCT116 p53 +/+ cells induced significant modifications in the activity of Complex I (NADH dehydrogenase or NADH:ubiquinone oxidoreductase) such that the activity was severely diminished compared to non-irradiated controls. The enzymatic assay showed that the efficiency of NADH oxidation to NAD+ was severely compromised. It is suspected that this impairment may be linked to the photoabsorption of biophotons in the blue wavelength range (492–455 nm). The photobiomodulation to Complex I was suspected to contribute greatly to the inefficiency of ATP synthase function since it resulted in a lower quantity of H+ ions to be available for use in the process of chemiosmosis. Other reactions of the ETC were not significantly impacted. Overall, these results provide evidence for a link between biophoton emission and biomodulation of the mitochondrial ATP synthesis process. However, there are many aspects of biological modulation by radiation-induced biophotons which will require further elucidation.



中文翻译:

辐射诱导的生物光子对氧化磷酸化(OXPHOS)的调节

辐射诱导的生物光子是旁观者信号的电磁形式。在人类细胞中,生物光子信号传导能够在未辐射的旁观者细胞中引发效应。但是,尚不清楚生物光子相互作用并作用于旁观者细胞的机制。已知涉及线粒体能量产生和ROS,但尚不清楚精确的相互作用。为了解决这个问题,我们研究了生物光子发射对氧化磷酸化(OXPHOS)配合物功能的影响。旁观者HCT116 p53 + / +细胞暴露于β发出的生物光子信号辐照的HCT116 p53 + / +细胞诱导复合物I(NADH脱氢酶或NADH:泛醌氧化还原酶)的活性发生显着改变,因此与未辐照的对照组相比,该活性大大降低。酶促测定表明,NADH氧化为NAD +的效率受到严重损害。怀疑这种损伤可能与蓝色波长范围(492–455 nm)中生物光子的光吸收有关。怀疑对复合物I的光生物调节对ATP合酶功能的低效率有很大贡献,因为它导致较低的H +量。离子可用于化学渗透过程中。ETC的其他反应未受到明显影响。总体而言,这些结果为生物光子发射与线粒体ATP合成过程的生物调节之间的联系提供了证据。然而,由辐射诱导的生物光子进行生物调节的许多方面需要进一步阐明。

更新日期:2018-02-22
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