## 4 Discussion  
As indicated by recent investigations, the O\({}_{2}\) loading of the optical fiber can destroy the GLPC centers and modify the optical fiber response to consecutive irradiation [10]. This is particularly interesting in the context of radiation-hardened optical fibers [17; 18], particularly in the ultraviolet and visible domains. In the present work we provided strong evidence, in the O\({}_{2}\)-loaded sample, of a GLPC increase (Figure 4) that is induced by electron irradiation. Such an increase is observed until the \(\sim\)40 th scan (dose \(\sim\)2.7 \(\times\) 10\({}^{7}\) Gy), then a limit value, confined within a factor \(\sim\)2, is reached. The resulting behavior is similar in the two investigated Ge-doped regions (5 wt% and 9 wt%), even if the growth of the signal is higher in the less-doped parts of the fibers, while in the higher-doped region, a growth of only \(\sim\)25% is recorded. We also note that due to the high dose rate in the first scan, each investigated point accumulates a dose of about 0.67 MGy. The observed behavior prompts two essential questions: what are the microscopic mechanisms behind the observed increase in the CL signal of GLPC centers, and what kind of point defects can arise from the interaction of an O\({}_{2}\) molecule with a GLPC in bulk silica? Our ab initio results suggest that the O\({}_{2}\) loading of the optical fiber, which is performed prior to irradiation, can lead to the formation of bulk DIOG defects in silica. In fact, our calculations indicate that the DIOG could be readily formed whenever an oxygen molecule is present near the GLPC, i.e., in the presence of O\({}_{2}\) excess inside Ge-doped silica, thus providing an explanation for the bleaching effect of the O\({}_{2}\) loading on the GLPC concentration (Figure 3a). Under electron irradiation, some GLPC centers are regenerated due to the release of excited/ionized O\({}_{2}\) species from a DIOG (Figure 7). Particularly, the reaction in the case of neutral species requires overcoming an energy barrier (\(\sim\)1.3 eV), being easily accessible during irradiation [15; 46], and representing an upper bound for the release of the excited/ionized O\({}_{2}\) species. Since O\({}_{2}\) at room temperature did not escape from the material, we approximated that (particularly when there is a starting excess of O\({}_{2}\) in the silica matrix) an equilibrium can be reached between the regeneration of GLPC under irradiation and the passivation by oxygen at room temperature which leads to the formation of dioxagermirane or other defects [10]. We note that electron-stimulated desorption may occur at the surface of samples as reported previously [47; 48]. Specifically, oxygen might be desorbed, and because the sample volume is mostly occupied by silica, oxygen vacancies might be generated in silica, and ODC-II centers could be generated during the irradiation occasionally. Yet, since the CL measurements were carried out at room temperature, oxygen diffusion is low so that, regarding the GLPC center (and hence its luminescence), the effect of this surface desorption in the bulk is not relevant. DIOG could release molecular oxygen, but the latter would not move far from the GLPC, so we do not expect it to lead to a remarkable desorption from the sample at room temperature within the total irradiation time. As the oxygen loading is often performed using diffusion mechanisms at temperatures around \(\sim\)500 \({}^{\circ}\)C [10], it could be speculated that a combination of excess oxygen and temperature could reconstruct the network at a GLPC site, similar to an oxygen molecule easily passivating an oxygen vacancy and forming a peroxy defect. The reconstruction reaction at a GLPC site may be a more complex network relaxation, analogous to the GLPC generation from an oxygen (mono-)vacancy which involves advanced \"rotation\" and \"puckering\" mechanisms [15].