One main function of telomeres is to maintain chromosome and genome stability. The rate of telomere shortening can be accelerated significantly by chemical and physical environmental agents. Reactive oxygen species are a source of oxidative stress and can produce modified bases (mainly 8-oxoG) and single strand breaks anywhere in the genome. The high incidence of guanine residues in telomeric DNA sequences makes the telomere a preferred target for oxidative damage. Our aim in this work is to evaluate whether chromosome instability induced by oxidative stress is related specifically to telomeric damage. We treated human primary fibroblasts (MRC-5) in vitro with hydrogen peroxide (100 and 200 µM) for 1 hr and collected data at several time points. To evaluate the persistence of oxidative stress-induced DNA damage up to 24 hrs after treatment, we analysed telomeric and genomic oxidative damage by qPCR and a modified comet assay, respectively. The results demonstrate that the genomic damage is completely repaired, while the telomeric oxidative damage persists. The analysis of telomere length reveals a significant telomere shortening 48 hrs after treatment, leading us to hypothesise that residual telomere damage could be responsible for the telomere shortening observed. Considering the influence of telomere length modulation on genomic stability, we quantified abnormal nuclear morphologies (Nucleoplasmic Bridges, Nuclear Buds and Micronuclei) and observed an increase of chromosome instability in the same time frame as telomere shortening. At subsequent times (72 and 96 hrs), we observed a restoration of telomere length and a reduction of chromosome instability, leaving us to conjecture a correlation between telomere shortening/dysfunction and chromosome instability. We can conclude that oxidative base damage leads to abnormal nuclear morphologies and that telomere dysfunction is an important contributor to this effect.

The degree of $B/B^{\prime }$ alternate cation order is known to heavily influence the magnetic properties of $A_{2}B{B}^{\prime }{\mathrm{O}}_6$ double perovskites although the nature of such disorder has never been critically studied. Our detailed x-ray absorption fine structure studies in conjunction with synchrotron radiation x-ray diffraction experiments on polycrystalline ${\mathrm{Sr}}_2{\mathrm{FeMoO}}_6$ samples with various degrees of disorder reveal that a very high degree of short range order is preserved even in samples with highly reduced long range chemical order. Based on these experimental results and with the help of detailed structural simulations, we are able to model the nature of the disorder in this important class of materials and discuss the consequent implications on its physical properties.

We have performed structural studies of a series of mixed-alkali phosphate glasses using diffraction experiments and reverse Monte Carlo simulations. We find that the alkali ions tend to preserve their local structural environment regardless of the glass composition. Furthermore, the distribution of the two types of cations in the structure is predominantly random. We propose that the long debated mixed-alkali effect is a natural consequence of the structural findings; a large energy mismatch for ionic jumps to dissimilar alkali sites resulting in blocking of low-dimensional migration pathways.