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The generation of reactive oxygen species (ROS) may be both beneficial to cells, performing functions in intracellular signaling and detrimental, modifying cellular biomolecules. ROS can cause DNA damage, such as base damage and strand breaks. Organisms respond to chromosome insults by activation of a complex and hierarchical DNA-damage response pathway. The extent of DNA damages determines cell fate: cell cycle arrest and DNA repair or cell death. The ATM is a central protein in the response to DNA double-strand breaks by acting as a transducer protein. Collected evidences suggest that ATM is also involved in the response to oxidative DNA damage.

In this work, the levels of DNA damage (8-oxo-7,8-dihidro-2’-desoxiguanosina, 8-oxodGuo) were evaluated in digestive glands of mussels exposed to different metals for 24 hours, as well as in coastal and farmed mussels. These experiments were carried out in order to evaluate the influence of uncontrolled abiotic factors on the production of 8-oxodGuo in mussels, since such lesions are extensively used as an indication of environmental contamination. Mussels exposed to lead or cadmium showed higher levels of oxidative DNA damage compared to the control group, and no difference was observed in mussels exposed to iron, indicating that metals can increase the levels of 8-oxodGuo in these organisms. On the other hand, wild mussels showed higher levels of 8-oxodGuo than farmed mussels, probably associated with high wave incidence and tidal oscilations. This data indicates that metals can increase 8-oxodGuo levels in mussels, but it also indicates that other environmental factors are capable of provoking such increases. Thus, for more appropriate use of DNA oxidative damage as a stress index related to the environmental contamination by pollutants such as metals, the sampling conditions should be considered, since this influences the observed results.

El anciano con fractura de cadera tiene alto riesgo de complicaciones y mortalidad hospitalaria. Las estadías hospitalarias cortas y el alta temprana con problemas clínicos activos pueden llevar a reinternaciones. OBJETIVOS: conocer la tasa de reinternaciones, los motivos y las variables predictoras de las mismas en los sujetos que tuvieron fracturas de cadera. MÉTODOS: Se trabajó una cohorte retrospectiva. Se incluyó a todos los pacientes ingresados en el Registro Institucional de Ancianos con Fractura de Cadera entre julio de 2014 y julio de 2017. Se describió la tasa de reinternación y su IC95%. Se utilizó un modelo de riesgo proporcional de Cox para describir factores de riesgo y el tiempo a la reinternación. RESULTADOS: Se incluyó a 858 pacientes. La mediana de días de internación fue de 6 (rango intercuartil [RIC 5-9]). El 86% (737) de los pacientes era de sexo femenino, con una mediana de edad de 86 años (RIC 81-89). La tasa de reinternación a los 30 días fue de 10% (IC95%: 8,3-12,5) y al año, de 39% (IC95%: 34,8-42,6). La principal causa fue la infección (30%). Los factores asociados fueron: edad (>85 años) Razón de Hazard o Hazard ratio (HR)1,3 (IC95%: 1-1,7; p 0,03), sexo femenino HR 0,5 (IC95%: 0,4-0,7; p7 días) HR 1,4 (IC95%: 1,2-1,9; p

To investigate oxidative lesions and strand breaks induction by singlet molecular oxygen (¹O2), supercoiled-DNA plasmid was treated with thermo-dissociated DHPNO2 and photoactivated-methylene blue. DNA lesions were detected by Fpg that cleaves DNA at certain oxidized bases, and T4-endoV, which cleaves DNA at cyclobutane pyrimidine dimers and apurinic/apyrimidinic (AP) sites. These cleavages form open relaxed-DNA structures, which are discriminated from supercoiled-DNA. DHPNO2 or photoactivated-MB treatments result in similar plasmid damage profile: low number of single-strand breaks or AP-sites and high frequency of Fpg-sensitive sites; confirming that base oxidation is the main product for both reactions and that ¹O2 might be the most likely intermediate that reacts with DNA.

Proteins are potential targets for singlet molecular oxygen (¹O2) oxidation. Damages occur only at tryptophan, tyrosine, histidine, methionine, and cysteine residues at physiological pH, generating oxidized compounds such as hydroperoxides. Therefore, it is important to understand the mechanisms by which ¹O2, hydroperoxides and other oxidized products can trigger further damage. The improvement and development of new tools, such as clean sources of ¹O2 and isotopic labeling approaches in association with HPLC/mass spectrometry detection will allow one to elucidate mechanistic features involving ¹O2-mediated protein oxidation.

It has been demonstrated that the enzyme acetylcholinesterase (AChE) is strongly inhibited by organophosphate and carbamate pesticides, and also by metals. However, recent reports indicate that some metals can activate AChE during acute exposure. In this work, we were interested in evaluating the effect of trace metal exposure (12, 24, 72 and 120 h) on the AChE activity of Perna perna mussel’s digestive gland. Mussels exposed to Fe or Cu showed no changes in AChE activity during the whole period. Mussels exposed to Cd for 72 h or to Pb for 12 hours showed higher AChE activity than the control group. Based on these results, we hypothesize that under acute exposure, metals might interact with acetylcholine receptors, thereby affecting their binding efficiency and leading to a response involving an initial increase in AChE synthesis.