Oxidative stress in bacteria and protein damage by reactive oxygen species

The advent of O2 in the atmosphere was among the first major pollution events occurred on earth The reaction between ferrous iron, very abundant in the reductive early atmosphere, and oxygen results in the formation of harmful superoxide and hydroxyl radicals, which affect all macromolecules (DNA, lipids and proteins). Living organisms have to build up mechanisms to protect themselves against oxidative stress, with enzymes such as catalase and superoxide dismutase, small proteins like thioredoxin and glutaredoxin, and molecules such as glutathione. Bacterial genetic responses to oxidative stress are controlled by two major transcriptional regulators (OxyR and SoxRS). This paper reviews major key points in the generation of reactive oxygen species in bacteria, defense mechanisms and genetic responses to oxidative stress. Special attention is paid to the oxidative damage to proteins

Gerencia de riesgos de Terminales Marítimas. Retención - Cobertura aseguradora -Transferencia Alternativa

Màster de Direcció d'Entitats Asseguradores i Financeres, Universitat de Barcelona, Facultat d'Economia i Empresa, Curs: 2003-2004, Tutor: Eduardo Llinàs VilaLos rápidos y continuos cambios en el transporte marítimo, durante los últimos treinta años, han dado un papel determinante a las Terminales Portuarias, en cuanto empresas independientes con sus propias necesidades y con sus propios recursos. El rápido desarrollo de esta actividad, imprescindible para el desarrollo de la economía mundial, hace necesaria una revisión de los riesgos a que esta actividad está expuesta, a fin de readaptar las medidas de prevención, control y financiación de riesgos a las nuevas necesidades. A lo largo de este trabajo, analizaremos en primer lugar el proceso de la Gerencia de Riesgos, entendida en un sentido amplio, para a continuación centrarnos en el análisis de los riesgos de una Terminal Marítima. A partir de una Matriz de Análisis de riesgos, procederemos a analizar uno por uno los riesgos que amenazan el desarrollo de la actividad, y en función del resultado de este análisis apuntaremos las técnicas de financiación más apropiadas

Iron in Friedreich Ataxia: A Central Role in the Pathophysiology or an Epiphenomenon?

Friedreich ataxia is a neurodegenerative disease with an autosomal recessive inheritance. In most patients, the disease is caused by the presence of trinucleotide GAA expansions in the first intron of the frataxin gene. These expansions cause the decreased expression of this mitochondrial protein. Many evidences indicate that frataxin deficiency causes the deregulation of cellular iron homeostasis. In this review, we will discuss several hypotheses proposed for frataxin function, their caveats, and how they could provide an explanation for the deregulation of iron homeostasis found in frataxin-deficient cells. We will also focus on the potential mechanisms causing cellular dysfunction in Friedreich Ataxia and on the potential use of the iron chelator deferiprone as a therapeutic agent for this disease.This work has been supported by grant SAF2017-83883-R from Ministerio de Economia Industria y Competitividad (Spain)