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Researchers at the University of Zaragoza and Consejo Superior de Investigaciones Científicas (CSIC) have made new findings from the project ROSAS, dedicated to the study of free radicals - responsible, among other things, the aging celulary by extension-related diseases, such as hypertension, fibrosis, mitochondrial disease (included within the so-called rare diseases) or Alzheimer's. Research has been published in the journal Proceedings of the National Academy of
Science, Molecular and Cellular Biology and Molecular Cell.

Among other achievements, researchers have identified a biomarker that could serve as early warning of oxidative stress caused by free radicals and hence the risk of developing diseases such as hypertension or fibrosis. Specifically, scientists at the Centro de Investigaciones Biológicas CSIC in Madrid have identified a cellular enzyme, the GAPDH (glyceraldehyde 3-phosphate dehydrogenase), which in normal conditions, interacts with certain structural elements of the messenger RNA, resulting in a low production of endothelin -1, a peptide involved in regulating vascular tone and related diseases such as hypertension or fibrosis.

"However, under conditions of oxidative stress that ability is impaired and, therefore, there is an increase in the production of endothelin-1," explains Santiago Pascual Rodriguez and Fernando Lamas, who are responsible for the investigation.

Other groups of investigators in this case from the University of Zaragoza, has corrected the model of organization of one of the fundamental processes of cells, the mitochondrial transport chain mail (CTEM). "This allows a better understanding of mitochondrial disease, a type of diseases caused by mutations in DNA, rare, incurable and for which no treatment," explains José Antonio Enriquez, director of the study.

The old model, dating from the 70s, stated that more than 80 proteins that are found in the mitochondria were associated in five large complexes sorted independently in the inner membrane of mitochondria. However, the group has shown that this view is incomplete and that the compounds are arranged in a more intricate what is believed and that even may be associated with one another depending on the needs of each cell, "apostille Enríquez.

This finding allows a better understanding of three crucial aspects of cell function: how to get energy from food, how your basic metabolic pathways and how they generate reactive oxygen species, such as free radicals, and what effect it has on mitochondrial DNA.

The CTEM has two distinct functions. On the one hand acts as a chemical that transmits cable electrons from food to oxygen, which then combines with hydrogen to form water. This allows the operation of the mechanism of the cell to produce DNA or the synthesis of certain molecules. At the same time, the passage of electrons through this "cable" releases energy that is dissipated by a hand in the form of heat and also accumulates as chemical energy in the molecule ATP, which then is used by multiple processes in the cell .

Using mouse cells grown in the laboratory and had been removed CTEM, researchers have also managed to replace it with a wire chemical much simpler, but equally capable of transmitting electrons from food to oxygen. Ie have recovered parts of the metabolism of the cell that were damaged in the absence of the CTEM. At the same time have been able to observe how much of the mitochondrial problems are mainly due to the lack of energy (ie, the malfunction of the cable) and what the failure of other metabolic processes, which has led to more precisely the molecular mechanisms of mitochondrial diseases.

"Mitochondrial diseases cause a malfunction of the processes taking place in mitochondria. Many of them affect the skeletal muscle and the central nervous system, but can affect any organ leading to demonstrations Multisistemic. In fact, mitochondrial deficiencies may lead to diabetes, neurodegenerative diseases and is postulated to participate in the development of Parkinson's and Alzheimer's, "Enriquez apostille.

The investigations are part of the project called ROSAS (Reactive Oxygen Species and Systems), a network of excellence in the ten participating research groups in Madrid, Catalonia, Valencia, Andalucia and Castilla Leon and funded by the Ministry of Consolider Ingenio 2010 Science and Innovation. Coordinated by Santiago Lamas, CSIC, ROSAS "aims to deepen the knowledge of free radicals and oxidative stress, and by extension that of the diseases associated with them to establish better strategies for diagnosis and monitoring," explains the researcher. can be described over three diseases in which the genesis or development involving free radicals in a decisive manner, such as Parkinson's, Alzheimer's, atherosclerosis and the various types of cancer.

Free radicals are a type of reactive oxygen species, small molecules that are formed as a byproduct of normal metabolism of oxygen and have an important role in cellular signaling, but that if too much accumulates, can cause oxidative stress and damage cellular structures, destroying and altering their genetic information and paving the way for cellular aging and various diseases.

Most of the free radicals produced by the cell are generated by CTEM, so the study of mitochondria and their processes is essential to understand how and diseases arising from them.