En el ganado vacuno, el estrés pre-sacrificio provoca la aparición de carnes conocidas como DFD (Dark, Firm, Dry), que se identifican por un descenso anómalo del pH muscular post-mortem y que muestran serios problemas de calidad, lo cual disminuye su valor comercial. El objetivo de este trabajo es conocer las diferencias en los procesos de estrés oxidativo, en los mecanismos de supervivencia/muerte celular (autofagia/apoptosis) y en biomarcadores proteómicos a las 24 h post-mortem, entre canales que mostraron un descenso normal de pH (pH = 5,4-5,8 a las 24 h post-mortem) utilizadas como CONTROL y canales con pH a las 24 h post-mortem (pH 24 ) > 6,0 clasificadas como DFD, con el fin de identificar los procesos del metabolismo muscular ligados a la aparición de carnes DFD.Se analizó el estrés oxidativo celular mediante el estudio de la actividad antioxidante total y los daños en macromoléculas (proteínas y lípidos). Las carnes DFD mostraron mayor actividad antioxidante (P < 0,05) a las 24 h post-mortem, así como mayor daño de proteínas (P < 0,05). También se analizaron biomarcadores de autofagia (Beclin-1 y LC3-II/LC3-I) y apoptosis (caspasa-3), así como los cambios producidos en el proteoma muscular. Los resultados demuestran la coexistencia de autofagia y apoptosis en el tejido muscular a las 24 h post-mortem, con diferencias de expresión significativas (P < 0,05) que permiten discriminar carnes DFD frente a carnes sin alteraciones de calidad (CONTROL).
BackgroundThe diversity between the muscle cellular interactome of dependent and independent elderly people is based on the interrelationships established between different cellular mechanisms, and alteration of this balance modulates cellular activity in muscle tissue with important functional implications. Methods Thirty patients (85 ± 8 years old, 23% female) scheduled to undergo hip fracture surgery participated in this study. During the surgical procedures, skeletal muscle tissue was obtained from the Vastus lateralis. Two groups of participants were studied based on their Barthel index: 15 functional-independent individuals (100-90) and 15 severely functional-dependent individuals (40-0). The expression of proteins from the most important cellular mechanisms was studied by western blot. Results Compared with independent elderly patients, dependent elderly showed an abrupt decrease in the capacity of protein synthesis; this decrease was only partially compensated for at the response to unfolded or misfolded proteins (UPR) level due to the increase in IRE1 (P < 0.001) and ATF6 (P < 0.05), which block autophagy, an essential mechanism for cell survival, by decreasing the expression of Beclin-1, LC3, and p62 (P < 0.001) and the antioxidant response. This lead to increased oxidative damage to lipids (P < 0.001) and that damage was directly associated with the mitochondrial impairment induced by the significant decreases in the I, III, IV, and V mitochondrial complexes (P < 0.01), which drastically reduced the energy capacity of the cell. The essential cellular mechanisms were generally impaired and the triggering of apoptosis was induced, as shown by the significantly elevated levels of most proapoptotic proteins (P < 0.05) and caspase-3/7 (P < 0.001) in dependents. The death of highly damaged cells is not detrimental to organs as long as the regenerative capacity remains unaltered, but in the dependent patients, this ability was also significantly altered, which was revealed by the reduction in the myogenic regulatory factors and satellite cell marker (P < 0.001), and the increase in myostatin (P < 0.01). Due to the severely disturbed cell interactome, the muscle contractile capacity showed significant damage. Conclusions Functionally dependent patients exhibited severe alterations in their cellular interactome at the muscle level. Cell apoptosis was caused by a decrease in successful protein synthesis, to which the cellular control systems did not respond adequately; autophagy was simultaneously blocked, the mitochondrion malfunctioned, and as the essential recovery mechanisms failed, these cells could not be replaced, resulting in the muscle being condemned to a loss of mass and functionality.
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