MITOCHONDRIAL APOPTOSIS MECHANISMS IN EXPERIMENTAL ACUTE LUNG INJURY
DOI:
https://doi.org/10.11603/2415-8798.2017.1.7343Keywords:
acute lung injury, mitochondria, apoptosis.Abstract
Considering the implementation of apoptosis cells mechanisms, an important place is given to the mitochondria, which form a complex system, being both targets and producers of reactive oxygen species. In recent years studies have shown clear evidence of the central role of mitochondria in the integration of most intracellular signaling pathways leading to cell death.
The aim of the study – to establish the role of mitochondria in apoptosis initiation as one of the mechanisms of acute lung injury.
Materials and Methods. The study was conducted on 106 white nonlinear mature male rats. It was investigated the ways of apoptosis initiating by the number of neutrophils, the level of ROS, percentage of neutrophils with decreased transmembrane potential of mitochondria, apoptosis using the reagents "ANNEXIN V FITC" ("Beckman Coulter",USA).
Results and Discussion. The study showed a significant effect of mitochondria-mediated pathway of apoptosis in the pathogenesis of acute lung injury, which was reproduced by intratracheal administration of the hydrochloride acid. In the first day of the experiment more informative and important changes in the bronchoalveolar lavage than in blood.
Conclusions. The signal way of apoptosis implementation in acute lung injury in rats is mitochondrial (positive correlation between the reduction of mitochondrial transmembrane potential (r=0.61; p <0.01) and the accumulation of reactive oxygen species (r=0.64; p<0.01) and increasing annexin-positive neutrophils through 2 hours), leading to irreversible changes in the cell.
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