Abstract
Mitochondria are considered to be important organelles in the cell and play a key role in the physiological function of the heart, as well as in the pathogenesis and development of various heart diseases. Under certain pathological conditions, such as cardiovascular diseases, stroke, traumatic brain injury, neurodegenerative diseases, muscular dystrophy, etc., mitochondrial permeability transition pore (mPTP) is formed and opened, which can lead to dysfunction of mitochondria and subsequently to cell death. This review summarizes the results of studies carried out by our group of the effect of astaxanthin (AST) on the functional state of rat heart mitochondria upon direct addition of AST to isolated mitochondria and upon chronic administration of AST under conditions of mPTP opening. It was shown that AST exerted a protective effect under all conditions. In addition, AST treatment was found to prevent isoproterenol-induced oxidative damage to mitochondria and increase mitochondrial efficiency. AST, a ketocarotenoid, may be a potential mitochondrial target in therapy for pathological conditions associated with oxidative damage and mitochondrial dysfunction, and may be a potential mitochondrial target in therapy for pathological conditions.
Highlights
Mitochondria are the main organelle in cells and play a key role in the normal functioning of the heart, as well as in the pathogenesis and development of various heart diseases [1]
AST is able to improve the functional state of RHM by increasing respiratory control index (RCI) and P/O ratio both with the administration of AST to rats and with direct addition of AST to isolated mitochondria
The AST administration increased the level of subunits of the respiratory chain complexes and ATP synthase in intact RHM samples, suggesting that AST prevents oxidative damage and increases mitochondrial efficiency
Summary
Mitochondria are the main organelle in cells and play a key role in the normal functioning of the heart, as well as in the pathogenesis and development of various heart diseases [1]. Since mitochondria are the main source of ROS [2], mitochondrial dysfunction leads to oxidative stress, which can result in various disorders in the cellular activity and to their death [3]. In addition to adding exogenous antioxidants, strategies that enhance endogenous defense pathways are candidates for the prevention or treatment of heart failure One of these enzymes is glutathione peroxidase, which is present in both the cytosol and mitochondria, which absorbs H2O2 and prevents the formation of hydroxyl radicals: overexpression of this enzyme in mice prevents the development of heart failure after myocardial infarction [12]. There are dietary antioxidants, such as vitamins E and C, that can reduce oxidative stress [15,16], increase the protection of the mitochondrial antioxidant system [17] and, as a result, prevent the development of cardiovascular disease. We present our findings, which shed light on the function of AST in heart failure and we hypothesized that mitochondria may be the target of the protective effect of AST
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