Abstract
Mitochondria are key organelles of the cell because their main function is the capture of energy-rich substrates from the cytoplasm and oxidative cleavage with the generation of carbon dioxide and water, processes that are coupled with the synthesis of ATP. Mitochondria are subject to oxidative stress through the formation of the mitochondrial permeability transition pore (mPTP). Various antioxidants are used to reduce damage caused by oxidative stress and to improve the protection of the antioxidant system. Astaxanthin (AST) is considered to be a dietary antioxidant, which is able to reduce oxidative stress and enhance the antioxidant defense system. In the present investigation, the effect of AST on the functional state of rat heart mitochondria impaired by isoproterenol (ISO) under mPTP functioning was examined. It was found that AST raised mitochondrial respiration, the Ca2+ retention capacity (CRC), and the rate of TPP+ influx in rat heart mitochondria (RHM) isolated from ISO-injected rats. However, the level of reactive oxygen species (ROS) production increased. In addition, the concentrations of cardiolipin (CL), Mn-SOD2, and the proteins regulating mPTP rose after the injection of ISO in RHM pretreated with AST. Based on the data obtained, we suggest that AST has a protective effect in rat heart mitochondria.
Highlights
Mitochondria are the center of cellular energy production and a major source of reactive oxygen species (ROS)
Because mitochondrial dysfunction induced by oxidative stress can affect the functional state in mitochondria [46], we examined the effects of mitochondrial permeability transition pore (mPTP) opening induced in rat heart mitochondria (RHM) by the administration of AST and injection of ISO on the membrane potential (∆ψm), and the Ca2+ retention capacity (CRC) in RHM isolated from each group of rats
It is known that regulatory proteins play an important role in the mPTP; we examined how the administration of AST and ISO influences the concentrations of proteins such as adenine nucleotide translocase (ANT), voltage-dependent anion channel (VDAC), subunit c, cyclic nucleotide -phosphodiesterase (CNPase), and subunit b of ATP synthase in RHM isolated from each group of rats
Summary
Mitochondria are the center of cellular energy production and a major source of reactive oxygen species (ROS). Since mitochondria are the main source of reactive oxygen species (ROS), their dysfunction results in oxidative stress, which causes the cells to enter into a diseased state [2]. Oxidative stress is considered to be one of the risk factors for the development of cardiovascular diseases [3]. It is the main cause of various human disorders such as metabolic syndrome and neurodegenerative, cardiovascular, and inflammatory diseases, as well as age-related failures. The impairment of mitochondrial function is responsible for various human diseases, including cardiovascular pathologies [6]
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