Astaxanthin Prevents Mitochondrial Impairment Induced by Isoproterenol in Isolated Rat Heart Mitochondria

Krestinina, Olga; Baburina, Yulia; Krestinin, Roman; Odinokova, Irina; Фадеева, И. С.; Sotnikova, Linda

doi:10.3390/antiox9030262

Cited by 35 publications

(26 citation statements)

References 57 publications

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“…One promising agent, an antioxidant called astaxanthin (AST), appears to have cardiovascular disease-related health benefits as shown in animal studies, as well as potential in the prevention and therapy of other pathological conditions associated with oxidative damage and mitochondrial dysfunction. AST treatment was found to improve the resistance of rat heart mitochondria to Ca 2+ -dependent stress, as well as decrease levels of CypD and increase levels of ADT in mitochondria in a model of experimental myocardial injury induced by isoproterenol [47,48].…”

Section: Discussionmentioning

confidence: 95%

mPTP Proteins Regulated by Streptozotocin-Induced Diabetes Mellitus Are Effectively Involved in the Processes of Maintaining Myocardial Metabolic Adaptation

Andelova

Waczulı́ková

Talian

et al. 2020

IJMS

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Mitochondrial permeability transition pores (mPTPs) have become an important topic in investigating the initiation and signaling pathways involved in cardioprotection. Experimental streptozotocin-induced diabetes mellitus (D) was shown to provide sufficient protection to the myocardium via compensatory mechanisms enabling mitochondria to produce energy under pathological conditions during the acute phase. The hypothesized involvement of mPTPs in these processes prompted us to use liquid chromatography and mass spectrometry-based proteomic analysis to investigate the effects of the acute-phase D condition on the structural and regulatory components of this multienzyme complex and the changes caused by compensation events. We detected ADT1, ATP5H, ATPA, and ATPB as the most abundant mPTP proteins. The between-group differences in protein abundance of the mPTP complex as a whole were significantly upregulated in the D group when compared with the control (C) group (p = 0.0106), but fold changes in individual protein expression levels were not significantly altered except for ATP5H, ATP5J, and KCRS. However, none of them passed the criterion of a 1.5-fold change in differential expression for biologically meaningful change. Visualization of the (dis-)similarity between the C and D groups and pairwise correlations revealed different patterns of protein interactions under the C and D conditions which may be linked to endogenous protective processes, of which beneficial effects on myocardial function were previously confirmed.

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Section: Discussionmentioning

confidence: 95%

mPTP Proteins Regulated by Streptozotocin-Induced Diabetes Mellitus Are Effectively Involved in the Processes of Maintaining Myocardial Metabolic Adaptation

Andelova

Waczulı́ková

Talian

et al. 2020

IJMS

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“…Earlier, we showed that AST enhances the activity of the respiratory chain complexes and increases the concentration of basic subunits of these complexes in intact RHM [ 33 ]. Here, we examined changes in the concentrations of the main subunits of the respiratory chain complexes in RHM isolated from each group of rats upon the opening/closing of the mPTP ( Figure 2 ).…”

Section: Resultsmentioning

confidence: 99%

“…Earlier, we showed that the pretreatment of rats with AST improves the functional state of the mitochondria by increasing the RCI and activity of respiratory chain complexes and ATP synthase in RHM injured by ISO [ 33 ]. Here, we used the same concentration of ISO and found that ISO injection decreased the RCI in RHM, whereas AST abolished the effect of ISO and increased the RCI in RHM.…”

Section: Discussionmentioning

confidence: 99%

“…Therefore, rat groups 1 and 3 were used as controls, and the animals in groups 2 and 4 were administrated AST (Natural, Hong Kong, China) for four weeks (hereafter referred to as AST groups 2 and 4). AST (5%, 150 mg/kg) [ 32 , 33 ] was dissolved in olive oil and administered orally using plastic feeding tubes (15 ga × 78 mm, Instech, Plymouth Meeting, Plymouth, PA, USA). Control animals received an equal amount of olive oil as a vehicle.…”

Section: Methodsmentioning

confidence: 99%

“…Moreover, oral administration of AST under oxidative stress induced by isoproterenol (ISO) increases the concentration of subunits of the respiratory chain complexes and ATP synthase both in intact RHM and after direct addition of AST to mitochondria. In addition, we observed that the pretreatment of rats with AST increased the activity of respiratory chain complexes and ATP synthase in RHM injured by ISO and suggested that AST prevents oxidative damage by increasing the efficiency of the mitochondria [ 33 ].…”

Section: Introductionmentioning

confidence: 99%

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Isoproterenol-Induced Permeability Transition Pore-Related Dysfunction of Heart Mitochondria Is Attenuated by Astaxanthin

et al. 2020

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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.

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Isoproterenol mechanisms in inducing myocardial fibrosis and its application as an experimental model for the evaluation of therapeutic potential of phytochemicals and pharmaceuticals

Bader Eddin,

Nagoor Meeran,

Kumar Jha

et al. 2024

Anim Models and Exp Med

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Cardiac injury initiates repair mechanisms and results in cardiac remodeling and fibrosis, which appears to be a leading cause of cardiovascular diseases. Cardiac fibrosis is characterized by the accumulation of extracellular matrix proteins, mainly collagen in the cardiac interstitium. Many experimental studies have demonstrated that fibrotic injury in the heart is reversible; therefore, it is vital to understand different molecular mechanisms that are involved in the initiation, progression, and resolution of cardiac fibrosis to enable the development of antifibrotic agents. Of the many experimental models, one of the recent models that has gained renewed interest is isoproterenol (ISP)–induced cardiac fibrosis. ISP is a synthetic catecholamine, sympathomimetic, and nonselective β‐adrenergic receptor agonist. The overstimulated and sustained activation of β‐adrenergic receptors has been reported to induce biochemical and physiological alterations and ultimately result in cardiac remodeling. ISP has been used for decades to induce acute myocardial infarction. However, the use of low doses and chronic administration of ISP have been shown to induce cardiac fibrosis; this practice has increased in recent years. Intraperitoneal or subcutaneous ISP has been widely used in preclinical studies to induce cardiac remodeling manifested by fibrosis and hypertrophy. The induced oxidative stress with subsequent perturbations in cellular signaling cascades through triggering the release of free radicals is considered the initiating mechanism of myocardial fibrosis. ISP is consistently used to induce fibrosis in laboratory animals and in cardiomyocytes isolated from animals. In recent years, numerous phytochemicals and synthetic molecules have been evaluated in ISP‐induced cardiac fibrosis. The present review exclusively provides a comprehensive summary of the pathological biochemical, histological, and molecular mechanisms of ISP in inducing cardiac fibrosis and hypertrophy. It also summarizes the application of this experimental model in the therapeutic evaluation of natural as well as synthetic compounds to demonstrate their potential in mitigating myocardial fibrosis and hypertrophy.

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Astaxanthin Prevents Mitochondrial Impairment Induced by Isoproterenol in Isolated Rat Heart Mitochondria

Cited by 35 publications

References 57 publications

mPTP Proteins Regulated by Streptozotocin-Induced Diabetes Mellitus Are Effectively Involved in the Processes of Maintaining Myocardial Metabolic Adaptation

mPTP Proteins Regulated by Streptozotocin-Induced Diabetes Mellitus Are Effectively Involved in the Processes of Maintaining Myocardial Metabolic Adaptation

Isoproterenol-Induced Permeability Transition Pore-Related Dysfunction of Heart Mitochondria Is Attenuated by Astaxanthin

Isoproterenol mechanisms in inducing myocardial fibrosis and its application as an experimental model for the evaluation of therapeutic potential of phytochemicals and pharmaceuticals

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