Effect of Melatonin on Rat Heart Mitochondria in Acute Heart Failure in Aged Rats

Odinokova, Irina; Baburina, Yulia; Kruglov, Alexey G.; Фадеева, И. С.; Zvyagina, Alena; Sotnikova, Linda; Акатов, В. С.; Krestinina, Olga

doi:10.3390/ijms19061555

Cited by 34 publications

(35 citation statements)

References 51 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The homogenate was centrifuged at 1000 × g for 10 minutes, and the pellet was removed. The mitochondria contained in the supernatant were sedimented at 10 000 × g for 10 minutes at 4°C 23 . The protein content in mitochondria was determined using the Bradford assay 24 .…”

Section: Methodsmentioning

confidence: 99%

Chrysin ameliorates aluminum phosphide‐induced oxidative stress and mitochondrial damages in rat cardiomyocytes and isolated mitochondria

Khezri

Sabzalipour

Jahedsani

et al. 2020

Environmental Toxicology

View full text Add to dashboard Cite

Apart from the anticancer, antioxidant, anti‐inflammatory effects, and inhibition of aromatase, chrysin is involved in the protection of cardiovascular disorders. Cardiovascular complications are the main cause of death induced by aluminum phosphide (AlP) which is related to oxidative stress and mitochondrial damages. For this purpose, we investigated the effect of chrysin as an antioxidant and mitochondrial protective agent against AlP‐induced toxicity in isolated cardiomyocytes and mitochondria obtained from rat heart ventricular. Using by biochemical and flow cytometry, cell viability, reactive oxygen species (ROS) formation, mitochondria membrane potential (MMP), lysosomal membrane integrity, malondialdehyde (MDA) content, and glutathione (GSH) and oxidized glutathione (GSSG) content were measured in isolated cardiomyocytes. Also, mitochondrial toxicity parameters such as mitochondrial NADH/succinate dehydrogenase activity, mitochondrial swelling, ROS formation, MMP collapse, and lipid peroxidation were analyzed in isolated mitochondria. Our results showed that the administration of chrysin (up to 10 μM) efficiently decreased (P < 0.05) cytotoxicity, oxidative, lysosomal, and mitochondrial damages induced by AlP, in isolated cardiomyocytes. Also, our finding in isolated mitochondria showed that chrysin (up to 10 μM) significantly (P < 0.05) decreased AlP‐induced mitochondrial toxicity. These findings demonstrated that chrysin as an antioxidant and mitochondrial protective agent exert protective effect in wild‐type cardiomyocyte treated with AlP. It was concluded that chrysin significantly reduced the toxicity of AlP in isolated cardiomyocytes and mitochondria. Due to the very low toxicity of chrysin for humans, it could be a promising agent in treatment of AlP poisoning.

show abstract

Section: Methodsmentioning

confidence: 99%

Chrysin ameliorates aluminum phosphide‐induced oxidative stress and mitochondrial damages in rat cardiomyocytes and isolated mitochondria

Khezri

Sabzalipour

Jahedsani

et al. 2020

Environmental Toxicology

View full text Add to dashboard Cite

show abstract

“…The animals of the control groups received an equal amount of olive oil as a vehicle. After two weeks, the rats of groups 3 and 4 were injected with ISO dissolved in physiological saline (85 mg/kg of body weight) twice at an interval of 24 h to induce mitochondrial disorders [27,40], and the rats of groups 1 and 2 were injected with saline. The next day after the 2nd injection of ISO or saline, RHM was isolated from the hearts of rats in each group.…”

Section: Animals and Treatmentmentioning

confidence: 99%

“…Mitochondria were isolated from the whole hearts by a standard technique [27]. Each heart was chopped, freed of blood vessels, and destroyed with a glass homogenizer in a tenfold volume of a medium containing 75 mM sucrose, 10 mM Tris-HCl (pH 7.4), 225 mM mannitol, 0.5 mM EDTA, 0.5 mM EGTA, and 0.1% BSA.…”

Section: Isolation Of Rat Heart Mitochondriamentioning

confidence: 99%

See 1 more Smart Citation

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

et al. 2020

Self Cite

View full text Add to dashboard Cite

Mitochondria are considered to be a power station of the cell. It is known that they play a major role in both normal and pathological heart function. Alterations in mitochondrial bioenergetics are one of the main causes of the origin and progression of heart failure since they have an inhibitory effect on the activity of respiratory complexes in the inner mitochondrial membrane. Astaxanthin (AST) is a xanthophyll carotenoid of mainly marine origin. It has both lipophilic and hydrophilic properties and may prevent mitochondrial dysfunction by permeating the cell membrane and co-localizing within mitochondria. The carotenoid suppresses oxidative stress-induced mitochondrial dysfunction and the development of diseases. In the present study, it was found that the preliminary oral administration of AST upregulated the activity of respiratory chain complexes and ATP synthase and the level of their main subunits, thereby improving the respiration of rat heart mitochondria (RHM) in the heart injured by isoproterenol (ISO). AST decreased the level of cyclophilin D (CyP-D) and increased the level of adenine nucleotide translocase (ANT) in this condition. It was concluded that AST could be considered as a potential mitochondrial-targeted agent in the therapy of pathological conditions associated with oxidative damage and mitochondrial dysfunction. AST, as a dietary supplement, has a potential in the prevention of cardiovascular diseases.

show abstract

“…Mitochondria were isolated from the whole hearts by the standard technique [39]. Each isolated heart was chopped, cleared of blood vessels, and destroyed with a glass homogenizer in a 10-fold volume of a medium containing 75 mM sucrose, 10 mM Tris-HCl (pH 7.4), 225 mM mannitol, 1 mM EDTA, and 0.1% BSA at 4 • C. The homogenate was centrifuged at 1000× g for 10 min, and the pellet was removed.…”

Section: Isolation Of Rat Heart Mitochondriamentioning

confidence: 99%

Astaxanthin Inhibits Mitochondrial Permeability Transition Pore Opening in Rat Heart Mitochondria

et al. 2019

Self Cite

View full text Add to dashboard Cite

The mitochondrion is the main organelle of oxidative stress in cells. Increased permeability of the inner mitochondrial membrane is a key phenomenon in cell death. Changes in membrane permeability result from the opening of the mitochondrial permeability transition pore (mPTP), a large-conductance channel that forms after the overload of mitochondria with Ca 2+ or in response to oxidative stress. The ketocarotenoid astaxanthin (AST) is a potent antioxidant that is capable of maintaining the integrity of mitochondria by preventing oxidative stress. In the present work, the effect of AST on the functioning of mPTP was studied. It was found that AST was able to inhibit the opening of mPTP, slowing down the swelling of mitochondria by both direct addition to mitochondria and administration. AST treatment changed the level of mPTP regulatory proteins in isolated rat heart mitochondria. Consequently, AST can protect mitochondria from changes in the induced permeability of the inner membrane. AST inhibited serine/threonine protein kinase B (Akt)/cAMP-responsive element-binding protein (CREB) signaling pathways in mitochondria, which led to the prevention of mPTP opening. Since AST improves the resistance of rat heart mitochondria to Ca 2+ -dependent stress, it can be assumed that after further studies, this antioxidant will be considered an effective tool for improving the functioning of the heart muscle in general under normal and medical conditions. membrane, which leads to the formation of mPTP in mitochondria, may be the cause of mitochondrial dysfunction and cell death. The composition of pore is not yet clearly established; therefore, by convention, the supposed structural components of mPTP are considered to be pore regulators. Among these are the voltage-dependent anion channel (VDAC) and the translocation protein (TSPO), which are localized in the outer mitochondrial membrane; adenine nucleotide translocase (ANT) of the inner membrane; cyclophilin D (CyP-D) and the phosphate carrier in the matrix; creatine kinase, localized in the intermembrane space; and hexokinase, localized in the cytosol [6]. We previously detected a protein in nonsynaptic, purified mitochondria from rat brains, which was identified as 2 ,3 -cyclic nucleotide-3 -phosphodiesterase (CNPase). CNPase is a myelin protein, which is also found in non-myelin-forming tissues [7][8][9]. We have shown that CNPase participates in the regulation of mPTP opening. Moreover, CNPase is colocalized with CyP-D, VDAC, ANT, and α-tubulin [8]. Subunit c, the mitochondrial (N,N-dicyclohexylcarbodiimide (DCCD)-binding proteolipid [10], also known as subunit 9 F 0 c, forms in cooperation with subunit a, the proton channel of F o F 1 -ATPase [11]. In mammals, subunit c of F o F 1 -ATP synthase has three isoforms (P1, P2, and P3), encoded by ATP5G1, ATPG2, and ATPG3 genes [12]. Recently, we showed that subunit c of F o F 1 -ATPase might be a structural and/or regulatory component of the mPTP complex, whose activity might be modulated by calcium-dependent phosphorylat...

show abstract

Effect of Melatonin on Rat Heart Mitochondria in Acute Heart Failure in Aged Rats

Cited by 34 publications

References 51 publications

Chrysin ameliorates aluminum phosphide‐induced oxidative stress and mitochondrial damages in rat cardiomyocytes and isolated mitochondria

Chrysin ameliorates aluminum phosphide‐induced oxidative stress and mitochondrial damages in rat cardiomyocytes and isolated mitochondria

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

Astaxanthin Inhibits Mitochondrial Permeability Transition Pore Opening in Rat Heart Mitochondria

Contact Info

Product

Resources

About