Simple kinetic model of mitochondrial swelling in cardiac cells

Chapa‐Dubocq, Xavier R.; Makarov, Vladimir I.; Javadov, Sabzali

doi:10.1002/jcp.26335

Cited by 41 publications

(28 citation statements)

References 45 publications

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“…Mitochondrial swelling can be accompanied by the release of compounds such as cytochrome c from the mitochondria [38,39]. Furthermore, this event is the main factor leading to mitochondriamediated cell death (apoptosis/necrosis) [40].…”

Section: Discussionmentioning

confidence: 99%

Toxicity of Atenolol and Propranolol on Rat Heart Mitochondria

2020

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Propranolol and atenolol are known as β receptor blocker drugs. These drugs are used to treat some heart diseases. There are controversies in the relationship between the use of beta-blocker drugs and the level of reactive oxygen species (ROS). Mitochondria as one of the most important sources of ROS are considered as one of the targets of drug-induced cardiotoxicity. The aim of this study was to evaluate the effects of propranolol and atenolol on mitochondria isolated from the heart. To achieve this aim, several markers of mitochondrial and cellular toxicity were evaluated. The key results of this study are the increased ROS level, collapse in mitochondrial membrane potential (MMP), mitochondrial swelling and cytochrome c release as well as disruption of respiratory chain complex II in mitochondria in isolated heart mitochondria after exposure to propranolol and atenolol. The results indicate an increase in caspase-3 activity and a decrease in the ATP level in cardiomyocytes after exposure to propranolol and atenolol. The underlying mechanisms of propranolol and atenolol induced cardiotoxicity may be associated with alterations in mitochondrial function, oxidative stress, and changes in the mitochondrial membrane.

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Section: Discussionmentioning

confidence: 99%

Toxicity of Atenolol and Propranolol on Rat Heart Mitochondria

2020

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“…An aliquot was used to determine protein concentration (2 µg/µL) by the Bradford method. The amount of mitochondrial protein is usually accepted as a mitochondrial quantity [27], and an equal amount (50 µg) of mitochondrial protein was used for each measurement in all experiments.…”

Section: Isolation Of Brain Mitochondriamentioning

confidence: 99%

“…The swelling of brain isolated mitochondria was evaluated according to Chapa-Dubocq et al [27], by measuring the changes in the absorbance of the mitochondrial suspensions at 540 nm using a GloMax ® Discover multimode plate reader (Promega, Italy). A volume corresponding to 50 µg of mitochondrial proteins was incubated with 50 µL of buffer (125 mM KCl, 1 mM MgCl 2 , 5 mM malate, 5 mM glutamate, 1 µM EGTA, and 20 mM Tris base) at pH 7.4.…”

Section: Mitochondrial Swellingmentioning

confidence: 99%

Regular Intake of Pistachio Mitigates the Deleterious Effects of a High Fat-Diet in the Brain of Obese Mice

et al. 2020

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Obesity has been associated with neurodegeneration and cognitive dysfunctions. Recent data showed that pistachio consumption is able to prevent and ameliorate dyslipidemia, hepatic steatosis, systemic and adipose tissue inflammation in mice fed a high-fat diet (HFD). The present study investigated the neuroprotective effects of pistachio intake in HFD mice. Three groups of mice were fed a standard diet (STD), HFD, or HFD supplemented with pistachio (HFD-P) for 16 weeks. Metabolic parameters (oxidative stress, apoptosis, and mitochondrial dysfunction) were analyzed by using specific assays and biomarkers. The pistachio diet significantly reduced the serum levels of triglycerides and cholesterol in the HFD model. No difference was observed in the index of insulin resistance between HFD and HFD-P. A higher number of fragmented nuclei were found in HFD cerebral cortex compared to STD and HFD-P. A decrease in reactive oxygen species, singlet oxygen and phosphorylated extracellular signal-regulated kinase, and an increase of superoxide dismutase 2 and heme oxygenase expression were found in the brains of the HFD-P samples compared to HFD. Furthermore, the impaired mitochondrial function found in HFD brain was partially recovered in HFD-P mice. These results suggest that the regular intake of pistachio may be useful in preventing obesity-related neurodegeneration, being able to reduce both metabolic and cellular dysfunctions.The positive effects of the Mediterranean diet on health have been well documented [9,10]. The longevity of one Mediterranean population, over 90 years old without dementia, was attributed to the nutraceutical components of the Mediterranean diet [11]. Functional food has been reported to delay or inhibit neurodegeneration, suggesting their employment as an alternative therapeutic strategy for correlated diseases [12][13][14].Benefits of nut consumption (mainly pistachios, walnuts, and almonds) have been described in studies on both animals and humans [15,16]. Daily nut consumption can improve dysmetabolic conditions such as obesity, type 2 diabetes, and related cardiovascular diseases [17,18]. In particular, Pistacia atlantica oleoresin has been proposed as an agent that protects the body against conditions associated with oxidative stress [19], including memory impairment, in lipopolysaccharide-treated rats [20]. Nevertheless, the potential beneficial impact of nut intake on neurodegenerative disorders, as well as on other cognitive-behavioral deficits, has been poorly explored.Compared to other nuts, pistachios possess a healthier nutritional profile, with low-fat content, high content of polyunsaturated fatty acids (13.3 g/100 g) and mono-unsaturated fatty acids (24.5 g/100 g), minerals (potassium, phosphorus, magnesium, and calcium) and vitamins (vitamin A, vitamin E, vitamin C, and vitamins B). Phytochemicals of pistachio show high bioavailability, contributing to the beneficial relationship between pistachio consumption and health-related outcomes [21]. Furthermore, recent data have demonstra...

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“…In a mathematical model, Oster et al (2011) postulated two independent mechanisms of regulation for the two modes: an activation by matrix pH and by mitochondrial Ca 2+ for the low and the high conductance states, respectively. Alternatively, to describe mitochondrial Ca 2+ swelling in cardiac cells, it was hypothesized that the pore switches from the low to the high conductance mode if the extramitochondrial Ca 2+ level increases (Chapa-Dubocq et al 2018), which remains to be established experimentally.…”

Section: Mitochondrial Permeability Transition Porementioning

confidence: 99%

Cytoplasmic and Mitochondrial Calcium Signaling: A Two-Way Relationship

Wacquier

Combettes

Dupont

2019

Cold Spring Harb Perspect Biol

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Intracellular Ca 2+ signals are well organized in all cell types, and trigger a variety of vital physiological processes. The temporal and spatial characteristics of cytosolic Ca 2+ increases are mainly governed by the fluxes of this ion across the membrane of the endoplasmic/sarcoplasmic reticulum and the plasma membrane. However, various Ca 2+ transporters also allow for Ca 2+ exchanges between the cytoplasm and mitochondria. Increases in mitochondrial Ca 2+ stimulate the production of ATP, which allows the cells to cope with the increased energy demand created by the stimulus. Less widely appreciated is the fact that Ca 2+ handling by mitochondria also shapes cytosolic Ca 2+ signals. Indeed, the frequency, amplitude, and duration of cytosolic Ca 2+ increases can be altered by modifying the rates of Ca 2+ transport into, or from, mitochondria. In this review, we focus on the interplay between mitochondria and Ca 2+ signaling, highlighting not only the consequences of cytosolic Ca 2+ changes on mitochondrial Ca 2+ , but also how cytosolic Ca 2+ dynamics is controlled by modifications of the Ca 2+ -handling properties and the metabolism of mitochondria.

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Simple kinetic model of mitochondrial swelling in cardiac cells

Cited by 41 publications

References 45 publications

Toxicity of Atenolol and Propranolol on Rat Heart Mitochondria

Toxicity of Atenolol and Propranolol on Rat Heart Mitochondria

Regular Intake of Pistachio Mitigates the Deleterious Effects of a High Fat-Diet in the Brain of Obese Mice

Cytoplasmic and Mitochondrial Calcium Signaling: A Two-Way Relationship

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