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Sentex, Emmanuelle; Laurent, Alexandra; Martine, Lucie; Grégoire, Stéphane; Rochette, Luc; Demaison, Luc

doi:10.1023/a:1007074330569

Cited by 12 publications

(2 citation statements)

References 39 publications

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“…Before considering the thermal effects of modulators of the level of cytosolic Ca 2+ , it should be noted that the entry of Ca 2+ through the plasma membrane or its release from the intracellular depot cannot be considered exclusively in terms of regarding the activation of SERCA or myosin ATPase [34,66,67]. Indeed, the entrance of Ca 2+ into the cytosol causes the immediate activation of three main heat-producing processes: ATP-dependent Ca 2+ pumping into the ER/SR, ∆Ψ m -dependent MCU-mediated Ca 2+ accumulation by mitochondria, and actin-myosin ATP-dependent contraction in muscle cells [71,[84][85][86][87][88][89][90][91] (Figures 2 and 3). In mitochondria, Ca 2+ causes a transient decrease in the mitochondrial transmembrane potential (∆Ψ m ), the activation of respiration, and the suppression of the ATP synthesis [71,85,92].…”

Section: Whole Cell Cell Surface and Cytosolmentioning

confidence: 99%

“…In mitochondria, Ca 2+ causes a transient decrease in the mitochondrial transmembrane potential (∆Ψ m ), the activation of respiration, and the suppression of the ATP synthesis [71,85,92]. A prolonged elevation in cytosolic Ca 2+ can evoke irreversible mitochondrial damage, the induction of the so-called permeability transition pore (PTP), which prevents the ATP synthesis and, as a consequence, the ATPase activity of SERCA [89][90][91]93]. In addition, PTP opening causes the mitochondrial uncoupling and activation of the hydrolysis of cytosolic ATP [90].…”

Section: Whole Cell Cell Surface and Cytosolmentioning

confidence: 99%

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Warm Cells, Hot Mitochondria: Achievements and Problems of Ultralocal Thermometry

Kruglov,

Romshin,

Nikiforova

et al. 2023

IJMS

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Temperature is a crucial regulator of the rate and direction of biochemical reactions and cell processes. The recent data indicating the presence of local thermal gradients associated with the sites of high-rate thermogenesis, on the one hand, demonstrate the possibility for the existence of “thermal signaling” in a cell and, on the other, are criticized on the basis of thermodynamic calculations and models. Here, we review the main thermometric techniques and sensors developed for the determination of temperature inside living cells and diverse intracellular compartments. A comparative analysis is conducted of the results obtained using these methods for the cytosol, nucleus, endo-/sarcoplasmic reticulum, and mitochondria, as well as their biological consistency. Special attention is given to the limitations, possible sources of errors and ambiguities of the sensor’s responses. The issue of biological temperature limits in cells and organelles is considered. It is concluded that the elaboration of experimental protocols for ultralocal temperature measurements that take into account both the characteristics of biological systems, as well as the properties and limitations of each type of sensor is of critical importance for the generation of reliable results and further progress in this field.

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Section: Whole Cell Cell Surface and Cytosolmentioning

confidence: 99%

Section: Whole Cell Cell Surface and Cytosolmentioning

confidence: 99%

Warm Cells, Hot Mitochondria: Achievements and Problems of Ultralocal Thermometry

Kruglov,

Romshin,

Nikiforova

et al. 2023

IJMS

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Dietary n-3 polyunsaturated fatty acids and coronary heart disease-related mortality: a possible mechanism of action

Demaison¹,

Moreau²

2002

Cellular and Molecular Life Sciences (CMLS)

105

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Epidemiological and interventional studies indicate that dietary n-3 PUFA reduces mortality due to coronary heart disease (CHD). They act at a low dose, since one or two meals with fatty fish per week is sufficient to provide protection when compared with no fish intake. These fatty acids are effective in providing primary prevention in low- and high-risk subjects and secondary prevention. At high doses, dietary n-3 PUFAs have several beneficial properties. First, they act favourably on blood characteristics: they are hypocholesterolemic and hypotriglyceridemic; they reduce platelet aggregation; they exhibit antithrombotic and fibrinolytic activities; they reduce blood viscosity and they exhibit antiinflammatory action. Second, they reduce ischemia/reperfusion-induced cellular damage. This effect is apparently due to the incorporation of eicosapentaenoic acid in membrane phospholipids. Third, they reduce ischemia and reperfusion arrhythmias. All the effects exerted by n-3 PUFAs at high doses are incompatible with the beneficial action on CHD mortality in humans observed at low doses, where their main properties are related to circulation in the form of free fatty acids. Numerous experimental studies have indicated that low concentrations of exogenous n-3 PUFAs reduce the severity of cardiac arrhythmias. This effect is probably responsible for the protective action of n-3 PUFA on CHD mortality. Further studies are necessary to confirm this assumption in animals. Such studies should take account of the fact that only a low dose of n-3 PUFA (20 mg/kg/day) is necessary to afford protection. Furthermore, since the beneficial effect of n-3 PUFAs on CHD mortality is observed in fish eaters versus no-fish eaters, and since populations in industrialised countries consume excess n-6 PUFAs, control animals in long-term dietary experiments should be fed a diet with only n-6 fatty acids as a source of PUFAs.

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High dietary sucrose triggers hyperinsulinemia, increases myocardial β-oxidation, reduces glycolytic flux and delays post-ischemic contractile recovery

et al. 2006

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Although the causal relationship between insulin resistance (IR) and hypertension is not fully resolved, the importance of IR in cardiovascular dysfunction is recognized. As IR may follow excess sucrose or fructose diet, the aim of this study was to test whether dietary starch substitution with sucrose results in myocardial dysfunction in energy substrate utilization and contractility during normoxic and post-ischemic conditions. Forty-eight male Wistar rats were randomly allocated to three diets, differing only in their starch to sucrose (S) ratio (13, 2 and 0 for the Low S, Middle S and High S groups, respectively), for 3 weeks. Developed pressure and rate x pressure product (RPP) were determined in Langendorff mode-perfused hearts. After 30 min stabilization, hearts were subjected to 25 min of total normothermic global ischemia, followed by 45-min reperfusion. Oxygen consumption, beta-oxidation rate (using 1-13C hexanoate and Isotopic Ratio Mass Spectrometry of CO2 produced in the coronary effluent) and flux of non-oxidative glycolysis were also evaluated. Although fasting plasma glucose levels were not affected by increased dietary sucrose, high sucrose intake resulted in increased plasma insulin levels, without significant rise in plasma triglyceride and free fatty acid concentrations. Sucrose-rich diet reduced pre-ischemic baseline measures of heart rate, RPP and non-oxidative glycolysis. During reperfusion, post-ischemic recovery of RPP was impaired in the Middle S and High S groups, as compared to Low S, mainly due to delayed recovery of developed pressure, which by 45 min of reperfusion eventually resumed levels matching Low S. At the start of reperfusion, delayed post-ischemic recovery of contractile function was accompanied by: (i) reduced lactate production; (ii) decreased lactate to pyruvate ratio; (iii) increased beta-oxidation; and (iv) depressed metabolic efficiency. In conclusion, sucrose rich-diet increased plasma insulin levels, in intact rat, and increased cardiac beta-oxidation and coronary flow-rate, but reduced glycolytic flux and contractility during normoxic baseline function of isolated perfused hearts. Sucrose rich-diet impaired early post-ischemic recovery of isolated heart cardiac mechanical function and further augmented cardiac beta-oxidation but reduced glycolytic and lactate flux.

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Untitled

Cited by 12 publications

References 39 publications

Warm Cells, Hot Mitochondria: Achievements and Problems of Ultralocal Thermometry

Warm Cells, Hot Mitochondria: Achievements and Problems of Ultralocal Thermometry

Dietary n-3 polyunsaturated fatty acids and coronary heart disease-related mortality: a possible mechanism of action

High dietary sucrose triggers hyperinsulinemia, increases myocardial β-oxidation, reduces glycolytic flux and delays post-ischemic contractile recovery

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