Oxidative stress time course in the rat diaphragm after freezing–thawing cycles

Sellarés, Jacobo; Mas, Sandra; Sánchez, Francesca; Marín, J. Toral; Gea, Joaquim; Barreiro, Esther

doi:10.1016/j.resp.2006.05.008

Cited by 7 publications

(5 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…SDHA is a critical component within both the TCA cycle and ETC, and consequently, its loss will impact negatively upon both mitochondrial processes. Whilst the precise functional role of UCP3 remains uncertain, its expression in cultured myotubes and rodent skeletal muscle has been linked to modulation of fatty acid oxidation [56–58], mitochondrial integrity, and to management of ROS/oxidative stress [59–62]. Likewise, in addition to catalysing the exchange of cytoplasmic ADP for mitochondrial ATP, ANT-1 can mediate fatty acid-induced uncoupling via its ability to transfer fatty acid anions across the inner mitochondrial membrane [63].…”

Section: Discussionmentioning

confidence: 99%

Proinflammatory NFkB signalling promotes mitochondrial dysfunction in skeletal muscle in response to cellular fuel overloading

Nisr

Shah

Ganley

et al. 2019

Cell. Mol. Life Sci.

View full text Add to dashboard Cite

Sustained nutrient (fuel) excess, as occurs during obesity and diabetes, has been linked to increased inflammation, impaired mitochondrial homeostasis, lipotoxicity, and insulin resistance in skeletal muscle. Precisely how mitochondrial dysfunction is initiated and whether it contributes to insulin resistance in this tissue remains a poorly resolved issue. Herein, we examine the contribution that an increase in proinflammatory NFkB signalling makes towards regulation of mitochondrial bioenergetics, morphology, and dynamics and its impact upon insulin action in skeletal muscle cells subject to chronic fuel (glucose and palmitate) overloading. We show sustained nutrient excess of L6 myotubes promotes activation of the IKKβ-NFkB pathway (as judged by a six-fold increase in IL-6 mRNA expression; an NFkB target gene) and that this was associated with a marked reduction in mitochondrial respiratory capacity (>50%), a threefold increase in mitochondrial fragmentation and 2.5-fold increase in mitophagy. Under these circumstances, we also noted a reduction in the mRNA and protein abundance of PGC1α and that of key mitochondrial components (SDHA, ANT-1, UCP3, and MFN2) as well as an increase in cellular ROS and impaired insulin action in myotubes. Strikingly, pharmacological or genetic repression of NFkB activity ameliorated disturbances in mitochondrial respiratory function/morphology, attenuated loss of SDHA, ANT-1, UCP3, and MFN2 and mitigated the increase in ROS and the associated reduction in myotube insulin sensitivity. Our findings indicate that sustained oversupply of metabolic fuel to skeletal muscle cells induces heightened NFkB signalling and that this serves as a critical driver for disturbances in mitochondrial function and morphology, redox status, and insulin signalling.

show abstract

Section: Discussionmentioning

confidence: 99%

Proinflammatory NFkB signalling promotes mitochondrial dysfunction in skeletal muscle in response to cellular fuel overloading

Nisr

Shah

Ganley

et al. 2019

Cell. Mol. Life Sci.

View full text Add to dashboard Cite

show abstract

“…We also did not detect an effect of taurine to reduce modified proteins in the diaphragm. It is possible that the techniques we employed were too insensitive, and that there may have been selective modification of a small number of critical proteins by sepsis that may have affected cellular function but may have escaped detection by our methodology (Sellares et al, 2007). The failure of taurine to quantitatively reduce levels of these particular protein modifications, however, is not without precedent, and other studies have reported that taurine may not alter levels of free radical mediated protein modifications (Zheng and Bizzozero, 2010).…”

Section: Discussionmentioning

confidence: 94%

Taurine administration ablates sepsis induced diaphragm weakness

Supinski

Wang

Schroder

et al. 2020

Respiratory Physiology & Neurobiology

View full text Add to dashboard Cite

Infection induced diaphragm weakness is a major contributor to death and prolonged mechanical ventilation in critically ill patients. Infection induced muscle dysfunction is associated with activation of muscle proteolytic enzymes, and taurine is known to suppress proteolysis. We therefore postulated that taurine administration may prevent infection induced diaphragm dysfunction. The purpose of this study was to test this hypothesis using a clinically relevant animal model of infection, i.e. cecal ligation puncture induced sepsis (CLP). Studies were performed on (n=5-7 mice/group): (a) sham operated controls, (b) animals with sepsis induced by CLP, (c) sham operated animals given taurine (75 mg/kg/d, intraperitoneally), and (d) CLP animals given taurine. At intervals after surgery animals were euthanized, diaphragm force generation measured in vitro, and diaphragm calpain, caspase and proteasomal activity determined. CLP elicited a large reduction in diaphragm specific force generation at 24 hours (1-150 Hz, p<0.001) and taurine significantly attenuated CLP induced diaphragm weakness at all stimulation frequencies (p<0.001). CLP induced significant increases in diaphragm calpain, caspase and proteasomal activity; taurine administration prevented increases in the activity of all three pathways. In additional time course experiments, diaphragm force generation remained at control levels over 72 hours in CLP animals treated with daily taurine administration, while CLP animals demonstrated severe, sustained reductions in diaphragm strength (p<0.01 for all time points). Our results indicate that taurine administration prevents infection induced diaphragm weakness and reduces activation of three major proteolytic pathways. Because this agent is has been shown to be safe, non-toxic when administered to humans, taurine may have a role in treating infection induced diaphragm weakness. Future clinical studies will be needed to assess this possibility.

show abstract

“…Combine Equation (18) with Equation ( 14), as shown in Equation (19). It is also assumed that, under different normal stress conditions, the peak shear stress of the rock is…”

Section: Determination Of Parameters Of Rock Damage Constitutive Modelmentioning

confidence: 99%

“…The failure process in rock under the action of the FTC is a change process of microstructural damage [4,16,17]: (1) the expansion force generated when the water contained in the rock voids is converted into ice, (2) thermal stress caused by the temperature difference between the surface and the interior of the rock, (3) the water pressure inside the rock caused by the freezing of the surface. In addition, there is also an expansive force phenomenon when ice crystals are formed [18,19].…”

Section: Introductionmentioning

confidence: 99%

Constitutive Characteristics of Rock Damage under Freeze–Thaw Cycles

Li,

Wang,

Cao

et al. 2024

Applied Sciences

View full text Add to dashboard Cite

Freeze–thaw effect is one of the most important environmental conditions that rocks may be subjected to. Through laboratory model tests, the damage characteristics of rocks under the FTC were studied. Based on assuming that the strength of rocks subject to the FTC follows the Weibull distribution, the cumulative damage variable of the number of FTCs was introduced. A cumulative damage constitutive model of shear strength attenuation of rock that meets the Mohr–Coulomb criterion is established. The rationality and applicability of the proposed damage constitutive model are verified by comparing the results of rock shear strength parameters under cyclic freeze–thaw loads.

show abstract

Oxidative stress time course in the rat diaphragm after freezing–thawing cycles

Cited by 7 publications

References 35 publications

Proinflammatory NFkB signalling promotes mitochondrial dysfunction in skeletal muscle in response to cellular fuel overloading

Proinflammatory NFkB signalling promotes mitochondrial dysfunction in skeletal muscle in response to cellular fuel overloading

Taurine administration ablates sepsis induced diaphragm weakness

Constitutive Characteristics of Rock Damage under Freeze–Thaw Cycles

Contact Info

Product

Resources

About