共查询到20条相似文献,搜索用时 109 毫秒
1.
Summary Isolated human term placenta mitochondria catalyse oxidation of external NADH in the presence of cytochrome c. This reaction is insensitive to the respiratory chain inhibitors such as rotenone and antimycin A, and is not coupled to phosphorylation. Comparison of the effect of Mg ++ ion on NADH plus cytochrome c oxidation by human term placental, human skeletal muscle and rat skeletal mitochondria showed that Mg ++ ion exerts an inhibitory effect in the case of human mitochondria and a stimulatory effect in the case of rat skeletal muscle mitochondria.This work has been supported by a grant from Ministry of Higher Education Science and Technology within the project No. 01.02. 相似文献
2.
Isolated human term placenta mitochondria catalyse oxidation of external NADH in the presence of cytochrome c. This reaction is insensitive to the respiratory chain inhibitors such as rotenone and antimycin A, and is not coupled to phosphorylation. Comparison of the effect of Mg++ ion on NADH plus cytochrome c oxidation by human term placental, human skeletal muscle and rat skeletal mitochondria showed that Mg++ ion exerts an inhibitory effect in the case of human mitochondria and a stimulatory effect in the case of rat skeletal muscle mitochondria. 相似文献
3.
Isolated rat skeletal muscle mitochondria took up about 40-ng-atoms O per mg protein, with glutamine as the only respiratory substrate. The mitochondria incubated in the presence of glutamine and KCN formed both ammonia and glutamate in equivalent amounts. The experiments reported here provide suggestive evidence that rat skeletal muscle mitochondria contain glutaminase (L-glutamine amidohydrolase EC 3.5.1.2.) activity. 相似文献
4.
Summary Isolated rat skeletal muscle mitochondria took up about 40-ng-atoms O per min per mg protein, with glutamine as the only respiratory substrate. The mitochondria incubated in the presence of glutamine and KCN formed both ammonia and glutamate in equivalent amounts. The experiments reported here provide suggestive evidence that rat skeletal muscle mitochondria contain glutaminase (L-glutamine amidohydrolase EC 3.5.1.2.) activity.This work was supported by the Polish Academy of Sciences within the project II. 1, 2, 6. 相似文献
6.
The remodeling of the mitochondrial network is a critical process in maintaining cellular homeostasis and is intimately related to mitochondrial function. The interplay between the formation of new mitochondria (biogenesis) and the removal of damaged mitochondria (mitophagy) provide a means for the repopulation of the mitochondrial network. Additionally, mitochondrial fission and fusion serve as a bridge between biogenesis and mitophagy. In recent years, the importance of these processes has been characterised in multiple tissue- and cell-types, and under various conditions. In skeletal muscle, the robust remodeling of the mitochondrial network is observed, particularly after injury where large portions of the tissue/cell structures are damaged. The significance of mitochondrial remodeling in regulating skeletal muscle regeneration has been widely studied, with alterations in mitochondrial remodeling processes leading to incomplete regeneration and impaired skeletal muscle function. Needless to say, important questions related to mitochondrial remodeling and skeletal muscle regeneration still remain unanswered and require further investigation. Therefore, this review will discuss the known molecular mechanisms of mitochondrial network remodeling, as well as integrate these mechanisms and discuss their relevance in myogenesis and regenerating skeletal muscle. 相似文献
7.
This study was designed to examine energetic behaviour of skeletal muscle subsarcolemmal and intermyofibrillar mitochondrial
populations. The data show that subsarcolemmal mitochondria exhibited a lower degree of coupling and efficiency than intermyofibrillar
ones, and can therefore be considered less efficient at producing ATP. In addition, subsarcolemmal mitochondria showed an
increased sensitivity to palmitate-induced uncoupling, in line with high adenine nucleotide translocator content and decreased
oxidative damage. We then determined the effect of 24 h fasting on energetic characteristics of skeletal muscle mitochondrial
populations. We found that fasting enhanced proton leak and decreased the degree of coupling and efficiency, both in the absence
and in the presence of palmitate only in subsarcolemmal mitochondria. Moreover, this mitochondrial population showed lower
oxidative damage, probably due to a counter-regulatory mechanism mediated by uncoupling protein 3. Subsarcolemmal and intermyofibrillar
mitochondria appear to exhibit different energetic characteristics and can be differently affected by physiological stimuli.
Received 28 September 2005; received after revision 9 November 2005; accepted 28 November 2005 相似文献
8.
Loss of cristae and matrix occur in the mitochondria of skeletal muscles prior to any observable changes in myofibrillar proteins during the development of rigor mortis. Care must be observed because ultrastructural changes in mitochondria in some studies may be attributed to a specific trauma, whereas the changes may be due to the lower pH in postmortem muscle. 相似文献
9.
Summary Loss of cristae and matrix occur in the mitochondria of skeletal muscles prior to any observable changes in myofibrillar proteins during the development of rigor mortis. Care must be observed because ultrastructural changes in mitochondria in some studies may be attributed to a specific trauma, whereas the changes may be due to the lower pH in postmortem muscle.Scientific Journal Series, Paper No. 9633, Minnesota Agricultural Experiment Station. 相似文献
10.
We investigated mitochondrial toxicity of four lipophilic stains (cerivastatin, fluvastatin, atorvastatin, simvastatin) and one hydrophilic statin (pravastatin). In L6 cells (rat skeletal muscle cell line), the four lipophilic statins (100 micromol/l) induced death in 27-49% of the cells. Pravastatin was not toxic up to 1 mmol/l. Cerivastatin, fluvastatin and atorvastatin (100 micromol/l) decreased the mitochondrial membrane potential by 49-65%, whereas simvastatin and pravastatin were less toxic. In isolated rat skeletal muscle mitochondria, all statins, except pravastatin, decreased glutamate-driven state 3 respiration and respiratory control ratio. Beta-oxidation was decreased by 88-96% in the presence of 100 micromol/l of the lipophilic statins, but only at higher concentrations by pravastatin. Mitochondrial swelling, cytochrome c release and DNA fragmentation was induced in L6 cells by the four lipophilic statins, but not by pravastatin. Lipophilic statins impair the function of skeletal muscle mitochondria, whereas the hydrophilic pravastatin is significantly less toxic. 相似文献
11.
Summary The gastrocnemius muscle of the rat showed no morphological, histometric or plasma membrane changes, after sciatic nerve stimulation with a 5 mA current for 30 to 60 min, 10 mA for 30 min and 15 mA for 5 min. However, 10 mA for 60 and 200 min gave rise to mitochondrial and plasma membrane abnormalities. These changes were absent after a rest period. The results indicated the sciatic nerve stimulation at 10 mA for 60 and 200 min caused reversible changes in the rat skeletal muscle mitochondria and plasma membrane. 相似文献
12.
The gastrocnemius muscle of the rat showed no morphological, histometric or plasma membrane changes, after sciatic nerve stimulation with a 5mA current for 30 to 60 min, 10 mA for 30 min and 15 mA for 5 min. However, 10 mA for 60 and 200 min gave rise to mitochondrial and plasma membrane abnormalities. These changes were absent after a rest period. The results indicated that the sciatic nerve stimulation at 10 mA for 60 and 200 min caused reversible changes in the rat skeletal muscle mitochondria and plasma membrane. 相似文献
16.
In mature human skeletal muscle, insulin-stimulated glucose transport is mediated primarily via the GLUT4 glucose transporter. However, in contrast to mature skeletal muscle, cultured muscle expresses significant levels of the GLUT1 glucose transporter. To assess the relative contribution of these two glucose transporters, we used a novel photolabelling techniques to assess the cell surface abundance of GLUT1 and GLUT4 specifically in primary cultures of human skeletal muscle. We demonstrate that insulin-stimulated glucose transport in cultured human skeletal muscle is mediated by GLUT4, as no effect on GLUT1 appearance at the plasma membrane was noted. Furthermore, GLUT4 mRNA and protein increased twofold (p < 0.05), after differentiation, whereas GLUT1 mRNA and protein decreased 55% (p < 0.005). Incubation of differentiated human skeletal muscle cells with a non-peptide insulin mimetic significantly (p < 0.05) increased glucose uptake and glycogen synthesis. Thus, cultured myotubes are a useful tool to facilitate biological and molecular validation of novel pharmacological agents aimed to improve glucose metabolism in skeletal muscle. 相似文献
17.
Hemoproteins are widely distributed among prokaryotes, unicellular eukaryotes, plants and animals [1]. Myoglobin, a cytoplasmic hemoprotein that is restricted to cardiomyocytes and oxidative skeletal myofibers in vertebrates, has been proposed to facilitate oxygen transport to the mitochondria [1-3]. This cytoplasmic hemoprotein was the first protein to be subjected to definitive structural analysis and has been a subject of long-standing and ongoing interest to biologists [1-3]. Recently, we utilized gene disruption technology to generate mice that are viable and fertile despite a complete absence of myoglobin [4]. This unexpected result led us to reexamine existing paradigms regarding the function of myoglobin in striated muscle. 相似文献
18.
Hypoxia refers to environmental or clinical settings that potentially threaten tissue oxygen homeostasis. One unique aspect
of skeletal muscle is that, in addition to hypoxia, oxygen balance in this tissue may be further compromised when exercise
is superimposed on hypoxia. This review focuses on the cellular and molecular responses of human skeletal muscle to acute
and chronic hypoxia, with emphasis on physical exercise and training. Based on published work, it is suggested that hypoxia
does not appear to promote angiogenesis or to greatly alter oxidative enzymes in skeletal muscle at rest. Although the HIF-1
pathway in skeletal muscle is still poorly documented, emerging evidence suggests that muscle HIF-1 signaling is only activated
to a minor degree by hypoxia. On the other hand, combining hypoxia with exercise appears to improve some aspects of muscle
O 2 transport and/or metabolism. 相似文献
19.
Syncoilin is a member of the intermediate filament protein family, highly expressed in skeletal and cardiac muscle. Syncoilin
binds α-dystrobrevin, a component of the dystrophin associated protein complex (DAPC) located at the muscle cell membrane,
and desmin, a muscle-specific intermediate filament protein, thus providing a link between the DAPC and the muscle intermediate
filament network. This link may be important for muscle integrity and force transduction during contraction, a theory that
is supported by the reduced force-generating capacity of muscles from syncoilin-null mice. Additionally, syncoilin is found
at increased levels in the regenerating muscle fibres of patients with muscular dystrophies and mouse models of muscle disease.
Therefore, syncoilin may be important for muscle regeneration in response to injury. The aims of this article are to review
current knowledge about syncoilin and to discuss its possible functions in skeletal muscle.
Received 21 May 2008; received after revision 10 July 2008; accepted 18 July 2008 相似文献
20.
The patterns of Glut1 and Glut3 glucose transporter protein and mRNA expression were assessed during embryogenesis of chicken
brain and skeletal muscle, Glut4 protein levels were also evaluated in skeletal muscle and heart, and Glut1 was examined in
the developing heart and liver. Glut1 protein expression was detectable throughout brain ontogeny but was highest during early
development. Glut1 mRNA levels in the brain remained very high throughout development. Glut3 protein was highest very early
and very late and mRNA was highest during the last half of development. In embryonic skeletal muscle, the levels of Glut1and
Glut3 proteins and mRNA were highest very early, and declined severely by mid-development. Glut1 protein and mRNA in the heart
also peaked early and then decreased steadily. Although Glut1 mRNA levels were consistently high in the embryonic liver, Glut1
protein expression was not detected. These results suggest that (1) Glut1 is developmentally regulated in chick brain, skeletal
muscle, and heart, (2) Glut1 mRNA is present in liver but does not appear to be translated, (3) Glut3 in brain increases developmentally
but is virtually absent in muscle, and (4) Glut4 protein and mRNA appear to be absent from chick heart and skeletal muscle.
Received 11 January 2001; accepted 14 February 2001 相似文献
|