Increasing Mitochondrial Membrane Phospholipid Content Lowers the Enzymatic Activity of Electron Transport Complexes

Biochemistry ◽  
2014 ◽  
Vol 53 (35) ◽  
pp. 5589-5591 ◽  
Author(s):  
Saame Raza Shaikh ◽  
E. Madison Sullivan ◽  
Rick J. Alleman ◽  
David A. Brown ◽  
Tonya N. Zeczycki
Keyword(s):  
Electron Transport ◽  
Enzymatic Activity ◽  
Mitochondrial Membrane ◽  
Membrane Phospholipid ◽  
Phospholipid Content ◽  
Electron Transport Complexes

Anaerobic respiration sustains mitochondrial membrane potential in a prolyl hydroxylase pathway-activated cancer cell line in a hypoxic microenvironment

2014 ◽  
Vol 306 (4) ◽  
pp. C334-C342 ◽  
Author(s):  
Eiji Takahashi ◽  
Michihiko Sato
Keyword(s):  
Membrane Potential ◽  
Electron Transport ◽  
Cell Line ◽  
Mitochondrial Membrane Potential ◽  
Cancer Cell ◽  
Mitochondrial Membrane ◽  
Cancer Cell Line ◽  
Prolyl Hydroxylase ◽  
Complex Ii ◽  
Pathway Activation

To elucidate how tumor cells produce energy in oxygen-depleted microenvironments, we studied the possibility of mitochondrial electron transport without oxygen. We produced well-controlled oxygen gradients (ΔO2) in monolayer-cultured cells. We then visualized oxygen levels and mitochondrial membrane potential (ΔΦm) in individual cells by using the red shift of green fluorescent protein (GFP) fluorescence and a cationic fluorescent dye, respectively. In this two-dimensional tissue model, ΔΦm was abolished in cells >500 μm from the oxygen source [the anoxic front (AF)], indicating limitations in diffusional oxygen delivery. This result perfectly matched GFP-determined ΔO2. In cells pretreated with dimethyloxaloylglycine (DMOG), a prolyl hydroxylase domain-containing protein (PHD) inhibitor, the AF was expanded to 1,500–2,000 μm from the source. In these cells, tissue ΔO2 was substantially decreased, indicating that PHD pathway activation suppressed mitochondrial respiration. The expansion of the AF and the reduction of ΔO2 were much more prominent in a cancer cell line (Hep3B) than in the equivalent fibroblast-like cell line (COS-7). Hence, the results indicate that PHD pathway-activated cells can sustain ΔΦm, despite significantly decreased electron flux to complex IV. Complex II inhibition abolished the effect of DMOG in expanding the AF, although tissue ΔO2 remained shallow. Separate experiments demonstrated that complex II plays a substantial role in sustaining ΔΦm in DMOG-pretreated Hep3B cells with complex III inhibition. From these results, we conclude that PHD pathway activation can sustain ΔΦm in an otherwise anoxic microenvironment by decreasing tissue ΔO2 while activating oxygen-independent electron transport in mitochondria.

Mitochondrial membrane modifications induced by adriamycin-mediated electron transport

1983 ◽  
Vol 32 (5) ◽  
pp. 889-893 ◽  
Author(s):  
E. Goormaghtigh ◽  
G. Pollakis ◽  
J.M. Ruysschaert
Keyword(s):  
Electron Transport ◽  
Mitochondrial Membrane

scholarly journals Palmitic Acid, but Not Lauric Acid, Induces Metabolic Inflammation, Mitochondrial Fragmentation, and a Drop in Mitochondrial Membrane Potential in Human Primary Myotubes

2021 ◽  
Vol 8 ◽  
Author(s):  
Domenico Sergi ◽  
Natalie Luscombe-Marsh ◽  
Nenad Naumovski ◽  
Mahinda Abeywardena ◽  
Nathan O'Callaghan
Keyword(s):  
Insulin Resistance ◽  
Membrane Potential ◽  
Electron Transport ◽  
Mitochondrial Membrane Potential ◽  
Electron Transport Chain ◽  
Mitochondrial Membrane ◽  
Chain Complex ◽  
Mitochondrial Fragmentation ◽  
Metabolic Inflammation ◽  
Transport Chain

The chain length of saturated fatty acids may dictate their impact on inflammation and mitochondrial dysfunction, two pivotal players in the pathogenesis of insulin resistance. However, these paradigms have only been investigated in animal models and cell lines so far. Thus, the aim of this study was to compare the effect of palmitic (PA) (16:0) and lauric (LA) (12:0) acid on human primary myotubes mitochondrial health and metabolic inflammation. Human primary myotubes were challenged with either PA or LA (500 μM). After 24 h, the expression of interleukin 6 (IL-6) was assessed by quantitative polymerase chain reaction (PCR), whereas Western blot was used to quantify the abundance of the inhibitor of nuclear factor κB (IκBα), electron transport chain complex proteins and mitofusin-2 (MFN-2). Mitochondrial membrane potential and dynamics were evaluated using tetraethylbenzimidazolylcarbocyanine iodide (JC-1) and immunocytochemistry, respectively. PA, contrarily to LA, triggered an inflammatory response marked by the upregulation of IL-6 mRNA (11-fold; P < 0.01) and a decrease in IκBα (32%; P < 0.05). Furthermore, whereas PA and LA did not differently modulate the levels of mitochondrial electron transport chain complex proteins, PA induced mitochondrial fragmentation (37%; P < 0.001), decreased MFN-2 (38%; P < 0.05), and caused a drop in mitochondrial membrane potential (11%; P < 0.01) compared to control, with this effect being absent in LA-treated cells. Thus, LA, as opposed to PA, did not trigger pathogenetic mechanisms proposed to be linked with insulin resistance and therefore represents a healthier saturated fatty acid choice to potentially preserve skeletal muscle metabolic health.

Study on the relationship of cPLA2, CK-MB, and membrane phospholipid content in acute myocardial infarction

2010 ◽  
Vol 26 (1) ◽  
pp. 64-68 ◽  
Author(s):  
Li Wei-hua ◽  
Han Jun-yu ◽  
Sun Chang-qing ◽  
Guo Yong-jun ◽  
Xie Qiang ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Membrane Phospholipid ◽  
Phospholipid Content ◽  
Relationship Of ◽  
The Relationship

scholarly journals Daptomycin Resistance in Enterococci Is Associated with Distinct Alterations of Cell Membrane Phospholipid Content

PLoS ONE ◽  
2012 ◽  
Vol 7 (8) ◽  
pp. e43958 ◽  
Author(s):  
Nagendra N. Mishra ◽  
Arnold S. Bayer ◽  
Truc T. Tran ◽  
Yousif Shamoo ◽  
Eugenia Mileykovskaya ◽  
...  
Keyword(s):  
Cell Membrane ◽  
Membrane Phospholipid ◽  
Phospholipid Content
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