scholarly journals Contribution of Mitochondrial F0F1-ATP Synthase and Adenine Nucleotide Translocator to Induced Thermogenesis in the Appendix of Sauromatum venosum Inflorescence

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Skubatz Hanna
1990 ◽  
Vol 265 (3) ◽  
pp. 731-734 ◽  
Author(s):  
R P Hafner ◽  
G C Brown ◽  
M D Brand

Oxidative phosphorylation can be treated as two groups of reactions; those that generate protonmotive force (dicarboxylate carrier, succinate dehydrogenase and the respiratory chain) and those that consume protonmotive force (adenine nucleotide and phosphate carriers. ATP synthase and proton leak). Mitochondria from hypothyroid rats have lower rates of respiration in the presence of ADP (state 3) than euthyroid controls. We show that the kinetics of the protonmotive-force generators are unchanged in mitochondria from hypothyroid animals, but the kinetics of the protonmotive-force consumers are altered, supporting proposals that the important effects of thyroid hormone on state 3 are on the ATP synthase or the adenine nucleotide translocator.


2007 ◽  
Vol 293 (5) ◽  
pp. E1320-E1324 ◽  
Author(s):  
Matthieu Arvier ◽  
Laëtitia Lagoutte ◽  
Gyasi Johnson ◽  
Jean-François Dumas ◽  
Benoit Sion ◽  
...  

The composition of the mitochondrial inner membrane and uncoupling protein [such as adenine nucleotide translocator (ANT)] contents are the main factors involved in the energy-wasting proton leak. This leak is increased by glucocorticoid treatment under nonphosphorylating conditions. The aim of this study was to investigate mechanisms involved in glucocorticoid-induced proton leak and to evaluate the consequences in more physiological conditions (between states 4 and 3). Isolated liver mitochondria, obtained from dexamethasone-treated rats (1.5 mg·kg−1·day−1), were studied by polarography, Western blotting, and high-performance thin-layer chromatography. We confirmed that dexamethasone treatment in rats induces a proton leak in state 4 that is associated with an increased ANT content, although without any change in membrane surface or lipid composition. Between states 4 and 3, dexamethasone stimulates ATP synthesis by increasing both the mitochondrial ANT and F1-F0 ATP synthase content. In conclusion, dexamethasone increases mitochondrial capacity to generate ATP by modifying ANT and ATP synthase. The side effect is an increased leak in nonphosphorylating conditions.


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