Perfusion cultures require optimum respiratory ATP supply to maximize cell‐specific and volumetric productivities

2019 ◽  
Vol 116 (5) ◽  
pp. 951-960 ◽  
Author(s):  
Max Becker ◽  
Lisa Junghans ◽  
Attila Teleki ◽  
Jan Bechmann ◽  
Ralf Takors
2018 ◽  
Vol 14 (2) ◽  
pp. 1700722 ◽  
Author(s):  
Moritz K. F Wolf ◽  
Aurélie Closet ◽  
Monika Bzowska ◽  
Jean‐Marc Bielser ◽  
Jonathan Souquet ◽  
...  

Author(s):  
Sylvain Mercille ◽  
Mark Johnson ◽  
Stéphane Lanthier ◽  
Amine A. Kamen ◽  
Bernard Massie
Keyword(s):  

Biologia ◽  
2006 ◽  
Vol 61 (1) ◽  
Author(s):  
Ján Pavlovkin ◽  
Miroslava Luxová ◽  
Ingrid Mistríková ◽  
Igor Mistrík

AbstractIn this study, the effects of Cd on root growth, respiration, and transmembrane electric potential (E m) of the outer cortical cells in maize roots treated with various Cd concentrations (from 1 µM to 1 mM) for several hours to one week were studied. The E m values of root cells ranged between −120 and −140 mV and after addition of Cd they were depolarized immediately. The depolarization was concentration-dependent reaching the value of diffusion potential (E D) when the Cd concentration exceeded 100 µM. The values of E D ranged between −65 to −68 mV (−66 ± 1.42 mV). The maximum depolarization of E m was registered approx. 2.5 h after addition of Cd to the perfusion solution and in some cases, partial (Cd > 100 µM) or complete repolarization (Cd < 100 µM) was observed within 8–10 h of Cd treatment. In the time-dependent experiments (0 to 168 h) shortly after the maximum repolarization of E m a continuous concentration-dependent decrease of E m followed at all Cd concentrations. Depolarization of E m was accompanied by both increased electrolyte leakage and inhibition of respiration, especially in the range of 50 µM to 1 mM Cd, with the exception of root cells treated with 1 and 10 µM Cd for 24 and 48 h. Time course analysis of Cd impact on root respiration revealed that at higher Cd concentrations (> 50 µM) the respiration gradually declined (∼ 6 h) and then remained at this lowest level for up to 24 h.All the Cd concentrations used in this experiment induced significant inhibition of root elongation and concentrations higher than 100 µM stopped the root growth within the first day of Cd treatment. Our results suggest that Cd does not cause irreversible changes in the electrogenic plasma membrane H+ ATPase because fusicoccin, an H+ ATPase activator diminished the depolarizing effect of Cd on the E m. The depolarization of E m in the outer cortical cells of maize roots was the result of a cumulative effect of Cd on ATP supply, plasmalemma permeability, and activity of H+ ATPase.


1986 ◽  
Vol 250 (5) ◽  
pp. C663-C675 ◽  
Author(s):  
D. P. Jones

Endogenous enzymes with different subcellular localizations provide in situ probes to study O2 and ATP concentration at various sites within cells. Results from this approach indicate that substantial intracellular concentration gradients occur under some O2- and ATP-limited conditions. These studies, along with electron microscopic analyses and mathematical modeling, indicate that clustering and distribution of mitochondria are major factors in determining the magnitude and location of the concentration gradients. The mitochondria appear to be clustered in sites of high ATP demand to maximize ATP supply under conditions of limited production. The size of such clusters is limited by the magnitude of the O2 gradient needed to provide adequate O2 concentrations for mitochondrial function within the clusters. Thus microheterogeneity of metabolite concentrations can occur in cells without membranal compartmentation and may be important in determining the rates of various high-flux processes.


2003 ◽  
Vol 374 (1) ◽  
pp. 37-40 ◽  
Author(s):  
Bernard KORZENIEWSKI ◽  
Jerzy A. ZOLADZ

Muscle training/conditioning improves the adaptation of oxidative phosphorylation in skeletal muscles to physical exercise. However, the mechanisms underlying this adaptation are still not understood fully. By quantitative analysis of the existing experimental results, we show that training-induced acceleration of oxygen-uptake kinetics at the onset of exercise and improvement of ATP/ADP stability due to physical training are mainly caused by an increase in the amount of mitochondrial proteins and by an intensification of the parallel activation of ATP usage and ATP supply (increase in direct stimulation of oxidative phosphorylation complexes accompanying stimulation of ATP consumption) during exercise.


Author(s):  
R. Heidemann ◽  
C. Zhang ◽  
H. Qi ◽  
J. Rule ◽  
C. Rozales ◽  
...  

2019 ◽  
Vol 132 (23) ◽  
pp. jcs234492 ◽  
Author(s):  
Topaz Altman ◽  
Danielle Geller ◽  
Elisabeth Kleeblatt ◽  
Tal Gradus-Perry ◽  
Eran Perlson

2018 ◽  
Vol 94 (2) ◽  
pp. 610-628 ◽  
Author(s):  
Maria R. Depaoli ◽  
Jesse C. Hay ◽  
Wolfgang F. Graier ◽  
Roland Malli

2020 ◽  
Vol 40 (8) ◽  
pp. 1151-1162
Author(s):  
Zaiwei Man ◽  
Jing Guo ◽  
Yingyang Zhang ◽  
Zhiqiang Cai

2020 ◽  
Vol 21 (7) ◽  
pp. 2428 ◽  
Author(s):  
Franziska Dengler

AMP-activated protein kinase (AMPK) is known as a pivotal cellular energy sensor, mediating the adaptation to low energy levels by deactivating anabolic processes and activating catabolic processes in order to restore the cellular ATP supply when the cellular AMP/ATP ratio is increased. Besides this well-known role, it has also been shown to exert protective effects under hypoxia. While an insufficient supply with oxygen might easily deplete cellular energy levels, i.e., ATP concentration, manifold other mechanisms have been suggested and are heavily disputed regarding the activation of AMPK under hypoxia independently from cellular AMP concentrations. However, an activation of AMPK preceding energy depletion could induce a timely adaptation reaction preventing more serious damage. A connection between AMPK and the master regulator of hypoxic adaptation via gene transcription, hypoxia-inducible factor (HIF), has also been taken into account, orchestrating their concerted protective action. This review will summarize the current knowledge on mechanisms of AMPK activation under hypoxia and its interrelationship with HIF.


Sign in / Sign up

Export Citation Format

Share Document