Relationship between rates of respiratory proton extrusion and ATP synthesis in obligately alkaliphilic Bacillus clarkii DSM 8720T

2012 ◽  
Vol 44 (2) ◽  
pp. 265-272 ◽  
Author(s):  
Toshikazu Hirabayashi ◽  
Toshitaka Goto ◽  
Hajime Morimoto ◽  
Kazuaki Yoshimune ◽  
Hidetoshi Matsuyama ◽  
...  
1994 ◽  
Vol 196 (1) ◽  
pp. 457-470 ◽  
Author(s):  
T A Krulwich ◽  
J Cheng ◽  
A A Guffanti

Both neutralophilic Bacillus subtilis and alkaliphilic Bacillus firmus OF4 depend upon electrogenic Na+/H+ antiporters, which are energized by the gradients established by respiration-coupled proton extrusion, to achieve Na(+)-resistance and pH homeostasis when the external pH is very alkaline. The interplay of proton and sodium cycles is discussed. In B. subtilis, pH homeostasis, up to pH9, can be achieved using K+ when Na+ is unavailable or when the gene encoding the Na+/H+ antiporter that is involved in Na(+)-dependent pH homeostasis is disrupted. That gene is a member of the tetracycline efflux family of genes. A second gene, encoding a Na+/H+ antiporter that functions in Na(+)-resistance, has been identified, and candidates for the K+/H+ antiporter genes are under investigation. Aggregate Na+/H+ antiport activity in B. subtilis is as much as 10 times lower than in the alkaliphile, and the neutralophile cannot regulate its internal pH upon a shift to pH 10.5. Upon such a shift, there is a pronounced reduction in the generation of a primary electrochemical proton gradient. The alkaliphile, by contrast, maintains substantial driving forces and regulates its internal pH in an exclusively Na(+)-coupled manner upon shifts to either pH 8.7 or 10.5. One gene locus has been identified and a second locus has been inferred as encoding relevant antiporter activities.


Extremophiles ◽  
1998 ◽  
Vol 2 (3) ◽  
pp. 217-222 ◽  
Author(s):  
T. A. Krulwich ◽  
Masahiro Ito ◽  
David B. Hicks ◽  
Raymond Gilmour ◽  
Arthur A. Guffanti

Extremophiles ◽  
2009 ◽  
Vol 13 (3) ◽  
pp. 491-504 ◽  
Author(s):  
Shinichi Ogami ◽  
Shoichi Hijikata ◽  
Tamotsu Tsukahara ◽  
Yasuhiro Mie ◽  
Toshihide Matsuno ◽  
...  

1998 ◽  
Vol 180 (15) ◽  
pp. 3799-3803 ◽  
Author(s):  
Masatoshi Sonoda ◽  
Hirokazu Katoh ◽  
Wim Vermaas ◽  
George Schmetterer ◽  
Teruo Ogawa

ABSTRACT The product of pxcA (formerly known ascotA) is involved in light-induced Na+-dependent proton extrusion. In the presence of 2,5-dimethyl-p-benzoquinone, net proton extrusion bySynechocystis sp. strain PCC6803 ceased after 1 min of illumination and a postillumination influx of protons was observed, suggesting that the PxcA-dependent, light-dependent proton extrusion equilibrates with a light-independent influx of protons. A photosystem I (PS I) deletion mutant extruded a large number of protons in the light. Thus, PS II-dependent electron transfer and proton translocation are major factors in light-driven proton extrusion, presumably mediated by ATP synthesis. Inhibition of CO2 fixation by glyceraldehyde in a cytochrome c oxidase (COX) deletion mutant strongly inhibited the proton extrusion. Leakage of PS II-generated electrons to oxygen via COX appears to be required for proton extrusion when CO2 fixation is inhibited. At pH 8.0, NO3 − uptake activity was very low in thepxcA mutant at low [Na+] (∼100 μM). At pH 6.5, the pxcA strain did not take up CO2 or NO3 − at low [Na+] and showed very low CO2 uptake activity even at 15 mM Na+. A possible role of PxcA-dependent proton exchange in charge and pH homeostasis during uptake of CO2, HCO3 −, and NO3 − is discussed.


2017 ◽  
Vol 2 (2) ◽  
pp. 34
Author(s):  
TA Popova ◽  
II Prokofiev ◽  
IS Mokrousov ◽  
Valentina Perfilova ◽  
AV Borisov ◽  
...  

Introduction: To study the effects of glufimet, a new derivative of glutamic acid, and phenibut, a derivative of γ-aminobutyric acid (GABA), on cardiac and cerebral mitochondria and endothelial functions in animals following exposure to stress and inducible nitric oxide synthase (iNOS) inhibition. Methods: Rats suspended by their dorsal cervical skin fold for 24 hours served as the immobilization and pain stress model. Arterial blood pressure was determined using a non-invasive blood pressure monitor. Mitochondrial fraction of heart and brain homogenates were isolated by differential centrifugation and analysed for mitochondrial respiration intensity, lipid peroxidation (LPO) and antioxidant enzyme activity using polarographic method. The concentrations of nitric oxide (NO) terminal metabolites were measured using Griess reagent. Hemostasis indices were evaluated. Platelet aggregation was estimated using modified version of the Born method described by Gabbasov et al., 1989. Results: The present study demonstrated that stress leads to an elevated concentration of NO terminal metabolites and LPO products, decreased activity of antioxidant enzymes, reduced mitochondrial respiratory function, and endothelial dysfunction. Inhibition of iNOS by aminoguanidine had a protective effect. Phenibut and glufimet inhibited a rise in stress-induced nitric oxide production. This resulted in enhanced coupling of substrate peroxidation and ATP synthesis. The reduced LPO processes caused by glufimet and phenibut normalized the endothelial function which was proved by the absence of average daily blood pressure (BP) elevation episodes and a significant increase in platelet aggregation level. Conclusion: Glufimet and phenibut restrict the harmful effects of stress on the heart and brain possibly by modulating iNOS activity.


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