Contrasting responses by respiration to elevated CO2 in intact tissue and isolated mitochondria

2007 ◽  
Vol 34 (2) ◽  
pp. 112 ◽  
Author(s):  
Dan Bruhn ◽  
Joseph T. Wiskich ◽  
Owen K. Atkin

The question of whether elevated concentrations of CO2 directly inhibit mitochondrial respiration in plants has received considerable attention. Although there is a growing consensus that elevated [CO2] rarely inhibits respiration of intact tissues, past studies have reported that elevated [CO2] does impact on O2 uptake in isolated mitochondria; what remains unclear, however, is the site(s) where elevated [CO2] impacts on mitochondrial electron transport (ETC). Here we investigated direct effects of [CO2] on respiratory activity of ETC enzymes, intact mitochondria and whole tissues using potato tubers (Solanum tuberosum L. cv. Desiree). Plots of O2 uptake against the redox poise of the ubiquinone (UQ) pool in isolated mitochondria were used to determine whether elevated [CO2] inhibits UQ-reducing and UQ-oxidising pathways differentially. Our results show that mitochondrial respiration was more inhibited via [CO2]/[HCO3–] effects on cytochrome c oxidase (COX) than on succinate dehydrogenase, with [HCO3–] rather than [CO2] inhibiting COX. However, the inhibitory effects at the mitochondrial level did not translate into inhibitory effects at the tissue level. Alternative oxidase (AOX) activity is normally absent in young potato tubers, as was the case in the present study. Thus, the lack of CO2-mediated inhibition at the tissue level was not the result of increases in AOX activity masking the effects of CO2 elsewhere in the respiratory system. We discuss whether the direct impact of elevated [CO2] on respiration is dependent on the rate of metabolic activity and flux control coefficients in individual tissues.

2002 ◽  
Vol 53 (369) ◽  
pp. 737-746 ◽  
Author(s):  
Tracy Lawson ◽  
Jim Craigon ◽  
Colin R. Black ◽  
Jeremy J. Colls ◽  
Geoff Landon ◽  
...  

1966 ◽  
Vol 21 (9) ◽  
pp. 879-888 ◽  
Author(s):  
Volkmar Loeschcke ◽  
Hermann Stegemann

Up to 25 proteins have been found in the sap of potato tubers by polyacrylamid electrophoresis. The mode of preparation and concentration of the plant material was investigated as well as the pretreatment of the polyacrylamid gel to avoid undue retardation of the migrating bands.Sulfite was the most active inhibitor of sap-browning compared with ascorbic acid and cysteine. which did not influence the protein pattern except for one line. The juice had to be dialyzed or filtered through Sephadex G 25 to remove an unkown acidic material which interferes with the more acidic proteins and causes spreading and diffusing of bands. Proteins were concentrated by means of Carbowax MW 20000. For best results ionic contaminations inherent in the gels was removed by electrophoresis before applying the proteins or dyes. Very few proteins were affected by decreasing the pore size of the gel. Ammonium sulfate (40% saturation) precipitated mainly those proteins which are similar in electrophoretic behavior to the albumin- and transferrinregion of human plasma.


2014 ◽  
Vol 4 (1) ◽  
pp. 1-6
Author(s):  
S. Shazia ◽  
F. Naz ◽  
A. Rauf ◽  
M. Inam-ul-Haq ◽  
S. Bushra

Potato (Solanum tuberosum L.) has various biotic constraints in its production due to pest attack. Among these, common scab caused by streptomyces scabies is an important disease in potato which causes economic loss with respect to plant yield and quality of tubers. The present study was conducted to determine the pathogenicity, pathogenic variation, characterization of morphological, physiological and biochemical aspects of Streptomyces associated with potato tubers grown in Rawalpindi district. Severity data and pathogenic variation of disease was studied by using different isolation and characterization techniques.


Plant Biology ◽  
2002 ◽  
Vol 4 (1) ◽  
pp. 77-85 ◽  
Author(s):  
M.-L. Fauconnier ◽  
J. Rojas-Beltrán ◽  
J. Delcarte ◽  
F. Dejaeghere ◽  
M. Marlier ◽  
...  

1989 ◽  
Vol 256 (2) ◽  
pp. G369-G376
Author(s):  
Z. Kizaki ◽  
R. G. Thurman

Livers from well-fed female Sprague-Dawley rats (100-150 g) were perfused at flow rates of 4 or 8 ml.g liver-1.min-1 to deliver O2 to the organ at various rates. During perfusion at normal flow rates (4 ml.g-1.min-1), glucagon (10 nM) increased O2 uptake in perfused liver by approximately 40 mumol.g-1.h-1. In contrast, glucagon increased O2 uptake by nearly 100 mumol.g-1.h-1 when livers were perfused at high flow rates. Increase in O2 uptake was directly proportional to flow rate and was blocked partially by infusion of phorbol myristate acetate (100 nM) before glucagon. Increase in O2 uptake due to elevated flow was not due to enhanced glucagon delivery, since infusion of 120 nM glucagon at normal flow rates only increased O2 uptake by approximately 40 mumol.g-1.h-1. On the other hand, when O2 tension in the perfusate was manipulated at normal flow rates, the stimulation of O2 uptake by glucagon increased proportional to the average O2 tension in the liver. Infusion of 8-bromo-adenosine 3',5'-cyclic monophosphate (BrcAMP; 25 microM) also increased O2 uptake more than twice as much at high compared with normal flow rates. In the presence of angiotensin II (5 nM), a hormone that increases intracellular calcium, glucagon increased O2 uptake by nearly 100 mumol.g-1.h-1 at normal flow rates. Infusion of glucagon or BrcAMP into livers perfused at normal flow rates increased state 3 rates of O2 uptake of subsequently isolated mitochondria significantly by approximately 25%. In contrast, perfusion with glucagon or BrcAMP at high flow rates increased mitochondrial respiration by 50-60%. Glucagon addition acutely to suspensions of mitochondria, however, had no effect on O2 uptake. These data are consistent with reports that glucagon administration in vivo or treatment of intact cells with glucagon increases O2 uptake of subsequently isolated mitochondria, a phenomenon that can account for the observed increase in O2 uptake in livers perfused at high flow rates with glucagon. Furthermore, these results are consistent with the hypothesis that the effect of glucagon on mitochondria is O2 dependent in the perfused liver. This is most likely due to an effect of intracellular calcium on a mechanism mediated via cAMP.(ABSTRACT TRUNCATED AT 250 WORDS)


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