Glucose decreases respiratory control ratio in EL-4 tumor cells

FEBS Letters ◽  
1992 ◽  
Vol 313 (2) ◽  
pp. 126-128 ◽  
Author(s):  
Vladimir L. Gabai
2013 ◽  
Vol 28 (suppl 1) ◽  
pp. 61-65 ◽  
Author(s):  
Leticia Botigeli Baldim ◽  
Ricardo Nejo Jr ◽  
Maria Eliza Jordani Souza ◽  
Maria Cecília Jordani Gomes ◽  
Maria Aparecida Neves Cardoso Picinato ◽  
...  

PURPOSE: To analyze the effects of hyperbaric oxygen therapy on liver function in rats previously subjected to ischemia and reperfusion. METHODS: A randomly distribution of 23 Wistar rats was conducted into three groups: SHAM, animals subjected to surgical stress without restricting blood flow by clamping the hepatic pedicle, IR, rats underwent hepatic vascular occlusion intermittently for two complete cycles of 15 minutes of ischemia followed by 5 min of reperfusion, IR / HBO, rats underwent hepatic pedicle clamping and thereafter exposed to hyperbaric oxygen pressure of 2 absolute atmospheres for 60 minutes. We evaluated liver function through mitochondrial function, determined by the stages 3 and 4 of respiration, respiratory control ratio (RCR) and mitochondrial permeability transition (Swelling). Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were also quantified . We analyzed the results using the Mann-Whitney test and were considered significant all results with p <0.05. RESULTS: There were significant differences between the results of stage 3 in SHAM vs IR group ; of the stage 4 in the groups IR vs SHAM and SHAM vs IR /HBO; of the Respiratory Control Ratio (RCR) in the group IR vs IR / HBO ; of alanine aminotransferase in the groups IR vs SHAM , SHAM vs IR/HBO and IR vs IR / HBO; aspartate aminotransferase in the groups SHAM vs IR and SHAM vs IR / HBO. CONCLUSION: The whole analysis of the mitochondiral function indicators permits us to conclude that the hyperbaric oxygen therapy acted as a protective agent of the mitochondrial function, minimizing the ischemia-reperfusion injury of the hepatic parenchyma.


1985 ◽  
Vol 63 (2) ◽  
pp. 373-379 ◽  
Author(s):  
James S. Ballantyne ◽  
Kenneth B. Storey

The mitochondria of the freezing-tolerant larvae of the goldenrod gall fly (Eurosta solidaginis) have been isolated and characterized. Proline is the preferred substrate of mitochondria from both warm- and cold-acclimated animals based on state 3 rates. Lipid is used as a substrate by warm- and cold-acclimated mitochondria assayed at 20 °C, but not by the mitochondria from cold-acclimated animals assayed at 1 °C. Cold-acclimated mitochondria assayed at 1 °C have a higher and broader optimal range of salt concentration for the oxidation of proline based on the respiratory control ratio (RCR) than those from warm-acclimated animals oxidizing the same substrate at 20 °C. The optimal pH for warm-acclimated mitochondria oxidizing proline at 20 °C is low (6.2) based on the RCR, but rises to pH 7.0 in cold-acclimated animals at 1 °C. It is suggested that the broad optimal salt concentration in the cold-acclimated animals and the very low optimal pH in warm-acclimated animals are adaptations for survival in this freezing-tolerant larva.


1982 ◽  
Vol 2 (1) ◽  
pp. 33-40 ◽  
Author(s):  
Jean-Pierre Nowicki ◽  
Eric T. MacKenzie ◽  
Brigitte Spinnewyn

A number of drugs used in the pharmacotherapy of cerebral metabolic and vascular disease have been studied for their effects on the respiration of mitochondria isolated from the rat brain. Some of these agents increased the respiratory control ratio by more than 5% from base-line values (at p < 0.05), namely, aminophylline, dihydroergotoxine, ifenprodil, nicergoline, raubasine, and vincamine. The ability of these agents to increase the efficiency of mitochondrial respiration could be correlated with two other attributes peculiar to these five drugs: their ability to contract cerebrovascular smooth muscle when studied in vitro and their ability to decrease the volume of infarcted brain tissue following experimental occlusion of the middle cerebral artery in the cat. Papaverine and its derivatives (naftidrofuryl, viquidil, YC-93) decreased respiratory control, an effect that might correlate with their capacity to effect a vasodilatation of the cerebral vessels and their inefficacy in models of acute cerebral infarction. There is a considerable body of evidence suggesting that one of the earliest and most fundamental perturbations of cerebral ischaemia is a loss of respiratory control. Ifenprodil, vincamine, and some related “anti-ischaemic” compounds are capable of increasing respiratory control in normal cerebral mitochondria, and this capacity might well help to explain their therapeutic potential in cerebrovascular disorders in which energy supply to the brain is limited.


2016 ◽  
Vol 62 (5) ◽  
pp. 572-576 ◽  
Author(s):  
T.A. Popova ◽  
V.N. Perfilova ◽  
G.A. Zhakupova ◽  
V.E. Verovsky ◽  
O.V. Ostrovskij ◽  
...  

Substitution of drinking water for 1.8% NaCl in pregnant rats caused a pronounced increase in arterial pressure by 24,3% and urinary protein by 117% to day 21 of pregnancy. State 4 respiration of isolated placental mitochondria in the group of negative control was 3- and 1.5-fold higher with malate/glutamate and succinate as substrates than in placental mitochondria isolated from uncomplicated pregnant animals. This led to a decrease of the respiratory control ratio. These results suggest that development of experimental preeclampsia is accompanied by mitochondrial dysfunction through uncoupling of oxidative phosphorylation. Daily administration of sulodexide to females with experimental preeclampsia (EP) per os at a dose of 30 LE during the whole period of gestation decreased manifestations of the disease as evidenced by a slight increase in blood pressure (by 8,6%) and less pronounces increase in urinary protein (by 58,9%). Sulodexide decreased development of mitochondrial dysfunction in EP rats as shown a decrease of non-stimulated ADP respiration with malate/glutamate and succinate (4.5- and 2.5-fold, respectively) as compared with the negative control group and the corresponding increase in the respiratory control ratio (2.5- and 1.5-fold, respectively). Thus, sulodexide reduces uncoupling of oxidative phosphorylation and enhances the functional activity of mitochondria in EP animals, possibly due to its antioxidant and endotelioprotective effects.


Author(s):  
R. F. Dunn ◽  
M. Worsfold ◽  
J. B. Peter

This is a preliminary report on our studies correlating the morphology and biochemical characteristics of mitochondria isolated from rat skeletal muscle. Figures 1 to 3 show sections of the mitochondrial preparations made on two separate occasions. These were sedimented from low speed supernatants at 3,500 g for 10 minutes (Figs. 1 and 2) or from a 3,500 g supernatant sedimented at 7,000 g for 10 minutes (Fig. 3). Polarographic traces of the respiration of the 3,500 g fractions from the two preparations, with pyruvate and malate as substrates, are shown in Figure 4.The mitochondria in the 70-3,500 g fraction from rat A (Fig. 1) were generally compact with closely packed cristae. Contamination with myofibrillar material was evident. In the 7,000 g fraction from the same animal, very few myofibrils were seen, and the mitochondria appeared distended and generally swollen (Fig. 3). The respiratory control ratio (RCR) of the 3,500 g mitochondria (Fig. 1) was 3.1 compared to 2.2 of the 7,000 g fraction (Fig. 3). Using our technique of preparation most of the mitochondria from rat skeletal muscle were sedimented at 3,500 g.


1990 ◽  
Vol 149 (1) ◽  
pp. 133-148 ◽  
Author(s):  
J. O'Brien ◽  
R. D. Vetter

Isolated mitochondria of the bivalve Solemya reidi Bernard oxidize sulphide and couple this oxidation to ADP phosphorylation. The products of mitochondrial sulphide oxidation were analyzed by HPLC using monobromobimane derivatization. Concurrent measurements of respiration were made using sulphide-insensitive oxygen electrodes. S. reidi mitochondria oxidized sulphide exclusively to thiosulphate. The reaction occurred in two steps. One sulphide molecule was first oxidized to sulphite. A second molecule of sulphide was then added oxidatively to form the free product thiosulphate. This oxidation was obligately linked to mitochondrial electron transport and could be inhibited by the cytochrome c oxidase inhibitor hydrogen cyanide, or by low oxygen concentration. The site II inhibitor antimycin A did not inhibit thiosulphate production, indicating that sulphide oxidation is linked through only one ATP coupling site (site III). A calculation of the respiratory potential for ATP synthesis by fully intact mitochondria indicated that 2.0-3.25 ATP per sulphide may be synthesized using the proton potential generated by sulphide oxidation. This estimate far exceeds the published phosphorylation ratios for S. reidi (0.5-1.2 ATP per sulphide). This difference may be accounted for by partial uncoupling of phosphorylation from sulphide-based respiration. This hypothesis is supported by the observation that the respiratory control ratio of mitochondria respiring on sulphide is 41% lower than that of mitochondria respiring on succinate. The respiratory control ratio is an index of the tightness of coupling of respiration to ADP phosphorylation. When the adenylate pool of a eukaryotic cell is mostly phosphorylated, respiration is very slow, owing to the maintenance of a high mitochondrial membrane potential. Uncoupling of oxidative phosphorylation from respiration would be an adaptive advantage to the animal in that it allows for continuous, rapid removal of the toxic molecule hydrogen sulphide.


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