Respiration and oxidative phosphorylation by muscle and heart mitochondria of hamsters with hereditary myocardiopathy and polymyopathy

1968 ◽  
Vol 46 (4) ◽  
pp. 323-329 ◽  
Author(s):  
Klaus Wrogemann ◽  
M. C. Blanchaer
Keyword(s):  
Skeletal Muscle ◽  
Oxidative Phosphorylation ◽  
Histological Examination ◽  
Creatine Phosphokinase ◽  
Respiratory Control ◽  
Isolation Procedure ◽  
Heart Mitochondria ◽  
Respiratory Control Ratio ◽  
Skeletal Muscle Mitochondria ◽  
Serum Creatine Phosphokinase

Mitochondria isolated from skeletal muscle and heart of normal Syrian hamsters and from hamsters of the BIO 14.6 myopathic strain aged 97–124 days were studied. Histological examination of the tissues and serum creatine phosphokinase determinations established that the disease was active in the dystrophic animals. In the mitochondrial isolation procedure the minced tissue was incubated before homogenization in a mannitol–sucrose–EDTA medium containing a proteinase (Nagarse). Polarographic estimations with pyruvate–malate as substrate, in the presence and absence of ADP, indicated that the rate of O2 uptake, ADP/O ratio, and respiratory control ratio (state 3 to 4 transition) of the heart mitochondria did not suffer significantly between the normal and myopathic groups. The findings with the skeletal muscle mitochondria were similar. L-α-Glycerophosphate oxidation also was not affected by the myopathy but the rate of NADH oxidation was 35% slower in the heart mitochondria of the BIO 14.6 strain.

OXIDATIVE PHOSPHORYLATION BY MUSCLE MITOCHONDRIA OF DYSTROPHIC MICE

1967 ◽  
Vol 45 (8) ◽  
pp. 1271-1278 ◽  
Author(s):  
Klaus Wrogemann ◽  
M. C. Blanchaer
Keyword(s):  
Skeletal Muscle ◽  
Oxidative Phosphorylation ◽  
Respiratory Control ◽  
Laboratory Strain ◽  
Adenosine Diphosphate ◽  
Isolation Procedure ◽  
Respiratory Control Ratio ◽  
Differential Centrifugation ◽  
Dystrophic Mice ◽  
Phosphorylation Rate

Oxidative phosphorylation was studied in mitochondria isolated from the skeletal muscle of control and dystrophic mice of the Jackson Laboratory strain 129/Re, aged 32–104 days. The isolation procedure included a preliminary incubation of the muscle minced in a medium containing a proteinase (Nagarse) followed by gentle homogenization and differential centrifugation. Polarographic estimations in the presence and absence of adenosine diphosphate (ADP) indicated that the rate of oxygen uptake, ADP/0 ratio, respiratory control ratio, and phosphorylation rate were not significantly different in the mitochondria isolated from control and dystrophic mice. Bovine serum albumin increased the ADP/0 and respiratory control ratios, but the values for the control and dystrophic preparations again did not differ significantly in the presence of albumin.

The Morphology and Biochemistry of Isolated Skeletal Muscle Mitochondria

1968 ◽  
Vol 26 ◽  
pp. 124-125 ◽  
Author(s):  
R. F. Dunn ◽  
M. Worsfold ◽  
J. B. Peter
Keyword(s):  
Skeletal Muscle ◽  
Preliminary Report ◽  
Respiratory Control ◽  
Respiratory Control Ratio ◽  
Rat Skeletal Muscle ◽  
Biochemical Characteristics ◽  
Muscle Mitochondria ◽  
Low Speed ◽  
Skeletal Muscle Mitochondria

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.

65 Fatty acid oxidation in human skeletal muscle mitochondria determined by oxidative phosphorylation as a function of age

Mitochondrion ◽  
2007 ◽  
Vol 7 (6) ◽  
pp. 422-423
Author(s):  
George Kypriotakis ◽  
Bruce H. Cohen ◽  
Sumit Parikh ◽  
Douglas S. Kerr ◽  
Charles L. Hoppel ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Oxidative Phosphorylation ◽  
Fatty Acid Oxidation ◽  
Human Skeletal Muscle ◽  
Acid Oxidation ◽  
Muscle Mitochondria ◽  
Skeletal Muscle Mitochondria

A magnesium-responsive defect of respiration and oxidative phosphorylation in skeletal muscle mitochondria of dystrophic hamsters

1970 ◽  
Vol 48 (12) ◽  
pp. 1332-1338 ◽  
Author(s):  
K. Wrogemann ◽  
M. C. Blanchaer ◽  
B. E. Jacobson
Keyword(s):  
Skeletal Muscle ◽  
Oxidative Phosphorylation ◽  
Respiratory Rate ◽  
Test System ◽  
Muscle Mitochondria ◽  
Skeletal Muscle Mitochondria ◽  
Muscle Necrosis ◽  
Presence And Absence ◽  
Stimulation Of

Skeletal muscle mitochondria were isolated in the presence and absence of the proteinase Nagarse from dystrophic hamsters of the BIO 14.6 strain, aged 45–196 days, and from normal hamsters. Mitochondria from the dystrophic animals prepared by glass-on-glass homogenization without Nagarse in 0.25 M sucrose – 1 mM EDTA, pH 7.4, did not differ from normal in their respiratory rate or capacity for oxidative phosphorylation. However, these functions were subnormal in mitochondria isolated with Nagarse from the same animals, both in the presence and absence of albumin. Respiration measured with an O2 electrode was reduced by 50–70% and the stimulation of O2 uptake normally seen after ADP addition was minimal or absent. This was most marked in mitochondria from young hamsters about 65 days old with muscle necrosis. The defect was ameliorated by addition to the Polarographie test system of an ATP trap or of Mg2+, one of the trap constituents. This ion, when added to the defective mitochondria prior to ADP and substrate, restored respiration and oxidative phosphorylation to values that did not differ significantly from those found with skeletal muscle mitochondria of normal hamsters.

scholarly journals The effect of sulodexide on placental mitochondria function in rats with experimental preeclampsia

2016 ◽  
Vol 62 (5) ◽  
pp. 572-576 ◽  
Author(s):  
T.A. Popova ◽  
V.N. Perfilova ◽  
G.A. Zhakupova ◽  
V.E. Verovsky ◽  
O.V. Ostrovskij ◽  
...  
Keyword(s):  
Oxidative Phosphorylation ◽  
Mitochondrial Dysfunction ◽  
Respiratory Control ◽  
Negative Control ◽  
Urinary Protein ◽  
Control Group ◽  
Respiratory Control Ratio ◽  
Pregnant Rats ◽  
Pronounced Increase ◽  
Uncoupling Of Oxidative Phosphorylation

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.

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