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PubMedDate not supplied

[Effect of heparin on the Mg++-ATPase of the muscle mitochondria of adult and young rabbits].

ATPase activity from freshly prepared, "aged" and "heparin" mitochondria was studied in adult, newborn and 7 day old rabbits. Heparin, incubated with the mitochondria within 2-2.5 hrs at 20 degrees C, increased the activity of endogenous ATPase in the newborn rabbits. Activities of Mg-2++-ATPase and Mg-2+-DNP-ATPase were decreased under effect of heparin in both adult and new born rabbits. In 7 day old rabbits, to the contrary, increased activity of Mg-2+-ATPase and its activation by 2,4-DNP were observed.

Adenosine Triphosphatases↗
PubMedDate not supplied

[IR-spectra of skeletal muscle mitochondria and endoplasmic reticulum].

The existance of alpha- and beta-protein conformation in human straight abdomen muscle mitochondria and microsomal fraction was established. The stability of beta-conformation was provided by hydrophobic and lipid protein interactions. The band at 1730 cm-1, C=O stretching of the carboxyl groups, was more intensive in mitochondria, presented in microsomal fraction and disappeared after its isooctane treatment. From the reducing of NH, OH stretching frequency in microsomes films, was made a conclusion that hydrogen bonds were stronger in that membrane.

Abdominal Muscles↗
PubMedDate not supplied

Functional behaviour of isolated heart muscle mitochondria after in situ ischemia. Polarographic analysis of mitochondrial oxidative phosphorylation.

Heart muscle mitochondria with satisfactory functional parameters of oxidative phosphorylation and with morphologically intact structure were isolated from canine myocardium employing a modified KEA-medium (0.18 M KCl, 10 mM EDTA, 0.5% bovine serum albumin, pH 7.1) according to Sordahl and Schwartz (1). The functional behaviour of mitochondria was investigated after different durations of in situ ischemia (cardioplegia, 15 degrees C) and correlated with metabolic findings. During ischemia the following changes were seen: 1. Successive reduction of electron flow. 2. Relatively small impairment of phosphorylation efficiency. 3. Less damage of FAD- than NAD-catalyzed oxidative phosphorylation. 4. A marked increase of electron flow and thus recovery of phosphorylation rate even after longer ischemic periods by addition of cytochrome c. As important factors of accelerating mitochondrial impairment during ischemia the myocardial ATP decrease, the lactate and H+-activity increase are discussed.

Adenosine Triphosphate↗
PubMed1979

4-Methyl-2-oxopentanoate oxidation by rat skeletal-muscle mitochondria.

1. Oxidative decarboxylation of 4-methyl-2-oxopentanoate (2-oxoisocaproate) by mitochondria of rat skeletal muscle showed biphasic kinetics. Two apparent Km values of 9.1 micronM and 0.78 mM were established. In broken mitochondria the rate of oxidation was lower and only the higher apparent Km value was found. 2. Isovalerylcarnitine inhibited 4-methyl-2-oxopentanoate oxidation in the presence and absence of carnitine, but isovaleryl-CoA had no inhibitory effect. 3. Addition of ADP enhanced 4-methyl-2-oxopentanolate oxidation. Malate, succinate and 2-oxoglutarate additionally increased the rate of oxidation, but in the absence of ADP succinate and 2-oxoglutarate inhibited. 4. Addition of rotenone and simultaneous addition of carbonyl cyanide p-trifluoromethoxyphenyl-hydrazone (FCCP) and valinomycin markedly decreased 4-methyl-2-oxopentanoate oxidation. 5. These observations indicate that the branched-chain 2-oxo acid dehydrogenase complex is situated on the inner side of the mitochondrial inner membrane. 6. In mitochondria and homogenates CO2 was only produced by oxidative decarbosylation of 4-methyl-2-oxopentanoate. In intact muscle oxidation of this oxo acid proceeds more to completeness. 7. The physiological significance of intermediate formation during oxidation of branched-chain amino acids is discussed.

Animals↗
PubMed1978

Calcium uptake in skeletal muscle mitochondria. I. The effects of chelating agents on the mitochondria from fatigued rats.

Female Wistar rats were used to determine the effects of the chelating agents, EDTA and EGTA, on the in vitro 45Ca2+ accumulation by mitochondria isolated from the skeletal muscle of fatigued animals. The rats were divided into three groups: sedentary-rested (SR), trained-rested (TR), trained-exhausted (TE). The trained groups were exercised on a treadmill for 1 h daily, five times a week, for 22 weeks. At the conclusion of the training program, the TE group was rapidly exercised to exhaustion immediately following their daily 1-h run. In the TR group EDTA reduced 45Ca2+ binding while both EDTA and EGTA appeared to increase mitochondrial Ca2+ and Mg2+ content. In the TE group, EDTA reduced endogenous mitochondrial Ca2+ and Mg2+ content, while both EDTA and EGTA increased 45Ca2+ binding. Since chelating Ca2+ and Mg2+ from the membrane may affect the structure and function of the mitochondria, it is suggested that the use of chelating agents during the isolation of mitochondria from the skeletal muscle of trained rats be viewed with caution.

Animals↗
PubMed1976

Effects of exercise training and exhaustion on 45Ca uptake by rat skeletal muscle mitochondria and sarcoplasmic reticulum.

Mitochondrial and sarcoplasmic reticular 45Ca2+ uptake and Ca2+-ATPase activity were determined in skeletal muscle from exercise trained and non-trained rats at rest or following short-term exhaustive exercise. In trained rats exercised to exhaustion, mitochondrial 45Ca2+ uptake was significantly depressed when compared to non-trained rats at rest. Ca2+-ATPase activity of sarcoplasmic reticulum from trained rats exercised to exhaustion was significantly increased as compared to trained rats at rest. These data suggest that the disruptive influence of Ca2+ accumulation in mitochondria isolated following exhaustive exercise may be diminished as a result of training.

Adenosine Triphosphatases↗
PubMed1977

Ultrastructural changes in muscle mitochondria in situ, including the apparent development of internal septa, associated with the uptake and release of calcium.

Treatment of mammalian muscle with the divalent cation ionophore A23187 causes the release of Ca2+ from the sarcoplasmic reticulum and allows the ultrastructural changes of the mitochondria during Ca2+-uptake to be demonstrated in situ. Electron micrographs reveal that the mitochondria swell dramatically during uptake, before contracting again when the accumulated Ca2+ is released once more into the cytoplasm. When maximally swollen, the mitochondria are apparently subdivided and internal "septa" are formed. The ultrastructural details concerning these internal membranous structures are shown in detail and their significance is discussed.

Animals↗
PubMed1975

Effects of thyroid hormone administration on skeletal muscle mitochondria.

The effects of thyroid hormone administration on the levels of a number of mitochondrial markers were measured in skeletal muscle and liver of normal rats. Injection of 18 mug of L-thyroxine (T4) per 100 g body wt every 4th day for 3 wk had no effect on the concentrations of cytochrome c, on citrate synthase activity, or on respiratory capacity of skeletal muscle. Injection of 200 mug of L-triiodothyronine (T3) daily for 5 days, or feeding 23 mg T4 and 7 mg T3/kg of diet for 2 wk, resulted in thyrotoxicosis and large increases in the activity of hepatic alpha-glycerophosphate dehydrogenase and other mitochondrial markers; however, the levels of activity of mitochondrial marker enzymes in gastrocnemius and quadriceps muscles were not significantly changed. Only when rats were fed 3 mg T4 and 1 mg T3/kg diet for a 6-wk period did we observe an increase in skeletal muscle mitochondrial markers. Thus, thyroxine treatment must be sufficiently prolonged if it is to be used as a tool for studying skeletal muscle mitochondrial biogenesis.

Administration, Oral↗
PubMed1978

The early effects of ischemia upon skeletal muscle mitochondria.

The effects of early ischemia were studied in the anterior tibial muscle of Sprague-Dawley rats after 2--24 hr of tourniquet compression at the thigh. Ragged-red fibers, moth-eaten fibers, cores and targets were seen in tissue examined by enzyme histochemistry and electron microscopy. Giant mitochondria, abnormalities of cristal arrangement, crystalloids, osmiophilic inclusion bodies and myeloid figures were dominant features of the mitochondrial reaction. The results of this experiment indicate that early ischemia induces a variety of changes described in other neuromuscular conditions such as dystrophy and the "mitochondrial myopathies". The pathogenesis of these changes and their relationship to human disease of muscle is discussed.

Adenosine Triphosphatases↗
PubMed1978

Calcium uptake in skeletal muscle mitochondria. II. The effects of long-term chronic and acute exercise.

In order to ascertain the effects of long-term exercise training and long-term exhaustive exercise on mitochondrial 45Ca2+ uptake and related variables in rat skeletal muscle, female rats were randomly divided into three groups: sedentary-rested (SR), trained-rested (TR), and trained-exhausted (TE). The trained groups were exercised five times per week on a treadmill for 22 weeks. At the conclusion of the training period, the TE group was exercised to exhaustion following their daily 1 h run. The 45Ca2+ uptake and endogenous mitochodrial Ca2+ content of skeletal muscle followed stepwise increases of approximately 25% and 50%, respectively, across the groups, suggesting that long-term exercise induces the mitochondria to play an important role as a Ca2+ uptake buffer. A 75--83% reduction in 45Ca2+ binding in the TE group suggests a selective loss and partial saturation of membrane phospholipids with exhaustive exercise. The TE group had a two-fold greater content of mitochondrial Mg2+ than did the rested groups. It is speculated that the mitochondria accumulate Mg2+ during acute exercise to maintain the functional integrity of the membrane, thus offsetting the deleterious effects of excessive Ca2+ uptake

Adaptation, Physiological↗
PubMed1977

Response of mitochondria of different types of skeletal muscle to thyrotoxicosis.

To determine the effect of long-term thyrotoxicosis on muscle mitochondria, we measured representative mitochondrial enzymes from three different types of skeletal muscle (fast-twitch red and fast-twitch white from the quadriceps, and slow-twitch red from the soleus) in rats given 3 mg L-thyroxine and 1 mg triiodo-L-thyronine per kilogram of diet for 12 wk. Marker enzymes of the electron transport chain and citric acid cycle (cytochrome oxidase, cytochrome c, and citrate synthase) increase approximately twofold in soleus muscle in response to this treatment. The fast-twitch muscles exhibit no more than 44% increases in these enzymes in response to the same treatment. Relative to initial concentration, 3-hydroxybutyrate dehydrogenase increased to the same extent in fast-twitch red muscle as it did in the soleus (70%). Mitochondrial alpha-glycerophosphate dehydrogenase increased 76% in red quadriceps and 170% in soleus, but did not change in white muscle in the thyrotoxic rats. This differential sensitivity of the three types of muscle provides a tool for studying the mechanisms underlying the action of thyroid hormones on muscle mitochondria.

Animals↗
PubMed1978

Morphologic and metabolic studies in a case of oculo-cranio-somatic neuromuscular disease.

A case resembling the syndrome of "ophthalmoplegia plus" or "oculo-cranio-somatic neuromuscular disease" is reported. A biopsy of deltoid muscle showed that 23% of the fibers were "ragged-red fibers" and were all type 1. Study of their ultrastructure revealed clusters of abnormal skeletal muscle mitochondria in subsarcolemmal and intermyofibrillar spaces. A liver biopsy also revealed a considerable increase in the number and size of the mitochondria. In some instances the mitochondria contained osmiophilic rounded inclusions surrounded by myelin-like structures. Metabolic studies revealed an increase of blood lactate concentration after very light exercise, while the O2 consumption was increased within the expected range. It is concluded that: a) the association of ophthalmoplegia and ultrastructural alterations of the mitochondria in muscle fibers may represent a specific nosographic entity: b) mitochondrial abnormalities are not limited to the skeletal muscles and c) the dysmetabolic basis of such a clinico-pathological entity might lie in an alteration of the mechanism which regulates the mitochondrial oxidative phosphorylation.

Adult↗