Biomedical subjects

A I Marzoev

Publications and source records attributed to A I Marzoev.

At least 19 recordsLinked to original sources

PubMed1985

[Electrical stability of mitochondrial membranes: the role of thyroid hormones and the fat component of the diet].

Electric stability of the membranes of the mitochondria and liposomes formed from mitochondrial lipids was studied. The mitochondria were isolated from the liver of euthyroid or hyperthyroid rats kept on the diets with varying degree of food fat unsaturation. In the first group animals, butter was used as a fatty component of the diet whereas the second group animals received sunflower oil. The electric stability of the membranes of the mitochondria and respective liposomes appeared lower in the first group animals as compared with those in the second group animals. Hyperthyrosis was accompanied by the increased electrical stability of mitochondrial lipids in both the groups. At the same time the liposomal membranes were similar as regards the electric stability, whereas the electric stability of the mitochondrial membranes in the first group hyperthyroid and euthyroid rats was lower than in the organelles of the second group animals. It is thus assumed that the electric stability of the mitochondria is determined not only by the chemical composition of lipids but also by other factors.

Animals↗

PubMed1985

[Blocking effect of cycloheximide on decreased mitochondrial resistance due to thyroid hormone action].

Administration of cycloheximide (20-25 micrograms/kg bw twice, interval 24 h) to hyperthyroid rats (300 micrograms/T4/100 g bw i. p. 48 h before sacrifice) inhibited the decrease in mitochondrial resistance to Ca2+ characteristic of hyperthyroidism. It was established in particular that calcium capacitance of the mitochondria and the time of the maintenance of transmembrane potential of these organelles under calcium loading were increased in the mitochondria of hyperthyroid animals given cycloheximide as compared with analogous parameters of the organelles of intact hyperthyroid rats. Moreover, the fluorescence intensity of NADPH in the mitochondria of the first group of animals was 37% greater and the rate of oxidation of these nucleotides several times lower than in the organelles of the second group animals. It is assumed that the described effects of cycloheximide on the mitochondria are linked with the inhibitory effect of the antibiotic on endogenous activity of mitochondrial phospholipase A2.

Animals↗

PubMed1984

[Effect of hypothyroidism on the structural and functional characteristics of the sarcoplasmic reticulum of rabbit skeletal muscles].

Structural and functional characteristics of sarcoplasmic reticulum vesicles (SRV) from skeletal muscle of normal and hypothyroid rabbits were investigated. The rate of Ca2+ absorption was decreased in hypothyroid animals and Ca2-ATPase activity in SRV of these animals was lower than that of control rabbits. The transport ratio (Ca2+/ATP) in hypothyroid rabbits was higher by 20% than in controls. In SRV of hypothyroid animals a decrease in the protein/lipid interaction and higher fluidity of membrane lipids were observed. Administration of L-thyroxine (300 mg/kg of body mass, intraperitoneally) normalized the SR lipids fluidity within about 40 hrs after the injection but did not affect significantly the patterns of protein/lipid interaction. Normal and hypothyroid SRV were similar in their protein spectrum as shown by electrophoresis in polyacrylamide gel. These alterations observed in the SRV structure and function are apparently related to modifications of membrane lipids.

Absorption↗

PubMed1984

[Transmembrane potential of rat liver mitochondria in hypothyreosis].

Transmembrane potential in liver mitochondria of hypothyroid rats was lower than that in normal animals. In hypothyroid rat mitochondria, the system responsible for maintaining the transmembrane potential was more resistant to the disturbing action of Ca2+ions. This was manifested in both the longer period of transmembrane potential under the limited content of Ca2+ and in the increased maximal dose of Ca2+, which is required for a quick decrease in transmembrane potential. Thyroxine injection (300 micrograms/100 g mass intraperitoneally) made in 48 h almost recovered the transmembrane potential value to that in the normal animals, with a dramatic lowering of the resistance of organelles to the disturbing action of Ca2+ being observed. Apparently, the increase in the resistance of hypothyroid rat mitochondria to the disturbing action of Ca2+ is connected with a reduction in the activity of mitochondrial phospholipids and with deceleration of lipid peroxidation in the mitochondria of hypothyroid animals.

Animals↗

PubMed1984

[Effect of thyroid state on the phospholipid regeneration rate of rat liver mitochondria].

The rate of phospholipid renewal in mitochondria of normal, hypothyroid, hyperthyroid and thyrotoxic rats was studied. Mitochondria were isolated from rat livers 24 and 48 hrs after administration of 3H-glycerol and 14C-palmitic acid. In mitochondria of hypothyroid animals, practically no phospholipid renewal is observed. In mitochondria of hyperthyroid and thyrotoxic rats, the rate of degradation of phospholipids labelled with glycerol, was approximately 1.5 times as low as that in controls. The decrease in the rate of renewal of the fatty acid residues in mitochondrial phospholipids was still more pronounced in hyperthyroid and thyrotoxic animals. Possible reasons for these changes connected with the thyroid state are discussed.

Animals↗

PubMed1984

[Thyroid hormones and the electrical stability of rat liver mitochondrial membranes].

The electrical stability of mitochondrial membranes isolated from the liver of normal, hypothyroid, hyperthyroid (0.1 mg L-thyroxine per 100 g bw for 9 days) and thyrotoxic (4 mg L-thyroxine per 100 g bw for 6 days) rats was investigated. The electrical stability of mitochondrial membranes was estimated by the amount of potassium acetate required for electrical breakdown of the mitochondria. Of the four mitochondrial populations, the organelles of hyperthyroid and thyrotoxic animals had the most stable membranes, whereas the electrical stability of the mitochondria of normal and hypothyroid rats was approximately the same. It is assumed that the increased electrical stability of the mitochondria seen in hyperthyroid conditions is linked with the hormone-induced modifications in the composition of membrane phospholipids rather than with a direct action of excess thyroxine on the organelles.

Animals↗

PubMed1983

[Thyroid hormones and phospholipase activity in rat liver mitochondria].

The rate of the hydrolysis of mitochondrial phospholipids isolated from the liver of rats given excess amount of thyroid hormones for a long time was higher than in normal animals. Activation of this process determined by endogenous phospholipase of mitochondria could be also observed in liver mitochondria isolated 2 days after a single injection of L-thyroxine into rats. It is assumed that the hyperthyrosis-induced acceleration of lipid peroxidation in these organelles might be one of the reasons for activation of endogenous phospholipase of mitochondria.

Animals↗

PubMed1982

[Activation of lipid peroxidation in liver mitochondria of rabbits with hyperthyroidism].

Lipid peroxidation (LPO) in liver mitochondria of normal and hyperthyroid rabbits was studied by recording chemiluminescence of mitochondrial suspensions, induced by Fe2+. It was shown that in mitochondria of the hyperthyroid animals, there takes place an increase in the "slow flash" amplitude of chemiluminescence and reduction in the latent period of the luminescence development, as compared to the similar phenomena in normal animals. Characteristic changes were also seen upon recording chemiluminescence of suspensions of the lipids isolated from mitochondria of normal and hyperthyroid animals. These data attest to LPO activation in liver mitochondria during hyperthyrosis. LPO activation is not the result of a direct action of thyroxine on the mitochondria, since the addition of the hormones to organelles in different concentrations (3.25 x 10(-8)- 1.6 x 10(-7) mol/mg protein) did not alter the chemiluminescence parameters. It is suggested that LPO activation seen in liver mitochondria during hyperthyrosis is determined by an increase in the unsaturated index of fatty acids of mitochondrial lipids.

Animals↗

PubMed1982

[Decrease of lipid peroxidation in liver mitochondria isolated from rabbits with hypothyroidism].

A study was made of chemiluminescence of mitochondria and liposomes formed of mitochondrial phospholipids obtained from the liver of normal and thyroidectomized rabbits. The Fe2+-induced chemiluminescence of mitochondria was characterized by a decrease in the amplitude of "slow flash" and by an increase in the latent period of this parameter occurrence under hypothyrosis. This is accounted for by the decreased rate of lipid peroxidation (LPO) in mitochondria, caused by the deficiency of thyroid hormones in the body. Forty-one hours after a single administration of L-thyroxine (300 micrograms/kgbw) to the rabbits the intensity of chemiluminescense of mitochondria and liposomes not only returned to that of the preparations obtained from the normal animals but even exceeded it approximately 1.5-fold. Apparently, such an abrupt intensification in LPO reactions is consequent on the increased rate of unsaturation of fatty acids in mitochondrial lipids, caused by the hormone administered.

Animals↗

PubMed1982

[Hyperthyroidism and the transmembrane potential of rat liver mitochondria].

Transmembrane potential of liver mitochondria in hyperthyroid rats was higher than that in euthyroid animals. Besides, a lower resistance to Ca2+ of the system responsible for the maintenance of the transmembrane potential was observed in the preparations from hyperthyroid rats. This was manifested in a decrease of the calcium dose required for the decay of the transmembrane potential and in a shorter period of Ca2+ retention by mitochondria. The observed decrease in the resistance to Ca2+ ions of the potential-maintaining system in hyperthyroid mitochondria is supposed to be determined by the increased activity of mitochondrial endogenous phospholipase.

Animals↗

PubMed1981

[Changes in spatial organization in sarcoplasmic reticulum membranes in rabbits with experimental thyrotoxicosis].

The structure of sarcoplasmic reticulum membranes (SR) of skeletal muscles from normal and thyrotoxic rabbits was studied with the use of the fluorescent probe pyrene. It was found that protein globules in SR preparations of thyrotoxic animals were submerged into the lipid bilayer to a greater extent than in the reticulum of normal animals. Electrophoresis in polyacrylamide gel revealed no detectable differences between SR of normal and thyrotoxic rabbits. The ratio protein/lipid in SR membranes remained 2:1 in rabbits with thyrotoxicosis.

Animals↗

PubMed1981

[Liver mitochondrial phospholipase activation in hyperthyroid rabbits].

Mitochondria obtained from hyperthyroid rabbit liver contained an approximately 4-fold greater amount of free fatty acids (FFA) than preparations from the control animals. The temperature dependence of FFA accumulation (29--38 degrees C) showed that the activation energy of mitochondrial lipid hydrolysis for control and experimental animals was 7 kcal/mole and 29 kcal/mole, respectively. The mitochondria were kept at 3 degrees C for 48 h. During this period there was an accumulation of fatty acids. The rate of the process in the mitochondria of hyperthyroid animals was several times than that in the control ones. This indicates the activation of mitochondrial phospholipase by the liver in hyperthyrosis. The increased mitochondrial phospholipase activity seen in hyperthyrosis is assumed to be determined by changes in the physical properties of lipid membranes.

Animals↗

PubMed1981

[Accumulation of lipid peroxidation products and suppression of the retinal electrical activity of vitamin E deficient rats exposed to high intensity light].

Induction of alimentary vitamin E deficiency in rats is accompanied by accumulation of lipid peroxidation products in the retina in vivo and by reduction of the magnitude of electroretinogram waves. Photodamage to the retina caused by the action of light of high intensity (10 000 lx for 3.5 h) is more pronounced in vitamin E deficient animals than in control rats fed standard laboratory chow. The exposure of rats to the light of high intensity results in accumulation of lipid peroxides, the magnitude of which is far greater in vitamin E deficient animals than in controls. The photodamage process is reversible and by the end of the 14th day after exposure to light the content of lipid peroxidation products in the retina and its electric activity are close to the values found in controls.

Animals↗

PubMed1981

[Hyperthyroidism: increase in the electrical stability of membranes from liver mitochondria lipids].

Electrical stability of the membranes was assessed in bilayer lipid membranes and liposomes. It was shown that the break down potential of the membranes prepared from mitochondrial phospholipids of hyperthyroid rabbits' liver is higher than that for the membranes from mitochondrial lipids of the control animals. It is suggested that the increased electrical stability of the membranes is consequent on the changes in the phospholipid content of liver mitochondrial membranes in hyperthyrosis.

Animals↗

PubMed1980

[Thyroxine: structural transformations in the membranes of rabbit skeletal muscle sarcoplasmic reticulum].

The structure of the membranes of sarcoplasmic reticulum fragments (SRF) normally and in thyrotoxicosis was studied by the spin-label and spin-probe methods and by chemifluorescence. The curves of temperature dependence of the regularity parameter show a typical break for the spin probe at 20 degrees C shifted by 4 degrees C to sower temperatures for thyrotoxins. The same shift was observed with temperature dependence for the correlation period of the spin label covalently bound to the thiol groups of Ca2+ dependent ATPase of sarcoplasmic reticulum. The latent period of thyrotoxins was reduced and the chemifluorescence intensity increased. The results obtained suggest the occurrence of considerable changes in the structure of SRF membranes in thyrotoxicosis.

Animals↗

PubMed1980

[Effect of thyroxine on the function of rabbit skeletal muscle sarcoplasmic reticulum].

Thyrotoxicosis in rabbits was induced by prolonged intraperitoneal injection of L-thyroxin. The development of thyroxicosis was assoiated with a decreased Ca2+ accumulation rate by sarcoplasmic reticulum (SR) fragments and a lowered Ca2+ dependent ATPase activity. As compared to the analogous parameters in normal animals. Ca2+ accumulation rate and ATPase activity of thyrotoxicosis animals decreased by 60 and 25%, respectively. The changes in the specific parameters of SR were also observed during incubation of normal SR samples in the medium containing thyroxin (10-5 M). The changes seen in SR functioning in thyrotoxicosis animals are likely to be related to structural rearrangements of lipoprotein surroundings of Ca-ATPase.

Animals↗

PubMed1977

[Effect of antioxidants and complexons on mitochondrial swelling induced by thyroxine].

The rate of thyroxin-induced swelling of rat liver mitochondria depended but little on the cation compositions of the medium (KCl, NaCl or choline chloride), this indicating that the enhancement of mitochondrial membrane permeability for cations in the presence of thyroxin was of negligible selectivity. The antioxidants alpha-tocopherol and beta-ionol in concentrations completely inhibiting the lipid perioxidation failed to affect the thyroxin-induced mitochondrial swelling; hence the latter could not be attributed to the lipoperoxidation. The kinetics of the swelling and the fact of its inhibition by EGTA imply the necessity of calcium ions in the activation of the process and make possible a postulation that the thyroxin-based mitochondrial swelling was based on the process of activation of the membrane phospholipase in these organellae.

Animals↗

PubMed1977

[Role of mitochondrial membrane lipid hydrolysis in their swelling induced by thyroxine].

The thyroxin-induced mitochondrial swelling was accompanied by an accumulation in organellas of free fatty acids which level was restored after the mitochondria contraction in the ATP presence. EGTA induced mitochondrial contractions as well, but with no free fatty acids utilization. Apparently, the thyroxin-induced mitochondrial swelling is the result of the membrane phospholipase activation and of the increase in the membrane cationic permeability due to the hydrolysis of membrane phospholipids.

Adenosine Triphosphate↗