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At least 1,693 records · Page 94Linked to original sources
PubMed1992

X-ray diffraction by crystals of beef heart ubiquinol: cytochrome c oxidoreductase.

Beef heart mitochondrial ubiquinol:cytochrome c oxidoreductase has been crystallized in the shape of hexagonal bipyramids. At present the crystals diffract X-rays to 4.7 A. From preliminary analysis the diffraction pattern appears to be consistent with space group P6(1)22 or P6(5)22 and with unit cell parameters a = b = 212 A and c = 352 A.

Animals↗
PubMed1988

Silymarin-induced mitochondrial Ca2+ release.

The effect of silymarin on different functions of mitochondria isolated from rat kidneys was studied. Addition of silymarin to mitochondria oxidizing succinate, induced stimulation of the respiratory State 4; while in mitochondria oxidizing NAD-dependent substrates, the drug produced inhibition of the oxygen consumption. It is also shown that silymarin induces mitochondrial swelling, a drop in the transmembrane potential, as well as Ca2+ release. It is proposed that due to its hydrophobic character, silymarin produces an alteration in the lipidic milieu of the inner membrane which is conductive to an inhibition of the electron transport in the NAD-CoQ span of the respiratory chain, as well as to the loss of the energy dependent accumulated Ca2+.

Animals↗
PubMed1984

Lipid changes with aging in cardiac mitochondrial membranes.

Mitochondrial membranes were isolated from the myocardium of young (4-month-old) and aged (33-month-old) male Long-Evans rats and compared in terms of cholesterol content and phospholipid and fatty acid composition. In aged rats, as compared to young, the major observations include: markedly higher cholesterol content; increased percentage of sphingomyelin and diphosphatidylglycerol (cardiolipin); in fatty acids, variable changes, with a predominant increase in the 16:0 in most phospholipids except cardiolipin, and sporadic increase in the longer chain (20:0, 24:0) fatty acids in cardiolipin; decreased unsaturation index for most phospholipids but increased for cardiolipin. These results are tentatively interpreted as indicative of an aging-related decrease in fluidity and energy transduction of mitochondrial membrane in the heart of aged rats and may be responsible, in part, for the decrements in cardiac function with aging.

Aging↗
PubMed1991

Hydrogen peroxide release by mitochondria increases during aging.

The effect of aging on the release of H2O2 by mitochondria was studied in the housefly in order to elucidate the causes of previously observed age-related increase in the level of oxidative stress. Intact flight muscle mitochondria of the housefly, supplemented with alpha-glycerophosphate, produce 1-2 nmol H2O2/min per mg protein, even in the absence of respiratory inhibitors. The rate of H2O2 secretion progressively increases approximately 2-fold during aging of the fly. Neither uncoupling of oxidative phosphorylation nor mechanical damage to mitochondria during the isolation procedure appear to be responsible for the age-related increase in H2O2 production. Activities of NADH-ferricyanide reductase, succinate-ubiquinone reductase, and NADH-, succinate- and alpha-glycerophosphate-cytochrome c reductases, were approximately 2-fold higher in mitochondria from the old than those from the young flies. However, the concentration of enzymatically reducible ubiquinone remained unchanged with age. Infliction of damage by exposure of mitochondria to free radical-generating systems in vitro caused an increase in the rate of H2O2 generation. Glutaraldehyde, an intermolecular crosslinking agent, induced an increase in the rate of H2O2 generation by mitochondria. Results of this study demonstrate that aging in the housefly is associated with an increase in the rate of H2O2 generation by mitochondria probably due, at least in part, to self-inflicted damage by mitochondria. Intermolecular cross-linking in the inner mitochondrial membrane can contribute towards the increased H2O2 generation.

Aging↗
PubMed1989

Regulation of succinate dehydrogenase and tautomerization of oxaloacetate.

Highly purified succinate-ubiquinone reductase catalyzes the oxidation of L- or D-malate with a Km and initial Vmax equal to approximately 10(-3) M and approximately 100 nmol/min/mg of protein, respectively. The malate dehydrogenase activity of succinate dehydrogenase rapidly decreases regardless of the presence of glutamate plus glutamate-oxaloacetate transaminase. The inhibitor trapping system, however, prevents the inactivation of succinate dehydrogenase under the conditions when the rate of tautomeric oxaloacetate enol in equilibrium oxaloacetate ketone interconversion is high. These results suggest that enol oxaloacetate is an immediate product of malate oxidation at the succinate dehydrogenase active site. Two proteins (Mr 37 and 80 kD) which catalyze the oxaloacetate tautomerase reaction were isolated from the mitochondrial matrix. Some physico-chemical and kinetic properties of these enzymes were characterized. The larger protein was identified as inactive aconitase. The system containing succinate dehydrogenase, L-malate, glutamate plus transaminase and oxaloacetate tautomerase was reconstituted. Such a system is capable of oxidizing malate to aspartate without rapid inactivation of succinate dehydrogenase. Taken together, the data obtained emphasize a significant role of enzymatic oxaloacetate tautomerization in the control of the succinate dehydrogenase activity in the mitochondrial matrix.

Animals↗