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Biomedical subjects

M Rugolo

Publications and source records attributed to M Rugolo.

47 records · Page 3Linked to original sources
PubMed1984

Increased accumulation of a lipophilic cation (tetraphenylphosphonium) in human embryo fibroblasts after infection with cytomegalovirus.

The distribution of a lipophilic cation, tetraphenylphosphonium (TPP+), has been used to monitor changes in mitochondrial and plasma membrane potentials within human embryo fibroblasts infected with human cytomegalovirus. An increase in TPP+ accumulation was observed throughout the whole viral replication cycle, beginning 6 h after infection. This effect requires an active viral DNA and seems to be dependent on the early transcription of the viral genome. In the early phase of viral replication, the increase in TPP+ accumulation is insensitive to mitochondrial inhibitors and sensitive to ouabain, and could be due to a hyperpolarization of the plasma membrane. Later during the infectious cycle, enhanced accumulation of the lipophilic cation is sensitive to mitochondrial inhibitors.

Cells, Cultured↗
PubMed1984

Magnesium transport by brain mitochondria: energy requirement and dependence on Ca2+ fluxes.

The association of Mg2+ ions with mitochondria isolated from guinea pig cerebral cortex is investigated and resolved into two components, that bound to the surface of both the outer and the inner membranes and that transported into the mitochondrial matrix. When rotenone-treated mitochondria are preincubated in a Mg2+-containing medium, Mg2+ binding can be measured and actual Mg2+ transport determined after the addition of succinate. Mg2+ uptake as well as retention within mitochondria is an energy-dependent process linked to substrate oxidation. EGTA completely prevents Mg2+ uptake, while the Ca2+ uniporter inhibitor Ruthenium Red, along with prevention of Mg2+ uptake, induces a slow efflux of accumulated Mg2+ ions. These findings suggest that both inward and outward Mg2+ movements follow Ca2+ fluxes across the mitochondrial membrane. Modulation of Mg2+ movements by mitochondria is therefore suggested to occur within nerve terminals.

Animals↗
PubMed1983

Studies on the transport of carnitine in the brain using synaptosomes isolated from guinea-pig cerebral cortex.

Synaptosomes isolated from guinea pig cerebral cortex accumulate L-carnitine from the medium in an active process, dependent on the sodium gradient across the plasma membrane and on (Na+ + K+)-ATPase activity. L-Carnitine uptake is inhibited by oxidative phosphorylation uncouplers and by ouabain, a known inhibitor of (Na+ + K+)-ATPase. In addition, the omission of Na+ or its replacement by Li+ inhibited the transport, which was also competitively inhibited by gamma-aminobutyrate. The kinetics of carnitine uptake show that the overall process would consist of two components: a passive diffusion and a carrier-mediated transport which is saturated at 1-2 mM carnitine concentration.

Animals↗
PubMed1983

Oxygen-induced inhibition of light-dependent uptake of tetraphenylphosphonium ions as a probe of a direct interaction between photosynthetic and respiratory components in cells of Rhodopseudomonas capsulata.

Light-generated and oxygen-dependent membrane potentials by heterotrophycally grown cells of Rhodopseudomonas capsulata have been investigated by using a tetraphenylphosphonium ion-selective electrode. The results show that respiratory electron transport affects the magnitude of photogenerated membrane potential while photosynthesis seems to either inhibit or stimulate respiration in coupled or uncoupled cells, respectively. These observations have been considered as evidence that the intracytoplasmic membrane system of R. capsulata contain respiratory and photosynthetic apparatuses which are strictly intermingled.

Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone↗
PubMed1983

Inhibition of the mitochondrial bc1 complex by dibromothymoquinone.

We have studied the effects of dibromothymoquinone (DBMIB) in various redox activities of the succinate-cytochrome c span of the mitochondrial respiratory chain. At concentrations higher than 50 mol/mol of cytochrome c1 the inhibitor produces a bypass of electron transfer on the substrate side of the bc1 complex, because of its autooxidation capability. This induces an artifactual overestimation of the real inhibition titer of the redox activity of this enzyme, which has been found to be 3-6 mol/mol of cytochrome c1 by following the ubiquinol-cytochrome c reductase activity. This action is reversed by addition of excess of sulphydryl compounds like cysteine.

Animals↗
PubMed1982

alpha-latrotoxin of black widow spider venom depolarizes the plasma membrane, induces massive calcium influx, and stimulates transmitter release in guinea pig brain synaptosomes.

The effect of alpha-latrotoxin from black widow spider venom upon guinea pig cerebral cortical synaptosomes is described. Plasma membrane potential (delta psi p), in situ mitochondrial membrane potential (delta psi m), Ca2+ transport, gamma-amino[3H]butyrate release, [3H]noradrenaline release, and synaptosomal ATP were monitored under parallel conditions. Potentials were determined both isotopically and with a tetraphenylphosphonium-selective electrode. alpha-Latrotoxin depolarizes delta psi p selectively, both in the presence and absence of Ca2+. A slight toxin-induced depolarization of delta psi m is a consequence of a massive Ca2+ uptake across the plasma membrane. Depolarization of delta psi p is insensitive to tetrodotoxin, and Ca2+ entry is only partially inhibited by verapamil. Release of [3H]noradrenaline and gamma-amino[3H]butyrate is markedly stimulated by the toxin in the presence of Ca2+, and this effect is only slightly reduced in Ca2+-free conditions.

Animals↗
PubMed1981

Parallel efflux of Ca2+ and Pi in energized rat liver mitochondria.

Addition of Ruthenium Red to energized rat liver mitochondria that have previously accumulated Ca2+ and phosphate from the external medium induces a parallel efflux of both these ions. Mersalyl or dithioerythritol, which decrease Ruthenium Red-insensitive Ca2+ efflux, also decrease phosphate efflux to the same extent. Conversely diazenedicarboxylic acid bis(NN-dimethylamide) (DDBA), which increases the Ruthenium Red-induced Ca2+ efflux concurrently increases phosphate release. Dithioerythritol and DDBA, reducing and oxidizing agents of thiol groups respectively, modify Ca2+ and Pi efflux without penetrating the mitochondrial inner membrane. Under all the adopted conditions the membrane potential is preserved. The release of resting respiration and the parallel efflux of Mg2+ and adenine nucleotides, events closely correlated to Ca2+ cycling, are equally prevented either by mersalyl, which inhibits phosphate transport, or dithioerythritol; DDBA has the opposite effect. These findings and the observation that suggest that Ca2+ and phosphate transport in energized liver mitochondria are closely related and dependent on the redox state of membrane-bound thiol groups.

Adenine Nucleotides↗
PubMed1981

Correlated effluxes of adenine nucleotides, Mg2+ and Ca2+ induced in rat-liver mitochondria by external Ca2+ and phosphate.

The presence of inorganic phosphate and Ca2+ in the external medium induces a closely parallel efflux of both endogenous adenine nucleotides and Mg2+ from rat liver mitochondria. These effluxes are (a) pH-dependent and inhibited by uncouplers, respiration inhibitors and external Mg2+; (b) completely prevented by bongkrekate, but stimulated by atractylate. ATP, ADP or AMP each inhibit the release of Mg2+ promoted by Ca2+ and phosphate; however, in the presence of oligomycin and P1,P5-di(adenosine-5')-pentaphosphate (an inhibitor of adenylate kinase) only ADP is effective. Also the release of accumulated Ca2+ observed when approximately 50% Mg2+ is discharged is retarded by bongkrekate and added Mg2+ whereas it is accelerated by atractylate. All adenine nucleotides have a significant effect in retarding the efflux of accumulated Ca2+ but, in the presence of oligomycin and P1,P5-di(adenosine-5')-pentaphosphate, only ADP is active. From these results we conclude that effluxes of Mg2+, Ca2+ and adenine nucleotide from rat liver mitochondria induced by external phosphate are interconnected and regulated by external ADP and Mg2+ levels.

Adenine Nucleotides↗
PubMed1978

Efflux of magnesium and potassium ions from liver mitochondria induced by inorganic phosphate and by diamide.

Addition to rat liver mitochondria of 2 mM inorganic phosphate or 0.15 mM diamide, a thiol-oxidizing agent, induced an efflux of endogenous Mg2+ linear with time and dependent on coupled respiration. No net Ca2+ release occurred under these conditions, while a concomitant release of K+ was observed. Mg2+ efflux mediated either by Pi or low concentration of diamide was completely prevented by EGTA, Ruthenium red, and NEM. These reagents also inhibited the increased rate of state 4 respiration induced both by Pi and diamide. At higher concentrations (0.4 mM), diamide induced an efflux of Mg2+ which was associated also with a release of endogenous Ca2+. Under these conditions EGTA completely prevented Mg2+ and K+ effluxes, while they were only partially inhibited by Ruthenium red and NEM. It is assumed that Mg2+ efflux, occurring at low diamide concentrations or in the presence of phosphate, is dependent on a cyclic in-and-out movement of Ca2+ across the inner mitochondrial membrane, in which the passive efflux is compensated by a continuous energy linked reuptake. This explains the dependence of Mg2+ efflux on coupled respiration, as well as the increased rate of state 4 respiration. The dependence of Mg2+ efflux on phosphate transport is explained by the phosphate requirement for Ca2+ movement.

Animals↗