PubMed Health⌕ Search

Biomedical subjects

L Landi

Publications and source records attributed to L Landi.

85 records · Page 5Linked to original sources

Coenzyme Q-3 as an antioxidant. Its effect on the composition and structural properties of phospholipid vesicles.

Coenzyme Q-3 incorporated into the lipid bilayer at physiological concentration provided an 80% inhibition of the lipid peroxidation induced by ferrous ions. In coenzyme Q-containing vesicles, the fluorescence lifetime and the fluorescence anisotropy decay of the probe, 1,6-diphenyl-1,3,5-hexatriene, were measured in order to find out if the presence of the quinone can cause variations in the membrane organization. Our data show that two distinct populations of the probe were present and that both populations were available to quenching by coenzyme Q. The overall effects of coenzyme Q on the static and dynamic properties of the model membranes were: a very small effect in the ordering of the fatty acid chain, and a more noticeable decrease of the probe correlation time and, therefore, an increase in membrane fluidity at increasing quinone concentration. When vesicles were peroxidized in the absence of the coenzyme Q, the fluidity markedly decreased; in its presence, the fluidity was nearly unchanged. The results suggest that the antioxidant properties of coenzyme Q can be ascribed to its ability to react with free radicals. The effect on the fluidity of the lipid bilayer might imply that a requisite for a molecule to act as an efficient antioxidant could be its ability to readily diffuse within the membrane.

Antioxidants↗

Histomorphometric evaluation of extraction sockets and deficient alveolar ridges treated with allograft and barrier membrane: a pilot study.

The aim of the study was to determine the fate of demineralized freeze-dried bone allograft (DFDBA) used in conjunction with a barrier membrane in the management of extraction sockets and deficient alveolar ridges, and to compare the amount of bone formed with that found in untreated sites. Ten biopsies were obtained from 8 grafted patients. Five biopsies were harvested from untreated sites during routine implant placement and analyzed for comparison. In the socket management procedure, DFDBA was packed tightly into the socket and covered with an expanded polytetrafluoroethylene (e-PTFE) membrane. Primary closure was achieved in all cases. In the ridge regeneration procedure, cortical columns were placed in the ridge projecting outward approximately 3 mm to create and maintain space for DFDBA particles packed between them; the columns were then covered by an e-PTFE membrane. Healing time ranged from 8 to 23 months. At the time of implant placement, bone cores (7 mm x 2 mm) were harvested, fixed in 10% formalin solution, and prepared for histologic examination. At the light microscopic level, no inflammation or fibrous encapsulation was observed. New bone formation on and around DFDBA particles was widespread. Histomorphometric analysis of the grafted specimens and untreated sites was carried out using the trabecular bone volume (TBV) index. The TBV in the maxillary test specimens was 55.03%, as compared to 57.33% of control cores. Unaltered DFDBA made up 8.7% of the test specimens. In the mandibular biopsies, the TBV was 56.6%, while for the controls it was 40.9%. The volume of DFDBA still present was 2.45%. The results tended to indicate that treatment with DFDBA in conjunction with cell occlusive membranes will result in new bone formation, predominantly by the process of conduction, which appears to be similar in amount and nature to that found in cores harvested from healed nonfunctional edentulous areas.

Adult↗

Fromation and stoichiometry of a lysozyme-phospholipid-mitochondrial protein ternary complex.

Mitochondrial membranes reconstituted from lipid-depleted mitochondria and aqueous phospholipid dispersions still have the phospholipid negative charges available for ionic interaction with the basic protein, lysozyme. The stoichiometry of the binding is of about 6 nmoles of lysozyme per 100 nmoles of phospholipid in membranes reconstituted with Asolectin, and of 10 nmoles of phospholipid phosphorus in membranes reconstituted with cardiolipin. Unextracted submitochondrial particles ETP also bind lysozyme (about 3 nmoles per 100 nmoles of phospholipid). These observations indicate that the phospholipid anionic groups are not completely shielded by the mitochondrial proteins, which might occupy areas between the nonpolar groups of the lipid molecules.

Animals↗

A conformational model of the action of general anesthetics at the membrane level. III. Anesthetics and the properties of membrane-bound enzymes: mitochondrial ATPase.

We have studied the effect of general anesthetics on the kinetic properties of the mitochondrial Mg2+-dependent ATPase. The enzyme is inhibited by anesthetics (alcohols, halotane, pentrane, ketamine) at concentrations of the order of those found to affect lipid-protein interactions. The inhibition appears usually uncompetitive with respect to the substrate, ATP, with a decrease of both Vmax and KM, indicating a possible stabilization of the enzyme-substrate complex. Arrhenius plots of ATPase activity show a striking increase in activation energy below 17-20 degrees C. Anesthetics affect the temperature dependence by increasing the activation energy above the break or abolishing the break whatsoever. An exception is diethyl ether, that induces a decrease in activation energy and a shift of the break to lower temperatures. Anesthetics make the ATPase insensitive to energy transfer inhibitor, oligomycin and dicyclohexyl carbodiimide. At low anesthetic concentration the oligomycin inhibition curve is changed from sigmoidal to hyperbolic, showing a loss of cooperativity in the inhibition.

Adenosine Triphosphatases↗

Reactions of oxygen radicals with the quinone ring of coenzyme Q.

Coenzyme Q, besides its role in electron transfer reactions, may act as a radical scavenger. The effect of oxygen radicals produced by ultrasonic irradiation on the quinone ring was investigated. Aqueous solutions of a Q homologue, completely lacking the side chain, were irradiated and the modifications were spectrophotometrically followed. The experimental results show that both degradation and reduction of the benzoquinone ring took place when the irradiation was performed in water. Data obtained when ultrasonic irradiation was carried out in the presence of OH. scavengers, as formate, organic and inorganic buffers, suggest: a) the responsible species for most the ubiquinol generated by sonication appeared to be the superoxide radical b) addition reactions of OH. radicals with the aromatic ring led probably to the degradation of Coenzyme Q molecules.

Formates↗

Incorporation of ubiquinones into lipid vesicles and inhibition of lipid peroxidation.

Ubiquinone incorporation into vesicles to evaluate its antioxidative effect on lipid peroxidation has been studied. Only sonication and not vortication allows comparable incorporation patterns of the various ubiquinone homologues into lipid vesicles. The measure of malondialdehyde, a convenient index for determining the extent of autoxidation, shows that both the naturally occurring homologues and synthetic shorter-chain ones, also in the oxidized form, possess similar antioxidant efficiency.

Antioxidants↗

Effects of extraction of ubiquinone on succinate-ferricyanide reductase activity.

The effects of extraction and reincorporation of ubiquinone on succinate dehydrogenase of mitochondrial membranes have been studied. The succinate dehydrogenase activity, measured with ferricyanide as electron acceptor, was diminished by approximatively 75% upon the extraction of ubiquinone and was restored when ubiquinone was reincorporated into the membranes. A study in a model system represented by ubiquinols incorporated in liposomes shows that the initial rates of ubiquinol oxidation by external ferricyanide are almost two order of magnitude lower than the rates of succinate-ferricyanide reductase in mitochondria. It is therefore concluded that the compound feeding electrons to ferricyanide in damaged mitochondria is either ubiquinone in a bound form or a compound between UQ and the antimycin block.

Animals↗