PubMed Health⌕ Search

Biomedical subjects

L Landi

Publications and source records attributed to L Landi.

At least 55 records · Page 3Linked to original sources
PubMed1992

Antioxidant activity of ubiquinone-3 in human low density lipoprotein.

The ability of ubiquinone-3, a short chain ubiquinone homologue, to prevent Cu2+ induced oxidation of human low density lipoprotein was investigated. The results are as follows: in the presence of ubiquinone-3 the extent of peroxidation, as determined by the formation of thiobarbituric acid reactive substances, was only one third of that found in its absence; the quinone can also prevent the fragmentation of apolipoprotein B-100 and the increase of the net negative surface charge of the particle.

Apolipoprotein B-100↗
PubMed1992

In vitro methods to evaluate metal-cell interactions.

The aim of this study was to test different metals, widely employed in constructing prosthetic devices, by in vitro methods. Biological effects of such materials were analyzed through four different assays on human lymphocytes and granulocytes. The lymphocyte proliferation assay gave quantitative results, while the viability test showed the morphological appearance of the cells correlated well with previous results. NK cytotoxicity and granulocyte chemokinesis tests provided interesting data on leucocyte performance when challenged with metals. Therefore the present study adds new basic information on cell behaviour when metal products are present in the body, e.g. around devices implanted in human tissues.

Biocompatible Materials↗
PubMed1991

The role of the side chain in the antioxidant activity of ubiquinones.

The question has been addressed whether the side chain contributes to the antioxidant activity of Ubiquinones. The length, the chemical composition and structure of the chain have been considered. The effect of the actual concentration of the quinone in egg lecithin vesicles has been investigated by means of both UV spectroscopy and time resolved fluorescence quenching experiments of 12-AS. The results indicate that the antioxidant properties of the quinone do not seem to depend on the side chain.

Antioxidants↗
PubMed1991

Ubiquinol prevents alpha-tocopherol consumption during liposome peroxidation.

In this study we investigated whether alpha-tocopherol can be spared by ubiquinol-3 during autoxidation of multilamellar liposome. A lipophilic azocompound, 2,2'-azobis-(2,4-dimethyl-valeronitrile), was chosen to initiate liposome autoxidation. The effect of either alpha-tocopherol, ubiquinol-3, or a mixture of them was compared. Rates of conjugated diene formation and concomitant disappearance of the two antioxidants was measured. Since the inhibition rate constant for the scavenging of peroxyl radical for alpha-tocopherol was higher than that for quinol-3, it was concluded that alpha-tocopherol is regenerated by ubiquinol-3.

Free Radicals↗
PubMed1990

Inhibition of autoxidation of egg yolk phosphatidylcholine in homogenous solution and in liposomes by oxidized ubiquinone.

The aim of this study was to obtain a quantification of the antioxidant activity of ubiquinone. To this purpose the oxidation of egg yolk phosphatidylcholine both in solvent and in liposomes initiated by an azocompound has been studied either in the absence or in the presence of ubiquinone-3, using alpha-tocopherol as a reference antioxidant. The two experimental systems gave similar results. In the presence of ubiquinone-3 the oxidation rate was reduced with respect to control experiments but was faster than that in the presence of alpha-tocopherol. The amount of ubiquinone required to decrease the autoxidation rate was so high as to prevent detection of the induction period. The stoichiometric factor was greater than 2 and the rate constant of inhibition was two orders of magnitude lower than that of alpha-tocopherol. It is concluded that high concentrations of ubiquinone are required to exhibit significant antioxidant activity. A possible mechanism compatible with the stoichiometric factor larger than 2 for the inhibiting effect of ubiquinone is also suggested.

Liposomes↗
PubMed1989

The influence of polyunsaturated fatty acids on spermine inhibition of lipoperoxidation. Studies on liposomes prepared with microsomal and mitochondrial phospholipids of sea bass (Dicentrarchus labrax L.) and rat liver.

1. Composition of phospholipids extracted from different organelles of European sea bass liver was determined and compared with that of phospholipids extracted from the same organelles of rat liver. 2. Spermine binding to the vesicles prepared from microsomal and mitochondrial phospholipids and their aggregation was studied: these parameters indicate that only the presence of acidic phospholipids and not their unsaturation was essential for polyamine action. 3. No correlation exists between polyunsaturated fatty acid and spermine inhibition of lipid peroxidation. In fact microsomal phospholipids, which have a low content of acidic phospholipids, and a prevalent presence of phosphatidylinositol, are not protected by spermine. 4. Mitochondrial phospholipids, which have high content of cardiolipin, elicit the capability of spermine to inhibit lipid peroxidation.

Animals↗
PubMed1989

Buffers can modulate the effect of sonication on egg lecithin liposomes.

When model membranes are prepared by ultrasonic irradiation of polyunsaturated phospholipids, radical production can induce a partial degradation of the polyunsaturated fatty acyl chains and the formation of lipid hydroperoxides. A suitable buffer employed during liposome preparation, like Hepes or Tris, is able to exhibit a protective effect against lipid peroxidation. Hepes has been found to be the most effective: a 10 mM concentration provides a 70% protection after 30 min sonication. Tris, in the same conditions, exhibits a 50% protection. These findings may be explained on the basis of the rate constants of these organic buffers with hydroxyl radicals.

Buffers↗
PubMed1989

Lipid peroxidation. Definition of experimental conditions for selective study of the propagation and termination phases.

To find experimental conditions to selectively study the propagation phase of lipoperoxidation we studied the lipoperoxidation, catalyzed by FeCl2, of liposomes in a buffering condition where Fe2+ autoxidation and oxygen active species generation does not occur. Liposomes from egg yolk phosphatidylcholine, prepared by vortex mixing, do not oxidize Fe2+; on the contrary they oxidize Fe2+ when prepared by ultrasonic irradiation. Dimyristoyl phosphatidylcholine liposomes prepared by ultrasonic irradiation do not oxidize Fe2+. During sonication polyunsaturated fatty acid residues autoxidize and lipid hydroperoxides (LOOH) are generated. Only when LOOH are present in the liposomes Fe2+ oxidizes and its rate of oxidation depends on the amount of LOOH in the assay. The reaction results in the generation of both LOOH and thiobarbituric acid reactive material (TBAR); it is inhibited by butylated hydroxytoluene and has a acidic pH optimum; it is not inhibited by catalase and OH scavengers. The reaction studied, thus, appears to be the chain branching and propagation phase of lipoperoxidation. When we studied the dependence of Fe2+ oxidation, LOOH and TBAR generation on FeCl2 concentration, we observed that at high FeCl2 concentrations the termination phase of lipoperoxidation was prevalent. Thus, by selecting the appropriate FeCl2 concentration the proposed experimental system allows study of either the propagation or the termination phase of lipoperoxidation.

Ferrous Compounds↗
PubMed1988

Differences in carbohydrate tolerance in Turner syndrome depending on age and karyotype.

Carbohydrate homeostasis was evaluated in 47 girls with Turner syndrome and in 25 "short normal" girls by means of an oral glucose tolerance test. Of the Turner patients 34% showed an impaired glucose tolerance vs 8% of the controls (chi 2 = 5.9, P less than 0.05). Mean glucose levels were significantly higher and mean insulin levels and insulinogenic index significantly lower in young Turner patients aged 5-12 years but not in adolescents aged 12-16 years. In both groups of patients, insulin levels and the insulinogenic index were significantly lower than those of the controls. In Turner patients between 12 and 16 years, carbohydrate tolerance improved and this may be explained by the lack of oestrogen release in these patients. Glucose tolerance was normal in patients with mosaicism. We conclude that (1) carbohydrate tolerance is defective in young children with Turner syndrome but improves in puberty due to the almost complete absence of oestrogen-progestogen secretion; (2) a difference in carbohydrate tolerance is evident depending on karyotype.

Adolescent↗
PubMed1987

Protective effect of endogenous coenzyme Q on both lipid peroxidation and respiratory chain inactivation induced by an adriamycin-iron complex.

Mitochondria from beef heart have been partially depleted of coenzyme Q by pentane extraction. It has been found that lipid peroxidation induced by an adriamycin-iron complex proceeds at a higher rate in this preparation than in coenzyme Q reincorporated mitochondria. Moreover in coenzyme Q depleted mitochondria both NADH and succinate oxidase activities result more affected. These observations indicate that endogenous coenzyme Q can effectively protect mitochondria from membrane lipid oxidative damage induced by adriamycin-iron and can reduce the inactivation of NADH and succinate oxidases.

Animals↗
PubMed1987

Effect of oxygen free radicals on ubiquinone in aqueous solution and phospholipid vesicles.

The purpose of this study was to evaluate the direct effect of oxygen free radicals produced by ultrasonic irradiation on ubiquinone and to compare the efficiency with which the antioxidant can compete with these radicals when it is both in aqueous solution and within the lipid bilayer. The main product obtained after insonation of aqueous solutions of ubiquinone-0 was ubiquinol, moreover some degradation occurred. The direct electron donor responsible for most of the ubiquinol generated by ultrasonic irradiation appeared to be superoxide radical. Addition reactions of hydroxyl radicals with aromatic ring structure led probably to degradation products of ubiquinone, which were not identified. Experiments were also performed to evaluate the efficiency with which ubiquinone-3 could react with oxygen radicals when it was within the lipid bilayer. The effect of presence or absence of a net surface charge was studied selecting a suitable bilayer including dimyristylphosphatidic acid or stearylamine in uncharged dimyristylphosphatidylcholine vesicles. In these systems hydroxyl radicals did not represent a potential danger for the antioxidant, the reaction between superoxide and ubiquinone-3 instead was significant only in positively charged membranes and gave rise to ubiquinol. It is suggested that ubiquinone acts as an antioxidant by stopping the propagation reaction.

Antioxidants↗
PubMed1986

Antioxidant behaviour of ubiquinone and beta-carotene incorporated in model membranes.

Experiments with model membranes, in which ubiquinone was incorporated, were performed in order to clarify the mechanism by which ubiquinone can prevent or control chain lipid peroxidation in biomembranes. Comparing the behavior of ubiquinone-containing vesicles with beta-carotene containing vesicles we suggest that a possible explanation of the ubiquinone antioxidant effect could be to scavenge singlet oxygen and to affect structurally the lipid bilayer inhibiting hydroperoxide decomposition.

Antioxidants↗
PubMed1985

Effect of ubiquinone extraction on the reaction of the mitochondrial bc1 complex with ferricyanide.

Depletion of endogenous ubiquinone by pentane extraction of mitochondrial membranes lowered succinate-ferricyanide reductase activity, whereas quinone reincorporation restored the enzymatic activity as well as antimycin sensitivity. The oxidant-induced cytochrome b extrareduction, normally found upon ferricyanide pulse in intact mitochondria in the presence of antimycin, was lost in ubiquinone-depleted membranes, even if cytochrome c was added. Readdition of ubiquinone-2 restored the oxidant-induced extrareduction with an apparent half saturation at 1 mol/mol bc1 complex saturating at about 5 mol/mol. These findings demonstrate a requirement for the ubiquinone pool of the cytochrome b extrareduction. Since the initial rates of cytochrome b reoxidation upon ferricyanide addition, in the presence of antimycin, did not saturate by any ferricyanide concentration in ubiquinone-depleted mitochondria, a direct chemical reaction between ferricyanide and reduced cytochrome b was postulated. The fact that such direct reaction is much faster in ubiquinone-depleted mitochondria may explain the lower antimycin sensitivity of the succinate ferricyanide reductase activity after removal of endogenous ubiquinone.

Animals↗
PubMed1984

Antioxidative effect of ubiquinones on mitochondrial membranes.

Peroxidation of mitochondria occurs extensively in ubiquinone-depleted membranes. Reincorporation into the membranes of either the physiological ubiquinone or a short-chain homologue protects mitochondria against peroxidation. The ability to prevent this phenomenon is more evident in mitochondria that have incorporated ubiquinone-3 and might be ascribed to an ordering structural effect on the lipid bilayer.

Animals↗
PubMed1984

Polyamine binding to phospholipid vesicles and inhibition of lipid peroxidation.

A study of the possible mechanism of inhibition by polyamines of lipid peroxidation was made utilizing vesicles prepared with mixed soy bean phospholipids. The results obtained can be summarized as follows: 1) Polyamines inhibit lipid peroxidation only when bound to the negative charges on vesicle surface. 2) Polyamines inhibit lipid peroxidation at concentrations lower than those required to cause precipitation of the vesicles and similar to those required for formation of the polyamine/phospholipid vesicle complex. 3) Spermine bound to vesicles, in contrast to free spermine, highly decreases the reactivity of both Fe2+ and Fe3+ versus superoxide.

Cations, Divalent↗
PubMed1984

On the mechanism of inhibition of NADH oxidase by ubiquinone-3.

The combined effects of rotenone and ubiquinone-3 on the kinetics of NADH dehydrogenase and NADH oxidase have been investigated. The two inhibitors do not show additivity; on the other hand, ubiquinone-3, when preincubated with the enzyme, partially removes rotenone sensitivity. The inhibition of NADH oxidase by ubiquinone-3 is the result of at least two combined effects: the competition of the less active ubiquinone-3 with endogenous ubiquinone-10 in the acceptor site of the dehydrogenase, and a nonspecific action on the structure of complex I. The latter effect is perhaps mediated by a physical change of the phospholipid bilayer similar to that observed with agents such as butanol, perturbing lipid-protein interactions in the membrane.

Animals↗