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Biomedical subjects

C Guarnieri

Publications and source records attributed to C Guarnieri.

At least 127 records · Page 7Linked to original sources

Effect of oxygen radicals and hyperoxia on rat heart ornithine decarboxylase activity.

Rat heart ornithine decarboxylate activity from isoproterenol-treated rats was inactivated in vitro by reactive species of oxygen generated by the reaction xanthine/xanthine oxidase. Reduced glutathione, dithiothreitol and superoxide dismutase has a protective effect in homogenates and in partially purified ornithine decarboxylase exposed to the xanthine/xanthine oxidase reaction, while diethyldithiocarbamate, which is an inhibitor of superoxide dismutase, potentiated the damage induced by O2- on enzyme activity. Dithiothreitol at concentrations above 1.25 mM had an inhibitory effect upon supernatant ornithine decarboxylase activity, while at 2.5 mM it was most effective in the recovery of ornithine decarboxylase activity, after the purification of the enzyme by the ammonium sulphate precipitation procedure. The ornithine decarboxylase inactivated by the xanthine/xanthine oxidase reaction showed a higher value of Km and a reduction of Vmax with respect to control activity. The exposure of rats to 100% oxygen for 3 h reduced significantly the isoproterenol-induced heart ornithine decarboxylase activity. The injection with diethyldithiocarbamate 1 h before hyperoxic exposure further reduced heart ornithine decarboxylase activity.

Animals↗

Myocardial mitochondrial functions in alpha-tocopherol-deficient and -refed rabbits.

In mitochondria from alpha-tocopherol-deficient rabbit hearts (30 days), there was a close correlation between the decline in respiration and the incidence of membrane peroxidation. In the same mitochondria, an increased formation of oxygen radicals was also observed, whereas superoxide dismutase activity was only slightly depressed. The exposure of mitochondria to exogeneous oxygen radicals generated by a xanthine-xanthine oxidase system caused a marked decrease in their oxidative phosphorylation capacity associated with an increase in lipid peroxidation breakdown. This was particularly evident in mitochondria from alpha-tocopherol-deficient rabbits. In mitochondria from deficient animals that had been rehabilitated with alpha-tocopherol, the toxic effect of oxygen radicals was less evident.

Adenosine Diphosphate↗

Effect of oxygen radicals on heart mitochondrial function in alpha-tocopherol deficient rabbits.

The mitochondria extracted from hearts of alpha-tocopherol deficient rabbits showed a decreased mitochondrial function and an increased formation of oxygen radicals associated with a decreased superoxide dismutase activity. The exposure of the alpha-tocopherol deficient mitochondria to exogeneous oxygen radicals caused a marked decrease in the mitochondrial function with respect to control mitochondria, which was partially reversed by the addition in vitro of alpha-tocopherol.

Animals↗

[Heart muscle mitochondria function in alpha-tocopherol deficient rabbits. (author's transl)].

In the mitochondria of alpha-tocopherol deficient rabbit hearts (30 days) there was a close correlation between the decline in respiration and the incidence of membrane peroxidation. The intraperitoneal injections of alpha-tocopherol (25 mg/kg) from the the 28th day to the 30th day to the vitamin E deficient rabbits prevented a decline in either the mitochondrial respiratory or in the lipid peroxidation breakdown. The addition of alpha-tocopherol "in vitro" to the alpha-tocopherol deficient cardiac mitochondria failed to improve their function. As a result of this study, the possibility that the alpha-tocopherol may protect the cardiac mitochondrial activity by preserving their integrity appears to be consolidated.

Animals↗

A possible role of rabbit heart cytosol tocopherol binding in the transfer of tocopherol into nuclei.

An alpha-tocopherol-binding macromolecule was isolated from the heart cytosol of rabbits fed for 1 month with an alpha-tocopherol-deficient diet. The amount of [3H]-tocopherol bound to nuclear chromatin was increased when the alpha-tocopherol-deficient heart nuclei were incubated in the presence of [3H]tocopherol-cytosol complex. In this condition, large amounts of [3H]tocopherol were associated with a subnuclear fraction that contained non-histone acidic proteins.

Animals↗

[Specific activity and release of norepinephrine in isolated and perfused rabbit hearts under various oxygen pressure].

The incorporation of 3H-tyrosine into norepinephrine of rabbit hearts perfused with Krebs-Henseleit solution containing 11 mM glucose and gassed with 95% O2 - 5% CO2 (control) or 80% O2 - 5% CO2 15% N2 (hypoxic) or 95% N2 - 5% CO2 (anoxic), was studied. In the control hearts a constant specific activity of norepinephrine without any release of catecholamine into coronary effluent was measured after 5, 15, 30, 60 minutes. The hypoxic perfusion while not causing any release of norepinephrine, produced a significant increase in tyrosine incorporation into norepinephrine. The specific activity of norepinephrine and its release into coronary effluent were increased by anoxic perfusion; this effect was most evident when the glucose was replaced with a solution containing 11 mM mannitol. These results suggest that the synthesis of norepinephrine in isolated hearts, lacking of sympathetic innervation, may be affected by different condition of oxygen supply.

Animals↗

RNA and protein synthesis in rat brain during exercise. Effect of arginine and some phosphorylated amino acids.

RNA and protein synthesis is noticeably depressed in the brain of swimming rats. Repeated oral administration of phosphothreonine, phosphoserine or arginine is susceptible of improving brain macromolecular synthesis. A parallel induction is observed on spermine and spermidine accumulation, particularly evident when arginine is used. The anti-fatigue effect of phosphorylated amino acids or arginine may be associated with the observed restoration of brain macromolecular synthesis via polyamine accumulation.

Amino Acids↗