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Biomedical subjects

F Stirpe

Publications and source records attributed to F Stirpe.

At least 199 records · Page 11Linked to original sources
PubMed1968

Regulation of rat liver pyruvate kinase. The effect of preincubation, pH, copper ions, fructose 1,6-diphosphate and dietary changes on enzyme activity.

1. Preincubation of partially purified rat liver L-type pyruvate kinase at 25 degrees for 10min. causes a marked increase in co-operativity with respect to both the substrate, phosphoenolpyruvate, and the allosteric activator, fructose 1,6-diphosphate. 2. The results are consistent with the existence of two forms of liver L-type pyruvate kinase, designated forms L(A) and L(B). It is postulated that form L(A) has a low K(m) for phosphoenolpyruvate (about 0.1mm) and is not allosterically activated, whereas form L(B) is allosterically activated by fructose 1,6-diphosphate, exhibiting in the absence of the activator sigmoidal kinetics with half-maximal activity at about 1mm-phosphoenolpyruvate. In the presence of fructose 1,6-diphosphate, form L(B) gives Michaelis-Menten kinetics with K(m) less than 0.1mm. It is further postulated that preincubation converts form L(A) into form L(B). 3. The influence of pH on the preincubation effect was studied. 4. The inhibition of pyruvate kinase by Cu(2+) was studied in detail. Though phosphoenolpyruvate and fructose 1,6-diphosphate readily protect the enzyme against Cu(2+) inhibition, little evidence of significant reversal of the inhibition by these compounds could be found. 5. The effects of starvation, fructose feeding and preincubation on the pyruvate kinase activity of crude homogenates of various tissues of the rat were also studied.

Animals↗
PubMed1967

Regulation of xanthine dehydrogenase in chick liver. Further experiments on the effects of inosine, actinomycin D and other factors.

1. It has been confirmed that the xanthine-dehydrogenase activity of chick liver is enhanced by starvation and by administration of inosine; the effects of these treatments are not additive. 2. Inosine has no effect when given to chicks depleted of the enzyme by feeding a low-protein diet. 3. Actinomycin D prevents the effect of inosine, but itself enhances the activity of xanthine dehydrogenase. 4. The xanthine-dehydrogenase activity is unchanged after addition of orotic acid to the diet, and is stimulated by injection of inorganic iron.

Acids↗
PubMed1967

Studies on the pathogenesis of liver necrosis by alpha-amanitin. Effect of alpha-amanitin on ribonucleic acid synthesis and on ribonucleic acid polymerase in mouse liver nuclei.

1. Injection of alpha-amanitin to mice causes a decreased incorporation of [6-(14)C]-orotic acid into liver RNA in vivo. 2. The activity of RNA polymerase activated by Mn(2+) and ammonium sulphate is greatly impaired in liver nuclei isolated from mice poisoned with alpha-amanitin, and is inhibited by the addition of the same toxin in vitro. 3. The activity of the Mg(2+)-activated RNA polymerase is only slightly affected by alpha-amanitin either administered to mice or added in vitro.

Animals↗
PubMed1965

Regulation of ascorbic acid and of xylulose synthesis in rat-liver extracts. The effect of alloxan-diabetes on the glucuronic acid pathway.

1. The synthesis of l-ascorbic acid and of l-xylulose from d-glucuronolactone, d-glucuronate, l-gulonate and l-gulonolactone has been studied with liver extracts from normal and alloxan-diabetic rats. 2. In diabetic animals the synthesis of ascorbic acid is impaired, and more from glucuronolactone and glucuronate than from gulonate and gulonolactone, whereas the formation of xylulose from gulonate and gulonolactone is enhanced. These changes are reversed by insulin therapy. 3. The activity of the NAD-linked gulonate dehydrogenase is enhanced during diabetes.

Journal Article↗
PubMedDate not supplied

On the distribution of ribosome-inactivating proteins amongst plants.

The extracts from various parts (mostly seeds) of 56 different plants were examined for inhibition of protein synthesis by a rabbit reticulocyte lysate. Most extracts inhibited protein synthesis with an ID50 (concentration giving 50% inhibition) of 100 micrograms extract protein per ml, or less. The extracts with high activity were partially purified by CM cellulose chromatography. Protein-containing fractions were separated which inhibited protein synthesis and resembled the ribosome-inactivating proteins from plants previously described. Thus, ribosome-inactivating proteins appear to be virtually ubiquitous in plants.

Animals↗
PubMedDate not supplied

Neuronotoxicity of axonally transported toxic lectins, abrin, modeccin and volkensin in rat peripheral nervous system.

In an attempt to find new and more useful suicide transport agents, the cytotoxic lectins abrin, modeccin and volkensin were pressure microinjected into peripheral nerves (vagus, hypoglossal and sciatic) of adult rats. After 33 h-5 days survival, the brainstems, spinal cords and corresponding sensory ganglia were examined histologically. All three lectins produced profound chromatolysis, and destruction of sensory and motor neurons projecting axons through the injected nerves. Volkensin and modeccin were significantly more potent than any previously reported suicide transport agent. It is concluded that abrin, modeccin and volkensin are effective, unselective suicide transport agents in the rat peripheral nervous system but none is clearly superior to ricin for making restricted sensory and motor neuron ablations. However, modeccin and volkensin are fundamentally different from any previously reported suicide transport agents with respect to spread within the CNS which destroyed neurons adjacent to those initially taking up and transporting the toxin. Possibly this is due to the different oligosaccharide binding specificity of modeccin and volkensin compared to other suicide transport agents. Modeccin and/or volkensin may prove useful in making lesions of CNS interneurons using the suicide transport strategy.

Abrin↗
PubMedDate not supplied

Toxicity of xanthine oxidoreductase to malignant B lymphocytes.

Reactive oxygen species (ROS) generated by xanthine oxidoreductase (XOR) were toxic to B lymphoma-derived Raji cells (positive for 8A monoclonal antibody, mAb). The sensitivity of these malignant cells to the hypoxanthine/XOR system was higher than that observed in peripheral human lymphocytes. The understanding of the mechanisms of cytotoxicity induced by XOR-produced ROS is essential in view of a possible clinical application. Cell death mostly had the feature of apoptosis and post-apoptotic necrosis and depended on the activity of XOR. Catalase, but not superoxide dismutase, protected cells from the toxicity of XOR, thus indicating that cell damage depended on the production of hydrogen peroxide. The toxicity of ROS was selectively targeted to malignant Raji cells by antibody-XOR conjugation, either directly, with an 8A-XOR conjugate, or indirectly, with an 8A mAb plus an anti-mouse IgG-XOR. Both direct and indirect immunotoxins induced apoptotic death to target cells in a dose-dependent manner. These conjugates showed no aspecific cytotoxicity in conditions very similar to the ex vivo treatment of cell suspension for bone marrow transplantation. Moreover, the prevalence of apoptotic death over necrosis may reduce the in vivo inflammatory response and its local and systemic consequences, thus becoming relevant in the construction of immunotoxins with therapeutic potential.

Animals↗