Search

Your search keyword '"De Bellis Vitti, G"' showing total 8 results
Start Over Author "De Bellis Vitti, G"
8 results on '"De Bellis Vitti, G"'

3. Unbalanced plasma control of TxA2 and PGI2 synthesis in Vitamin E deficient rats

Author

Falanga, A, Doni, M, Delaini, F, de Bellis Vitti, G, Imberti, L, Donati, M, Gaetano, G, Doni, MG, Donati, MB, Falanga, A, Doni, M, Delaini, F, de Bellis Vitti, G, Imberti, L, Donati, M, Gaetano, G, Doni, MG, and Donati, MB

Abstract

Factors contributing to the antioxidant power of plasma may play a role in the control of arachidonic acid (AA) metabolism. The purpose of this study was to evaluate the possible effects of vitamin E deficiency on platelet and vascular prostaglandin synthesis. CD-COBS male rats were fed for 7 mo a diet containing either 1 or 75 mg/kg vitamin E. At the end of this period, serum levels of vitamin E were 0.4 +/- 0.1 and 10 +/- 0.6 micrograms/ml in the two groups, respectively. Malondialdehyde (MDA) generation by AA was significantly higher in platelet-rich plasma from vitamin E-deficient rats. Thromboxane B2 (TxB2) in serum from vitamin E-deficient rats increased about 16 times compared with controls, whereas 6-keto-PGF1 alpha levels increased only 3 times. The ratio between TxB2 and 6-keto-PGF1 alpha, increased therefore manyfold in vitamin E-deficient animals. MDA formation and [14C]AA metabolism in washed platelets were similar in the two groups of animals. No significant difference was found in the PGI2 (prostacyclin) antiaggregating activity released from the aortic rings resuspended in buffer. In contrast, the capacity of plasma to stimulate PGI2 activity from "exhausted" aortic rings (prostacyclin-stimulating factor) was significantly reduced in vitamin E-deficient animals. In conclusion, vitamin E deficiency induces an unbalanced plasma regulation of AA metabolism. This results in an excessive production of platelet TxA2 compared with vascular PGI2 generation. On the other hand, vitamin E deficiency does not seem to affect directly the enzymatic pathways of AA metabolism

Published
1983

6. Unbalanced plasma control of TxA2 and PGI2 synthesis in Vitamin E deficient rats

Author

M.B. Donati, G. De Bellis Vitti, M. G. Doni, G. de Gaetano, L. Imberti, Anna Falanga, F Delaini, Falanga, A, Doni, M, Delaini, F, de Bellis Vitti, G, Imberti, L, Donati, M, and Gaetano, G

Subjects
Blood Platelets, Male, Vitamin, medicine.medical_specialty, Antioxidant, Physiology, medicine.medical_treatment, Prostacyclin, 6-Ketoprostaglandin F1 alpha, Arachidonic Acids, Thromboxane A2, chemistry.chemical_compound, Physiology (medical), Internal medicine, medicine, Animals, Vitamin E Deficiency, Tocopherol, Arachidonic Acid, plasma control, TxA2, PGI2 synthesis, Vitamin E, Chemistry, Vitamin E, Thromboxanes, Rats, Inbred Strains, Malondialdehyde, Epoprostenol, Rats, Thromboxane B2, Endocrinology, lipids (amino acids, peptides, and proteins), Vitamin E deficiency, Cardiology and Cardiovascular Medicine, medicine.drug
Abstract

Factors contributing to the antioxidant power of plasma may play a role in the control of arachidonic acid (AA) metabolism. The purpose of this study was to evaluate the possible effects of vitamin E deficiency on platelet and vascular prostaglandin synthesis. CD-COBS male rats were fed for 7 mo a diet containing either 1 or 75 mg/kg vitamin E. At the end of this period, serum levels of vitamin E were 0.4 +/- 0.1 and 10 +/- 0.6 micrograms/ml in the two groups, respectively. Malondialdehyde (MDA) generation by AA was significantly higher in platelet-rich plasma from vitamin E-deficient rats. Thromboxane B2 (TxB2) in serum from vitamin E-deficient rats increased about 16 times compared with controls, whereas 6-keto-PGF1 alpha levels increased only 3 times. The ratio between TxB2 and 6-keto-PGF1 alpha, increased therefore manyfold in vitamin E-deficient animals. MDA formation and [14C]AA metabolism in washed platelets were similar in the two groups of animals. No significant difference was found in the PGI2 (prostacyclin) antiaggregating activity released from the aortic rings resuspended in buffer. In contrast, the capacity of plasma to stimulate PGI2 activity from "exhausted" aortic rings (prostacyclin-stimulating factor) was significantly reduced in vitamin E-deficient animals. In conclusion, vitamin E deficiency induces an unbalanced plasma regulation of AA metabolism. This results in an excessive production of platelet TxA2 compared with vascular PGI2 generation. On the other hand, vitamin E deficiency does not seem to affect directly the enzymatic pathways of AA metabolism.

Published
1983

7. Warfarin inhibits both procoagulant activity and metastatic capacity of Lewis lung carcinoma cells. Role of vitamin K deficiency.

Author

Colucci M, Delaini F, de Bellis Vitti G, Locati D, Poggi A, Semeraro N, and Donati MB

Subjects
Animals, Blood Coagulation Factors pharmacology, Mice, Mice, Inbred C57BL, Neoplasm Metastasis prevention & control, Neoplasms, Experimental blood, Blood Coagulation drug effects, Lung Neoplasms blood, Vitamin K Deficiency blood, Warfarin pharmacology
Abstract

Chronic vitamin K deficiency, either dietary or pharmacologically induced with warfarin, depressed significantly the growth of lung secondaries in a spontaneously metastasizing murine tumor, the Lewis Lung Carcinoma. This effect was associated with a marked depression of the procoagulant activity of cancer cells, which could contribute to fibrin deposition around the tumor. Cellular anticoagulation may thus be an important mechanism in the antimetastatic effect of warfarin.

Published
1983
Full Text
View/download PDF

8. Platelet survival and function in rats with enhanced thrombotic tendency.

Author

Delaini F, Dejana E, Reyers I, Vicenzi E, De Bellis Vitti G, Poggi A, and Donati MB

Subjects
6-Ketoprostaglandin F1 alpha blood, Adenosine Diphosphate pharmacology, Animals, Arachidonic Acid, Arachidonic Acids pharmacology, Blood Platelets cytology, Blood Platelets drug effects, Cell Survival, Collagen pharmacology, Doxorubicin pharmacology, Epoprostenol blood, In Vitro Techniques, Male, Platelet Aggregation drug effects, Rats, Thrombosis etiology, Thromboxane B2 blood, Blood Platelets physiology, Thrombosis blood
Abstract

We have investigated the relevance of some laboratory tests of platelet function in predicting conditions of thrombotic tendency. For this purpose, we studied platelet survival, platelet aggregation in response to different stimuli, TxB2 and 6-keto-PGF1 alpha production in serum of rats bearing a nephrotic syndrome induced by adriamycin. These animals show a heavy predisposition to the development of both arterial and venous thrombosis. The mean survival time was normal in nephrotic rats in comparison to controls. As to aggregation tests, a lower aggregating response was found in ADR-treated rats using ADP or collagen as stimulating agents. With arachidonic acid (AA) we observed similar aggregating responses at lower AA concentrations, whereas at higher AA concentrations a significantly lower response was found in nephrotic rats, despite their higher TxB2 production. Also TxB2 and 6-keto-PGF1 alpha levels in serum of nephrotic rats were significantly higher than in controls. No consistent differences were found in PGI2-activity generated by vessels of control or nephrotic rats. These data show that platelet function may appear normal or even impaired in rats with a markedly increased thrombotic tendency. On the other hand, the significance of high TxB2 levels in connection with mechanisms leading to thrombus formation remains a controversial issue.

Published
1985

Catalog

Books, media, physical & digital resources
See catalog results