The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
MeSH Review


Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.

Disease relevance of Favism


High impact information on Favism

  • Deferoxamine and favism [5].
  • In one of the commonest, G6PD Mediterranean, which is associated with favism among other clinical manifestations, a single amino acid replacement was found (serine----phenylalanine): it must be responsible for the decreased stability and the reduced catalytic efficiency of this enzyme [6].
  • Association between ACP1 and favism: a possible biochemical mechanism [7].
  • Active involvement of catalase during hemolytic crises of favism [8].
  • To test the hypothesis that an autosomal enzyme is involved in the pathogenesis of favism, we carried out a beta-glucosidase assay in small intestine biopsies from normal subjects and G6PD deficient subjects with or without favism [9].

Chemical compound and disease context of Favism

  • In vitro incubation of normal and G6PD-deficient erythrocytes with divicine, a pyrimidine aglycone present in fava beans and strongly implicated in the pathogenesis of favism, reproduces most of these events, including drop of calcium ATPase, increased intracellular calcium, and leakage of erythrocyte potassium [1].
  • Lactose absorption in patients with glucose 6-phosphate dehydrogenase deficiency with and without favism [10].
  • Divicine has long been thought to be a mediator of an acute hemolytic crisis, known as favism, in susceptible individuals who ingest fava beans (Vicia faba) [11].
  • Our results corroborate the concept that intraerythrocytic inhibition of glutathione reductase mimicks the biochemistry of drug-sensitive glucose-6-phosphate dehydrogenase deficiency (favism), an inherited condition which confers protection from malaria [12].
  • Correspondingly, the calcium permeability of erythrocytes, estimated as the fraction of intracellular calcium exchangeable with externally added 45Ca2+, was invariably enhanced in favism and returned to normal patterns after several months from the acute hemolytic crisis [13].

Biological context of Favism


Anatomical context of Favism


Gene context of Favism


Analytical, diagnostic and therapeutic context of Favism


  1. Favism: disordered erythrocyte calcium homeostasis. De Flora, A., Benatti, U., Guida, L., Forteleoni, G., Meloni, T. Blood (1985) [Pubmed]
  2. Several mutations including two novel mutations of the glucose-6-phosphate dehydrogenase gene in Polish G6PD deficient subjects with chronic nonspherocytic hemolytic anemia, acute hemolytic anemia, and favism. Jablonska-Skwiecinska, E., Lewandowska, I., Plochocka, D., Topczewski, J., Zimowski, J.G., Klopocka, J., Burzynska, B. Hum. Mutat. (1999) [Pubmed]
  3. Glucose-6-phosphate: a key compound in glycogenosis I and favism leading to hyper- or hypolipidaemia. Schmitz, G., Hohage, H., Ullrich, K. Eur. J. Pediatr. (1993) [Pubmed]
  4. Reproductive performance of hens fed field beans and potential relationships to vicine metabolism. Naber, E.C., Vogt, H., Harnish, S., Krieg, R., Ueberschaer, K.H., Rauch, H.W. Poult. Sci. (1988) [Pubmed]
  5. Deferoxamine and favism. Ekert, H., Rawlinson, I. N. Engl. J. Med. (1985) [Pubmed]
  6. Diverse point mutations in the human glucose-6-phosphate dehydrogenase gene cause enzyme deficiency and mild or severe hemolytic anemia. Vulliamy, T.J., D'Urso, M., Battistuzzi, G., Estrada, M., Foulkes, N.S., Martini, G., Calabro, V., Poggi, V., Giordano, R., Town, M. Proc. Natl. Acad. Sci. U.S.A. (1988) [Pubmed]
  7. Association between ACP1 and favism: a possible biochemical mechanism. Bottini, E., Bottini, F.G., Borgiani, P., Businco, L. Blood (1997) [Pubmed]
  8. Active involvement of catalase during hemolytic crises of favism. Gaetani, G.F., Rolfo, M., Arena, S., Mangerini, R., Meloni, G.F., Ferraris, A.M. Blood (1996) [Pubmed]
  9. Favism: looking for an autosomal gene associated with glucose-6-phosphate dehydrogenase deficiency. Mareni, C., Repetto, L., Forteleoni, G., Meloni, T., Gaetani, G.F. J. Med. Genet. (1984) [Pubmed]
  10. Lactose absorption in patients with glucose 6-phosphate dehydrogenase deficiency with and without favism. Meloni, T., Colombo, C., Ogana, A., Mannazzu, M.C., Meloni, G.F. Gut (1996) [Pubmed]
  11. Chemical analysis and hemolytic activity of the fava bean aglycon divicine. McMillan, D.C., Schey, K.L., Meier, G.P., Jollow, D.J. Chem. Res. Toxicol. (1993) [Pubmed]
  12. Glutathione reductase-deficient erythrocytes as host cells of malarial parasites. Zhang, Y., König, I., Schirmer, R.H. Biochem. Pharmacol. (1988) [Pubmed]
  13. Mechanisms of perturbation of erythrocyte calcium homeostasis in favism. Damonte, G., Guida, L., Sdraffa, A., Benatti, U., Melloni, E., Forteleoni, G., Meloni, T., Carafoli, E., De Flora, A. Cell Calcium (1992) [Pubmed]
  14. Tf, Gc and Cp phenotypes in favism and G-6-PD deficiency. Farhud, D.D., Hedayat, S., Amirshahi, P., Tavakoli, S., Daneshmand, P., Sawhney, K.S., Montazemi, K. Indian J. Med. Res. (1978) [Pubmed]
  15. Divicine induces calcium release from rat liver mitochondria. Graf, M., Frei, B., Winterhalter, K.H., Richter, C. Biochem. Biophys. Res. Commun. (1985) [Pubmed]
  16. Lymphocyte changes in favism: in vitro evidence of a modifying effect of bilirubin and hemoglobin on T-lymphocyte receptors. Schilirò, G., Sciotto, A., Russo, A., Bottaro, G., Minniti, C., Musumeci, S., Russo, G. Acta Haematol. (1983) [Pubmed]
  17. Serum glutamic oxalacetic transaminase, glutamic pyruvic transaminase, gamma-glutamyl transpeptidase and glutamic dehydrogenase levels in favism. Meloni, T., Pilo, G., Gallisai, D., Dore, A. Acta Haematol. (1979) [Pubmed]
  18. Inactivation of red cell glutathione peroxidase by divicine and its relation to the hemolysis of favism. Mavelli, I., Ciriolo, M.R., Rotilio, G. Biochim. Biophys. Acta (1985) [Pubmed]
  19. Haptoglobin therapy for acute favism: a Japanese boy with glucose-6-phosphate dehydrogenase Guadalajara. Ohga, S., Higashi, E., Nomura, A., Matsuzaki, A., Hirono, A., Miwa, S., Fujii, H., Ueda, K. Br. J. Haematol. (1995) [Pubmed]
  20. Oxidative inactivation of the calcium-stimulated neutral proteinase from human red blood cells by divicine and intracellular protection by reduced glutathione. Morelli, A., Grasso, M., De Flora, A. Arch. Biochem. Biophys. (1986) [Pubmed]
  21. Megaesophagus in an asthmatic patient and beta2 stimulant treatment by inhalation. Stabellini, G., Calastrini, C., Becchetti, A., Gagliano, N., Moscheni, C., Marcuzzi, A., Fiocchi, O. Biomed. Pharmacother. (2004) [Pubmed]
WikiGenes - Universities