Favism

Mager, J.; Razin, A.; Hershko, Alon Y.

doi:10.1016/b978-0-12-395739-9.50015-5

Cited by 19 publications

(12 citation statements)

References 81 publications

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“…1). Fava beans also contain high amounts of ascorbate and varying amounts of L-DOPA glucoside [7,[20][21][22]. Divicine and isouramil share common effects and similar was also observed that oxidant treatments cause p72 Syk phosphorylation and binding to oxidized band 3 molecules inducing their selective phosphorylation.…”

Section: The Favic Crisis a Model For Oxidant Induced Acute Hemolysismentioning

confidence: 99%

Life and Death of Glucose-6-Phosphate Dehydrogenase (G6PD) Deficient Erythrocytes Role of Redox Stress and Band 3 Modifications

Arese

Gallo²,

Pantaleo³

et al. 2012

Transfus Med Hemother

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G6PD catalyzes the first, pace-making reaction of pentosephosphate cycle (PPC) which produces NADPH. NADPH maintains glutathione and thiol groups of proteins and enzymes in the reduced state which is essential for protection against oxidative stress. Individuals affected by G6PD deficiency are unable to regenerate reduced glutathione (GSH) and are undefended against oxidative stress. G6PD deficiency accelerates normal senescence and enhances the precocious removal of chronologically young, yet biologically old cells. The term hemolytic anemia is misleading because RBCs do not lyse but are removed by phagocytosis. Acute hemolysis by fava bean ingestion in G6PD deficient individuals (favism) is described being the best-studied natural model of oxidant damage. It bears strong analogies to hemolysis by oxidant drugs or chemicals. Membrane alterations observed in vivo during favism are superimposable to changes in senescent RBCs. In summary, RBC membranes isolated from favic patients contained elevated amounts of complexes between IgG and the complement fragment C3b/C3c and were prone to vesiculation. Anti-band 3 IgG reacted to aggregated band 3-complement complexes. In favism extensive clustering of band 3 and membrane deposition of hemichromes were also observed. Severely damaged RBCs isolated from early crises had extensive membrane cross-bonding and very low GSH levels and were phagocytosed 10-fold more intensely compared to normal RBCs.

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Section: The Favic Crisis a Model For Oxidant Induced Acute Hemolysismentioning

confidence: 99%

Life and Death of Glucose-6-Phosphate Dehydrogenase (G6PD) Deficient Erythrocytes Role of Redox Stress and Band 3 Modifications

Arese

Gallo²,

Pantaleo³

et al. 2012

Transfus Med Hemother

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“…1,2,10 In particular, this legume has not yet been incorporated in weaning food formulations where an inexpensive source of good quality protein is in demand.…”

Section: ±9mentioning

confidence: 99%

“…10,11 A number of methods have so for been devised for the assay of vicine and convicine; 12±19 hence many fababean varieties have been examined for these compounds. 17,20±23 If, in fact, vicine and convicine are the factors responsible for favism, then it is imperative that they be eliminated by either genetic breeding or suitable processing techniques.…”

Section: ±9mentioning

confidence: 99%

Removal of favism-inducing factors vicine and convicine and the associated effects on the protein content and digestibility of fababeans (Vicia faba L)

Jamalian

1999

J. Sci. Food Agric.

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“…On the basis of previous studies with rats (Yannai and Marquardt 1986;Arbid and Marquardt 1986) and other in vitro studies (Mager et al 1965(Mager et al , 1980Arese etaf 1981;Baker et a1 1984) it appears that DV first causes a reduction of GSH concentration in the RBC. If the dosage is sufficiently high, there is near complete depletion of GSH which is then followed by peroxidative changes in the haemoglobin and other components of the RBC.…”

Section: Influence Of Ip Injections Of Vitamin E On DV Toxicitymentioning

confidence: 90%

Protection against the toxic effects of the favism factor (divicine) in rats by vitamins E, A and C and iron chelating agents

Marquardt

Arbid

1988

J Sci Food Agric

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Five experiments were carried out with weanling Sprague-Dawley rats to determine if prior administration of either free-radical scavenging compounds (vitamins A, C and E) or chelating agents (EDTA and desferoxamine) affected the toxicity of divicine (DV). In all experiments, intraperitoneal (IP) injections of 250 mg g-' body weight of DV alone resulted in 100% mortalities within 24 h with most of the deaths occurring before 4 h. Death was accompanied by a rapid decrease in the concentration of glutathione (GSH) in the red blood cells (RBC) and the574 nm/428 nm absorbance ratio of haemoglobin. The first experiment demonstrated that IP injections of different amounts of vitamin E, 1 h prior to DV injection, prevented the decrease in the haemoglobin absorbancy ratio and GSH concentration and greatly reduced mortalities. In rats that received 1000 IUof vitamin E kg-1 body weightprior to DVinjection, mortality was only 20%. The second experiment demonstrated that the optimal time for IP administration of vitamin E was 1 to 4 h prior to DV injection although some protection was obtained after 94 h. In contrast, the optimal time for intramuscular injections was 24 h prior to DV administration. A dosage of 250 or 500 IU of vitamin E kg-' body weight provided complete protection (zero mortalities) against the toxic effects of DV. In the third experiment, the addition of varying amounts of vitamin E to the diet resulted in a dosedependent mortality curve with no deaths occurring in rats fed diets containing the highest concentrations of vitamin E. The fourth experiment also demonstrated that vitamin A, vitamin C, EDTA and desferoxamine each *Present address: National Research Centre, El-Tahrir St, Dokki, Cairo, Egypt.155 J. Sci. Food Agric. 0022-5142/88/$03.50 0 Society of Chemical Industry, 1988. Printed in Great Britain 156 R R Marquardt, M S S Arbidprotected rats to varying degrees against the toxic effects of DV. In the final experiment it appeared that the combined injections of a free-radical scavenging compound (vitamin E) and a metal chelator (desferoxamine) provide more protection than vitamin E alone. These results demonstrate for the first time in vivo that certain vitamins, especially vitamin E, and metal chelators can provide varying and in some cases 100% protection against the toxic effects of DV.

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Favism

Cited by 19 publications

References 81 publications

Life and Death of Glucose-6-Phosphate Dehydrogenase (G6PD) Deficient Erythrocytes Role of Redox Stress and Band 3 Modifications

Life and Death of Glucose-6-Phosphate Dehydrogenase (G6PD) Deficient Erythrocytes Role of Redox Stress and Band 3 Modifications

Removal of favism-inducing factors vicine and convicine and the associated effects on the protein content and digestibility of fababeans (Vicia faba L)

Protection against the toxic effects of the favism factor (divicine) in rats by vitamins E, A and C and iron chelating agents

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Favism

Cited by 19 publications

References 81 publications

Life and Death of Glucose-6-Phosphate Dehydrogenase (G6PD) Deficient Erythrocytes  Role of Redox Stress and Band 3 Modifications

Life and Death of Glucose-6-Phosphate Dehydrogenase (G6PD) Deficient Erythrocytes  Role of Redox Stress and Band 3 Modifications

Removal of favism-inducing factors vicine and convicine and the associated effects on the protein content and digestibility of fababeans (Vicia faba L)

Protection against the toxic effects of the favism factor (divicine) in rats by vitamins E, A and C and iron chelating agents

Contact Info

Product

Resources

About

Life and Death of Glucose-6-Phosphate Dehydrogenase (G6PD) Deficient Erythrocytes Role of Redox Stress and Band 3 Modifications

Life and Death of Glucose-6-Phosphate Dehydrogenase (G6PD) Deficient Erythrocytes Role of Redox Stress and Band 3 Modifications