Megaloblastic anaemias (MA) are frequently associated with haemolysis. The pathogenesis of these finding is not clear, but it is thought depend on the greater destruction of abnormal and fragile megaloblastic erythrocytes. Vitamin B-12 and folate deficiencies are the ommonest cause of MA; these deficiencies may simultaneously induce a significant alteration in homocysteine metabolism leading to yperhomocysteinemia. Blood cells have enzymes involved in homocysteine metabolism. Considering the possible effects of yperhomocysteinemia in erythrocyte toxicity (due to oxidative damage and/or to interaction with sultbydryl residues of structural and tzymatic proteins), the aim of our study was to evaluate (1) the homocysteine blood cells production in patients with MA due to vitamin B-12 and folate deficiency and (2) the possible role and mechanism of hyperhomocysteinemia in MA haemolysis. After incubation at 37 C, blood samples from MA patients showed higher and significant levels of Hcy, LDH, lipid peroxidation parameters (MDA), and ghost protein-bound cy than controls. Haemolysis ( %) was higher in MA patients than controls and was significantly correlated with Hey accumulation in the medium, lipid peroxidation indices and ghost protein-bound Hey. No significant (or significantly lower) alterations through time in considered parameters were observed in the corresponding samples incubated at 4degreesC or in samples incubated with methionine-free medium lower Hey production). Our data, deriving from an in vitro experience, suggest a possible role of Hey accumulation due to vitamin B12 and)late deficiencies in haemolysis associated to MA due to vitamin deficiency.

A role for homocysteine increase in haemolysis of megaloblastic anaemias due to vitamin B-12 and folate deficiency: results from an in vitro experience / Ventura, Paolo; R., Panini; S., Tremosini; Salvioli, Gianfranco. - In: BIOCHIMICA ET BIOPHYSICA ACTA. MOLECULAR BASIS OF DISEASE. - ISSN 0925-4439. - STAMPA. - 1739 (1):(2004), pp. 33-42.

A role for homocysteine increase in haemolysis of megaloblastic anaemias due to vitamin B-12 and folate deficiency: results from an in vitro experience

VENTURA, Paolo;SALVIOLI, Gianfranco
2004

Abstract

Megaloblastic anaemias (MA) are frequently associated with haemolysis. The pathogenesis of these finding is not clear, but it is thought depend on the greater destruction of abnormal and fragile megaloblastic erythrocytes. Vitamin B-12 and folate deficiencies are the ommonest cause of MA; these deficiencies may simultaneously induce a significant alteration in homocysteine metabolism leading to yperhomocysteinemia. Blood cells have enzymes involved in homocysteine metabolism. Considering the possible effects of yperhomocysteinemia in erythrocyte toxicity (due to oxidative damage and/or to interaction with sultbydryl residues of structural and tzymatic proteins), the aim of our study was to evaluate (1) the homocysteine blood cells production in patients with MA due to vitamin B-12 and folate deficiency and (2) the possible role and mechanism of hyperhomocysteinemia in MA haemolysis. After incubation at 37 C, blood samples from MA patients showed higher and significant levels of Hcy, LDH, lipid peroxidation parameters (MDA), and ghost protein-bound cy than controls. Haemolysis ( %) was higher in MA patients than controls and was significantly correlated with Hey accumulation in the medium, lipid peroxidation indices and ghost protein-bound Hey. No significant (or significantly lower) alterations through time in considered parameters were observed in the corresponding samples incubated at 4degreesC or in samples incubated with methionine-free medium lower Hey production). Our data, deriving from an in vitro experience, suggest a possible role of Hey accumulation due to vitamin B12 and)late deficiencies in haemolysis associated to MA due to vitamin deficiency.
1739 (1)
33
42
A role for homocysteine increase in haemolysis of megaloblastic anaemias due to vitamin B-12 and folate deficiency: results from an in vitro experience / Ventura, Paolo; R., Panini; S., Tremosini; Salvioli, Gianfranco. - In: BIOCHIMICA ET BIOPHYSICA ACTA. MOLECULAR BASIS OF DISEASE. - ISSN 0925-4439. - STAMPA. - 1739 (1):(2004), pp. 33-42.
Ventura, Paolo; R., Panini; S., Tremosini; Salvioli, Gianfranco
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11380/309767
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