Possible mechanisms of homocysteine toxicity

Perna, Alessandra F.; Ingrosso, Diego; Lombardi, Cinzia; Acanfora, F; Satta, Ersilia; Cesare, Concetta Maria; Violetti, Eleonora; Romano, Maria Maddalena; Santo, Natale G. De

doi:10.1046/j.1523-1755.63.s84.33.x

Cited by 110 publications

(93 citation statements)

References 20 publications

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“…6 How homocysteine may produce its ill effects is unclear, but elevated concentrations may induce endothelial dysfunction or abnormalities of coagulation factors and platelets. 7 In normal subjects, homocysteine concentrations may be lowered easily by using folic acid. This B vitamin is converted into 5-methyltetrahydrofolate, which donates a methyl group to homocysteine and reconstitutes the methionine from which homocysteine has been derived.…”

Section: See P 369mentioning

confidence: 99%

Renal Disease, Homocysteine, and Cardiovascular Complications

Robinson

2004

Circulation

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Section: See P 369mentioning

confidence: 99%

Renal Disease, Homocysteine, and Cardiovascular Complications

Robinson

2004

Circulation

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“…Severe hyperhomocysteinemia, on the other hand, is prevalently found in patients with rare genetic disorders or renal impairment [1][2][3][4]. In any case, total plasma homocysteine (Hcy) can be considered an effective marker of cardiovascular disease.…”

Section: Introductionmentioning

confidence: 99%

Homocysteine‐induced endothelial cell adhesion is related to adenosine lowering and is not mediated by S‐adenosylhomocysteine

et al. 2007

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Hyperhomocysteinemia is a cardiovascular risk factor and may contribute to the pathogenesis of atherosclerosis by altering endothelial functions. The mechanism of homocysteine-induced cell adhesion has been here investigated using EA.hy 926 cells. Homocysteine induces a stereospecific, time-and dosedependent cell adhesion which is prevented by adenosine. The dramatic increase of S-adenosylhomocysteine induced by adenosine-2 0 ,3 0 -dialdehyde does not cause cell adhesion, indicating that no apparent relationship exists between this process and intracellular S-adenosylhomocysteine content. Homocysteine-induced cell adhesion is abolished by pre-treatment with adenosine-2 0 ,3 0 -dialdehyde, demonstrating that the adenosine depletion caused by reversal of S-adenosylhomocysteine hydrolase reaction is responsible for homocysteine-induced cell damage.

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“…3 Most recently, we have reported that increases in plasma homocysteine (Hcys) levels resulted in proteinuria and glomerulosclerosis in Sprague Dawley rats, and hHcys participated in the development of arterial and glomerular sclerosis in Dahl salt-sensitive hypertensive (SS) rats. 4 However, the mechanisms leading to increases in plasma Hcys levels in SS rats remain unknown.…”

mentioning

confidence: 99%

Hyperhomocysteinemia Associated With Decreased Renal Transsulfuration Activity in Dahl S Rats

Chen²,

Muh³

et al. 2006

Hypertension

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Abstract-Elevated plasma homocysteine (Hcys) has been reported to participate in the development of arterial and glomerular sclerosis in Dahl salt-sensitive hypertensive (SS) rats. The mechanism resulting in hyperhomocysteinemia in these animals remains unknown. Disposal of Hcys in the kidneys plays an important role in regulating the plasma Hcys level. We, therefore, examined the activities and expressions of the enzymes involved in the metabolism of Hcys in the kidneys of SS rats, compared with that of Brown Norway rats and SSBN13 rats, a consomic subcolony of SS rats that carries a substituted chromosome 13 from Brown Norway rats. High-performance liquid chromatography analysis demonstrated that plasma Hcys levels were significantly higher in SS rats. The conversion of S-adenosylhomocysteine into Hcys via S-adenosylhomocysteine hydrolase by renal tissue was not different among these 3 rat strains. However, the metabolic rate of Hcys into cysteine was markedly reduced in the SS rat kidneys. The mRNA and protein levels of cystathionine ␤-synthase (CBS), one of the key enzymes in the transsulfuration pathway in the kidneys, were significantly lower in SS rats. In microdissected nephron segments, CBS mRNA was shown to be mainly present in renal proximal tubules (PTs). The mRNA levels of CBS in the PTs were also significantly decreased in SS rats, accompanied by a reduced CBS activity in PTs. We conclude that hyperhomocysteinemia is associated with a decreased activity and expression of CBS in renal PTs because of the defect of chromosome 13 in SS rats. (Hypertension. 2006; 47:1094-1100.)

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Possible mechanisms of homocysteine toxicity

Cited by 110 publications

References 20 publications

Renal Disease, Homocysteine, and Cardiovascular Complications

Renal Disease, Homocysteine, and Cardiovascular Complications

Homocysteine‐induced endothelial cell adhesion is related to adenosine lowering and is not mediated by S‐adenosylhomocysteine

Hyperhomocysteinemia Associated With Decreased Renal Transsulfuration Activity in Dahl S Rats

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