Total Plasma Homocysteine and Cardiovascular Risk Profile

Nygård, Ottar; Vollset, Stein Emil; Refsum, Helga; Stensvold, Inger; Tverdal, Aage; Nordrehaug, Jan Erik; Ueland, Per Magne; Kvåle, Gunnar

doi:10.1001/jama.1995.03530190040032

Cited by 797 publications

(152 citation statements)

References 54 publications

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“…The consensus of most laboratories is that a normal level of plasma homocysteine is somewhere between 4 and 16 mm (Nygard et al, 1995;Thomson et al, 2000). The degree of elevation of homocysteine depends on the degree of folic acid deficiency; thus, plasma homocysteine levels can range from high normal to >100 mm (McCully, 1993;Guttormsen et al, 1996;Blom, 1998;El-Khairy et al, 1999;Langman and Cole, 1999).…”

Section: Discussionmentioning

confidence: 99%

Oxidative damage to cellular and isolated DNA by homocysteine: implications for carcinogenesis

2003

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Homocysteine is considered to be an important risk factor for cancer as well as cardiovascular diseases. To clarify whether homocysteine has potential carcinogenicity, we investigated formation of 8-oxo-7,8-dihydro-2 0 -deoxyguanosine (8-oxodG), which is known to be correlated with the incidence of cancer, induced by homocysteine in human cultured cell lines. Homocysteine increased the amount of 8-oxodG in human leukemia cell line HL-60, whereas the amount of 8-oxodG in its hydrogen peroxide (H 2 O 2 )-resistant clone HP100 was not increased. We investigated the mechanism for oxidative DNA damage by homocysteine using 32 P-labeled DNA fragments obtained from human tumor suppressor genes and a protooncogene. There were two mechanisms by which homocysteine caused DNA damage in the presence of Cu(II). A low concentration of homocysteine (20 lm) frequently induced piperidine-labile sites at thymine residues, whereas a high concentration of homocysteine (100 lm) resulted in damage principally to guanine residues. Catalase inhibited DNA damage by 20 lm homocysteine, indicating the participation of H 2 O 2 , but was ineffective in preventing DNA damage by 100 lm homocysteine. Experiments using a singlet oxygen probe showed that 100 lm homocysteine enhanced chemiluminescence intensity in deuterium oxide more than that in H 2 O. These results indicated that the metal-dependent DNA damage through H 2 O 2 is likely to be a more relevant mechanism for homocysteine carcinogenicity.

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Section: Discussionmentioning

confidence: 99%

Oxidative damage to cellular and isolated DNA by homocysteine: implications for carcinogenesis

2003

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“…22,23 Tobacco and caffeinated coffee are also associated with increased Hcy concentrations. 24,25 A number of chronic diseases can produce hyperhomocysteinemia. Chronic renal failure regardless of etiology, duration, or type of dialysis elevates Hcy by an unknown mechanism.…”

Section: Etiology Of Hyperhomocysteinemiamentioning

confidence: 99%

The association of homocysteine and coronary artery disease

Gauthier¹,

Keevil²,

McBride³

2003

Clinical Cardiology

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Summary: Hyperhomocysteinemia has been associated with increased risk of atherosclerosis and myocardial infarction by a number of prospective case-control studies. A variety of genetic mutations, nutritional deficiencies, disease states, and drugs can elevate homocysteine concentrations. Treatment with folic acid with or without B-complex vitamins effectively lowers homocysteine levels. Whether therapy corresponds with decreased risk of coronary events is unknown, but may be promising. This article reviews the biochemistry of homocysteine metabolism, pathogeneisis, and etiology of hyperhomocysteinemia, along with its association with coronary artery disease, screening, and treatment.

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“…High homocysteine level is seen in patients with intimal-medial wall thickening in the carotid artery. Robinson et al found a positive correlation between increased serum homocysteine levels and increasing CAD risk [19].…”

Section: Resultsmentioning

confidence: 98%