Homocysteine and vascular disease

Berwanger, Christoph; Jeremy, JY; Stansby, Gerard

doi:10.1002/bjs.1800820604

Cited by 48 publications

(15 citation statements)

References 63 publications

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“…They calculated the odds ratio of a 5 mol/L increment of plasma HCy level for coronary artery disease of 1.6, cerebrovascular disease of 1.5, and for peripheral vascular disease of 6.8. These results have been supported by a further 40 subsequent studies [3]. Thirty percent of patients presenting to vascular clinics-the figure may be nearer 50% to 60% in patients undergoing vascular intervention [4]-have elevated plasma HCy, compared with 2% to 5% in the normal population [5].…”

Section: Introductionsupporting

confidence: 56%

The Use of an In Vivo Model to Study the Effects of Hyperhomocysteinaemia on Vascular Function

Hansrani

Stansby

2008

Journal of Surgical Research

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Section: Introductionsupporting

confidence: 56%

The Use of an In Vivo Model to Study the Effects of Hyperhomocysteinaemia on Vascular Function

Hansrani

Stansby

2008

Journal of Surgical Research

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“…Normal plasma levels of HC are in the range of 1 ± 10 mM (Berwanger et al, 1995) but in homocysteinaemic patients plasma HC levels of 100 ± 500 mM have been detected (Malinow, 1994). In the present study, addition of HC alone, at a concentration of 100 mM, had no signi®cant eect on endothelium-dependent relaxation.…”

Section: Discussionmentioning

confidence: 42%

“…Elevated plasma levels of the sulphur-containing amino acid homocysteine (HC) are suggested to be a powerful independent risk factor for premature atherosclerosis and other in¯ammatory vascular diseases (Berwanger et al, 1995;McCully, 1996). Vascular endothelial cell dysfunction is considered to be a major factor in the development of atherosclerosis (Ross, 1993), and recent studies have shown that mild to moderate elevations in plasma levels of HC (20 ± 35 mM) are associated with impaired endothelium-dependent arterial dilatation in both humans (Tawakol et al, 1997;Woo et al, 1997) and monkeys (Lentz et al, 1996) in vivo.…”

Section: Introductionmentioning

confidence: 99%

Investigation of the inhibitory effects of homocysteine and copper on nitric oxide‐mediated relaxation of rat isolated aorta

Emsley

Jeremy

Gomes

et al. 1999

British J Pharmacology

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Elevated plasma levels of homocysteine (HC) and copper have both been associated with the development of inflammatory vascular diseases, such as atherosclerosis. In this study, the effects of a combination of HC and copper on nitric oxide (NO)‐mediated relaxation of isolated rat aortic rings were investigated. Exposure to HC (10–100 μM; 30 min) had no effect on relaxation to acetylcholine (ACh; 0.01–10 μM, n=4). Pre‐incubation of aortic rings with a higher concentration of HC for an extended period (1 mM; 180 min) significantly inhibited endothelium‐dependent relaxation (n=4), but this inhibition was prevented by the presence of the copper chelator bathocuprione (10 μM, 180 min, n=6). Exposure to HC (100 μM) and copper (10–100 μM; 30 min) caused a copper concentration‐dependent inhibition of endothelium‐dependent relaxation (n=4). This inhibitory effect was reduced in the presence of either superoxide dismutase (SOD; 100 u ml−1; n=4) or catalase (100 u ml−1; n=4), and further reduced by the presence of both enzymes (n=5). HC and copper (100 μM; 30 min) significantly inhibited endothelium‐independent relaxation to glyceryl trinitrate (0.01–10 μM; n=8). In contrast, HC (1 mM), alone or in combination with copper (100 μM), did not inhibit relaxation to the endothelium‐independent relaxant sodium nitroprusside (0.01–10 μM; n=4). These data indicate that the presence of copper greatly enhances the inhibitory actions of HC on NO‐mediated relaxation of isolated aortic rings. The reduction of inhibition by catalase and SOD indicates a possible role for copper‐catalyzed generation of superoxide and hydrogen peroxide leading to an increased inactivation or decreased production of endothelium‐derived NO. British Journal of Pharmacology (1999) 126, 1034–1040; doi:10.1038/sj.bjp.0702374

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“…It has been recognized that PCOS is associated with cardiovascular disease risk factors such as obesity, insulin resistance, type 2 diabetes, elevated blood pressures and dyslipidemia. However, all of these abnormalities are also common in obese subjects [17,18].…”

Section: Discussionmentioning

confidence: 94%

The relationship between copper, homocysteine and early vascular disease in lean women with polycystic ovary syndrome

Çelik

Baştu

Abalı

et al. 2013

Gynecological Endocrinology

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This study investigates copper (Cu) levels and vascular dysfunction in lean women with polycystic ovary syndrome (PCOS). 44 subjects with PCOS, diagnosed according to Rotterdam criteria, and 42 healthy subjects matched for body mass index and age. Comparison of serum Cu, homocysteine, carotid intima-media thickness (CIMT), brachial artery flow mediated dilation (FMD) was carried out between PCOS patients and the control group. Clinical study was done in Namik Kemal University School of Medicine. The CIMT and concentration of Cu in PCOS patients was significantly higher than the healthy controls. FMD levels in PCOS patients were significantly lower than those in controls. In PCOS patients, CIMT was correlated with estrogen and Cu levels. However, FMD was correlated with age and Cu levels. Among these contributing factors, Cu levels were correlated with a change in CIMT and FMD. CIMT and FMD in PCOS patients were related to Cu levels as well as several cardiovascular risk factors. Thus, increased Cu levels may be responsible for the increased risk of early vascular disease in women with PCOS.

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Homocysteine and vascular disease

Cited by 48 publications

References 63 publications

The Use of an In Vivo Model to Study the Effects of Hyperhomocysteinaemia on Vascular Function

The Use of an In Vivo Model to Study the Effects of Hyperhomocysteinaemia on Vascular Function

Investigation of the inhibitory effects of homocysteine and copper on nitric oxide‐mediated relaxation of rat isolated aorta

The relationship between copper, homocysteine and early vascular disease in lean women with polycystic ovary syndrome

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