Disease relevance of HOMOCYSTINE

• This platelet mitogen is also active in vivo, since experimentally produced lesion of atherosclerosis induced mechanically by diet or by homocystine can be prevented if platelets are missing, as in thrombocytopenia, or if platelet function is impaired as a result of the use of platelet inhibitors such as dipyridamole [1].
• Homocystine, atherosclerosis and thrombosis: implications for oral contraceptive users [2].
• RESULTS: Increasing dietary homocystine produced a proportionate increase in plasma homocysteine and an increase in intimal hyperplasia [3].
• Hypertension and ischemic heart disease were significantly more prevalent in the NAION patients with elevated plasma homocystine [4].
• Increasing dietary homocystine increased plasma homocysteine and was followed by increases in the replicative index thus producing increased intimal hyperplasia and lumenal stenosis [3].

Psychiatry related information on HOMOCYSTINE

• These data, despite the relatively small numbers, suggest that early treatment with good biochemical control (lifetime plasma free homocystine median < 11 micromol/L) seems to prevent mental retardation [5].

High impact information on HOMOCYSTINE

• Genetic heterogeneity, technical differences of differences in plasma homocystine concentrations could account for these descrepant results [6].
• Homocystine-induced arteriosclerosis. The role of endothelial cell injury and platelet response in its genesis [7].
• We conclude that homocystine-induced endothelial cell injury resulted in arteriosclerosis through platelet-mediated intimal proliferation of smooth muscle cells that can be prevented by drug-induced platelet dysfunction [7].
• In a group of 138 men, aged 31 to 65 years (mean 53), referred for cardiac catheterization, plasma homocystine was measured before and 6 hours after an oral l-methionine load (0.1 g/kg) [8].
• Thirty-nine subjects found to have normal coronary arteries had a mean post-load plasma homocystine level of 0.59 +/- 0.37 mumol/liter [8].

Chemical compound and disease context of HOMOCYSTINE

• Two biochemical markers for homocystinuria, homocystine and methionine, were markedly elevated during periods when our patient manifested dystonia [9].
• Isotachophoretic analyses of cystine, homocystine and cystathionine in urines from patients with inborn errors of metabolism [10].
• Intimal hyperplasia group received either (1) control or (2) 4.5 g/kg DL-homocystine diets for two weeks followed by CEA and treated with diluent or 5.0 microg Saratin [11].
• Effect of maternal exposure to homocystine on sodium valproate-induced neural tube defects in the mouse embryos [12].
• Male Sprague-Dawley rats underwent carotid endarterectomy (CEA) and treatment with either placebo or varying regimens of clopidogrel, including chronic, pre-CEA bolus, chronic plus pre-CEA bolus, and chronic plus post-CEA bolus; a homocystine diet was used to elevate both plasma homocysteine and the degree of intimal hyperplasia [13].

Biological context of HOMOCYSTINE

• Her evaluation showed an elevated random serum homocystine level, a low serum vitamin B12 level, and an increased mean corpuscular volume (MCV) without anemia [14].
• When endothelial cells were cultured in the presence of methionine (10 mmol/l) or homocystine (10 mmol/l), differences occurred between the viability and function of the heterozygote and normal cells in terms of 51Cr release and ability to prevent platelet adherence [15].
• Patients were investigated for haemoglobin, serum iron, total iron binding capacity (TIBC), serum Vitamin B12, serum and blood folate, methylmalonic acid (MMA), homocystine and glomerular filtration rate [16].
• Results suggested that homocystine induced endothelial-modulated vasoconstriction in coronary vessels [17].
• Results show that homocystine induced cellular proliferation [18].

Anatomical context of HOMOCYSTINE

• There is considerable evidence that homocystine has a direct damaging effect on vascular endothelium and other tissues [19].
• These results suggest that dietary homocystine changes the distribution of body water and that sulfur amino acids can affect membrane porosity and/or membrane thickness [20].
• Homocysteine and homocystine were without effect on the synthesis of vascular PGI2 by umbilical artery segments [control, 0.22 +/- 0.03 to 0.21 +/- 0.03 ng/mg with D,L-homocysteine and 0.20 +/- 0.04 control to 0.19 +/- 0.04 ng/mg with D,L-homocystine] [21].
• In myocytes superfused with 500 microM homocystine, maximum I(to) density was decreased by approximately 40% from baseline (P < 0.05) [22].
• The total number of platelets that adhere to confluent monolayers increases for heterozygote cells cultured in the presence of methionine to 0.98 X 10(7) platelets cm-2 (normal cells, range: 0.56-0.72 X 10(7) platelets cm-2) and in the presence of homocystine to 1.41 X 10(7) platelets cm-2 (normal cells, range: 0.94-1.06 X 10(7) platelets cm-2) [15].

Associations of HOMOCYSTINE with other chemical compounds

• At 4 weeks, the homocystine diet induced a fourfold increase in plasma homocysteine (control: 6.5+/-0.4 micromol/l, homocystine: 26.2+/-2.5 micromol/l), and a reduction in the cerebral eNOS and GLUT-1 expression levels with a concomitant increase in the level of VCAM-1 expression [23].
• Five patients had high values of homocystine with folate deficiency and/or B12 deficiency and renal impairment [16].
• Urinary homocystine levels in a newborn infant with cystathionine synthase deficiency [24].
• The normal value for homocystine alone is 29.9 +/- 16.8 (n = 24) mg per g creatinine [25].

Gene context of HOMOCYSTINE

• Oxidized forms of Hcy (Hcy thiolactone, homocystine) were less effective in affecting AP-1 [26].
• Vitamin B12 injections normalized her fasting homocystine level and her MCV [14].
• Homocystine treatment did not cause significant alterations in CBS levels (P=0.992) [3].
• Plasma levels of fibrinogen and homocystine and serum levels of plasminogen activator inhibitor-1 (PAI-1) were obtained before and 6 months after initiation of treatment [27].
• AIM OF THE STUDY: The aim of this study was to determine if homocystine would augment VPA-induced exencephaly in an experimental model [12].

Analytical, diagnostic and therapeutic context of HOMOCYSTINE

• In smokers, fibrinogen, PAI-1, and homocystine were reduced more (P =.002, P =.0009, and P <.0001, respectively) than in nonsmokers in the whole study cohort [27].
• Homocystine induces collagen expression in a dose- and time-dependent manner, as measured by Northern blot (mRNA) analysis [18].
• A single intravenous injection of homocystine led to an increase in the number of circulating endothelial cells in the blood of rats [28].

References