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PubMed1990

Synthesis and 11C-labelling of the ACTH fragment analogue H-Met(O2)-Glu-His-Phe-D-Lys-Phe-OH (Org 2766) via its homocystine-containing precursor.

The hexapeptide dimer (H-Hcy-Glu-His-Phe-D-Lys-Phe-OH)2 was synthesized using solution methods and characterized. Its conversion into H-Met(O2)-Glu-His-Phe-D-Lys-Phe-OH, Org 2766, was studied on a small scale in as short a time as possible; reduction of the disulfide bond using Na/NH3, reaction with CH3I, oxidation with H2O2 and catalyst and purification by HPLC were carried out starting with 2 mg of the dimer in a total preparation time of approximately 22 min, starting with the addition of CH3I. The preparation of the 11C-labelled analogue was carried out by methylation with 11CH3I. Restrictions imposed by working with carbon-11 will be discussed.

Adrenocorticotropic Hormone↗
PubMed1998

Reduction-oxidation (Redox) and vascular tissue level of homocyst(e)ine in human coronary atherosclerotic lesions and role in extracellular matrix remodeling and vascular tone.

Hyperhomocyst(e)inemia in patients with coronary and peripheral arterial occlusion has been demonstrated by others. Redox-state of homocyst(e)ine causes dysfunction of endothelial cells and promote growth of vascular smooth muscle cells. The role of tissue, protein bound and unbound, oxidative mixed disulfides in the development of fibrous plaque in atherosclerotic lesion is not known. Redox-state around the fibroblasts and vascular smooth muscle cells modulates the expression of extracellular matrix (ECM) components (Tyagi et al. 1996, J Cell Biochem, 61: 139-151). To determine the role of tissue homocystine in fibrotic atherosclerotic plaque development, coronary arteries were isolated from ischemic explanted hearts (n = 10). Apparently normal vascular tissue was obtained from idiopathic cardiomyopathic explanted hearts (n = 10). Tissue extract were prepared from atherosclerotic lesions and from normal arteries devoid of adventitia. Interaction of homocystine with Ellman's reagent (5, 5'-dithio-bis-2-nitro benzoic acid) catalyzed by limiting amount of reducing agent (catalyst) generated change in optical density (OD) at 412 nm in dose dependent fashion. We have generated a standard curve between change at 412 nm and amount of homocystine. The change in OD at 412 nm with increasing amount (0-25 microg) of homocystine demonstrated linearity. The protein-bound oxidized disulfides were precipitated by trichloroacetic acid (TCA) and free-oxidative disulfides in the supernatant were collected. The pathophysiological amount of protein-bound disulfide in atherosclerotic tissue (1.0 +/- 0.2 microg/mg total protein) was 10 times that in normal tissue (0.1 +/- 0.01 microg/mg, p < 0.001). The amount of free oxidative disulfide in atherosclerotic tissue (1.5 +/- 0.3 microg/mg) was 15 times that in normal tissue (0.12 +/- 0.02 microg/mg, p < 0.001). To determine the role of homocystine in ECM expression, ECM collagenase activity in the presence and absence of homocystine was measured by zymography. The effect of homocysteine on collagenase activity was biphasic, increased at < [0.01 mM] and inhibited at > [0.1 mM]. To determine whether homocystine regulates vascular tone, isometric measurements were carried out using normal coronary rings. Results suggested that homocystine induced endothelial-modulated vasoconstriction in coronary vessels. Tissue oxidative disulfides and the homocystine may contribute to the development of fibrotic atherosclerotic lesions and vascular dysfunction.

Arteries↗
PubMed1998

Homocysteine redox receptor and regulation of extracellular matrix components in vascular cells.

Dynamic changes in the reduction-oxidation (redox) state of the tissue lead to the pathophysiological condition. Reduced homocysteine causes dysfunctions in endothelium. The proliferation of smooth muscle cells may lead to occlusive vascular disease, ischemia, and heart failure, but whether fibrosis and hypertension are a consequence of smooth muscle proliferation is unclear. Redox changes during hyper-homocyst(e)inemia may be one of the causes of premature atherosclerotic heart disease. To examine the effect of homocystine on human vascular smooth muscle cells (HVSMC), we isolated HVSMC from idiopathic dilated cardiomyopathic hearts. Coronaries in these hearts were apparently normal. HVSMC numbers in culture were measured by hemocytometer in the presence and absence of homocystine. Results show that homocystine induced cellular proliferation. This proliferation was reversed by the addition of the antioxidant N-acetylcysteine (NAC). Homocystine induces collagen expression in a dose- and time-dependent manner, as measured by Northern blot (mRNA) analysis. The 50% inhibitory concentration of 5 microM for collagen was estimated. The induction of collagen was reversed by the addition of NAC and reduced glutathione. To localize the receptor for homocystine on HVSMC, we synthesized fluorescamine-labeled homocystine conjugate. Incubation of labeled homocystine with HVSMC demonstrated membrane and cytosol localization of homocystine binding. The receptor-ligand binding was disrupted by NAC. Based on sodium dodecyl sulfate-polyacrylamide gel electrophoresis fluorography, we observed a 40- to 25-kDa homocystine redox receptor in HVSMC. Our results suggested that the redox homocysteine induces HVSMC proliferation by binding to the redox receptor and may exacerbate atherosclerotic lesion formation by inducing collagen expression.

Acetylcysteine↗
PubMed2004

The impact of third-generation beta-blocker antihypertensive treatment on endothelial function and the prothrombotic state: effects of smoking.

BACKGROUND: The significance of beta-blockers in the treatment of cardiovascular diseases is well established. The effect of vasodilating beta-blockers on endothelial function and prothrombotic state has not been investigated. METHODS: The study comprised 550 consecutive patients with uncomplicated essential hypertension. They were treated with celiprolol, carvedilol or nebivolol monotherapy (171, 179, and 200 patients, respectively), achieving comparable blood pressure reduction. 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. RESULTS: The three drugs differentiated in regard to homocystine (P <.00001) and fibrinogen level changes (P =.00003), but not (P = NS) in PAI-1 change. In smokers, differentiation was found in all three parameters (P =.0002, P =.001, and P =.006 for fibrinogen, PAI-1, and homocystine, respectively), but in nonsmokers differentiation was found only in homocystine change (P =.00003). 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. The effect of nebivolol was more prominent in smokers than nonsmokers in reducing all three parameters (P =.0001,.003, and.003, respectively), whereas in celiprolol and carvedilol-treated groups, differentiation between smokers and nonsmokers was significant (P =.00003 and.01, respectively) only in homocystine level change. CONCLUSIONS: In hypertensive smokers, nebivolol resulted in a significant decrease of plasma PAI-1, fibrinogen and homocystine. Celiprolol also significantly affected these parameters but to a lesser degree, whereas carvedilol had no significant favorable action. In nonsmokers, homocystine was reduced significantly by nebivolol. We conclude that smoking status should be a determinant of antihypertensive treatment choice.

Adrenergic beta-Antagonists↗
PubMed1992

Excess levels of cysteine and homocysteine induce tibial dyschondroplasia in broiler chicks.

The effect of excessive levels of cysteine and homocysteine on tibial dyschondroplasia (TD) in broiler chicks was studied. In the first experiment, graded levels of L-cysteine as well as one level of L-homocysteine were supplemented to a corn-soybean-based diet adequate in sulfur amino acids. Levels equal to or above 0.5% supplemental cysteine increased the incidence of TD, and levels equal to or above 0.75% supplemental cysteine increased the severity of TD above that found in chicks fed the basal diet. Also, L-homocysteine at 0.5% induced TD. In the second experiment, graded levels of DL-homocystine were added to the basal diet to determine the threshold value of homocystine needed to induce TD, and a level of ammonium sulfate isosulfurous to 0.45% homocystine was added to a basal diet. The results showed that 0.45% DL-homocystine was the lowest level that increased the severity of TD above that found in chicks fed the basal diet and that sulfate did not induce TD. In the third experiment, a 2 x 2 factorial design was used to investigate the interaction between DL-homocystine and copper. Copper supplementation lessened the severity of TD caused by DL-homocystine. Copper supplementation also tended to improve growth, especially in birds fed DL-homocystine.

Ammonium Sulfate↗
PubMed2004

Effects of dietary folic acid supplementation on cerebrovascular endothelial dysfunction in rats with induced hyperhomocysteinemia.

This study shows, for the first time, that hyperhomocysteinemia induces endothelial dysfunction in a rat brain, and that this can be alleviated by dietary folic acid supplementation. Our experiments examined the effects of folic acid supplementation on the endothelial nitric oxide synthase (eNOS) expression in the hyperhomocysteinemic rat brain, and related the observed changes in eNOS expression to the expression of the cell adhesion molecule and the glucose transporter protein. The animals were raised on an experimental diet containing 0.3% homocystine for 2 weeks and then they were placed either on a 0.3% homocystine, 0.3% homocystine with 8 mg/kg folic acid, or folic acid (8 mg/kg) diet for 2 weeks. The cerebrovascular eNOS activity was examined immunohistochemically. Cerebral levels of eNOS, glucose transporter-1 (GLUT-1), and the vascular cell adhesion molecule-1 (VCAM-1) proteins were evaluated by Western blot analysis. 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. Dietary folic acid supplementation caused a significant decrease in the plasma homocysteine levels, a concomitant increase in the hyperhomocysteinemia-induced reduction in the cerebral eNOS and GLUT-1 expression levels, and a decrease in the hyperhomocysteinemia-induced VCAM-1 expression levels.

Animals↗
PubMed1997

Newborn screening for homocystinuria.

It is becoming increasingly apparent that pyridoxine responsive homocystinuria patients are being missed by newborn screening programs. The possibility that screening for homocystine, rather than the methionine, might be more effective was investigated by comparing homocystine and methionine levels of non-responsive patients at diagnosis. The plasma methionine levels of 11 infants were much more abnormal than the homocystine levels. Urine homocystine was low or not detectable and always less than methionine. Therefore, methionine determination is much more effective than homocystine determination for newborn screening for homocystinuria. It seems that a second blood specimen at a later age may be required to find the pyridoxine responsive infants.

Homocystine↗