Hyperhomocyst(e)inemia in @entity1 with coronary and peripheral @entity432 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 @entity1525 in the development of @entity82 in @entity731 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 @entity43433 in @entity731 development, coronary arteries were isolated from ischemic explanted hearts (n = 10). Apparently normal vascular tissue was obtained from idiopathic @entity299 (n = 10). Tissue extract were prepared from @entity731 and from normal arteries devoid of adventitia. Interaction of @entity43433 with Ellman's reagent ( @entity8865 ) 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 @entity43433 . The change in OD at 412 nm with increasing amount (0-25 microg) of @entity43433 demonstrated linearity. The protein-bound oxidized @entity1525 were precipitated by @entity2804 ( @entity2974 ) and free-oxidative @entity1525 in the supernatant were collected. The pathophysiological amount of protein-bound @entity1520 in @entity731 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 @entity1520 in @entity731 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 @entity43433 in ECM expression, ECM collagenase activity in the presence and absence of @entity43433 was measured by zymography. The effect of @entity1255 on collagenase activity was biphasic, increased at < [0.01 mM] and inhibited at > [0.1 mM]. To determine whether @entity43433 regulates vascular tone, isometric measurements were carried out using normal coronary rings. Results suggested that @entity43433 induced endothelial-modulated vasoconstriction in coronary vessels. Tissue oxidative @entity1525 and the @entity43433 may contribute to the development of @entity455 .

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

@entity1 :: ('9606', 'Species') :: ['patients'] @entity82 :: ('MESH:D005355', 'Disease') :: ['fibrous plaque'] @entity455 :: ('MESH:D014652', 'Disease') :: ['fibrotic atherosclerotic lesions and vascular dysfunction'] @entity1255 :: ('MESH:D006710', 'Chemical') :: ['homocysteine'] @entity43433 :: ('MESH:D006711', 'Chemical') :: ['homocystine'] @entity8865 :: ('MESH:D004228', 'Chemical') :: ["5, 5'-dithio-bis-2-nitro benzoic acid"] @entity2974 :: ('CHEBI:30956', 'Chemical') :: ['TCA'] @entity1520 :: ('CHEBI:48343', 'Chemical') :: ['disulfide'] @entity299 :: ('MESH:D006331', 'Disease') :: ['cardiomyopathic explanted hearts'] @entity432 :: ('MESH:D001157', 'Disease') :: ['arterial occlusion'] @entity731 :: ('MESH:D050197', 'Disease') :: ['atherosclerotic', 'atherosclerotic lesion', 'atherosclerotic lesions', 'fibrotic atherosclerotic plaque'] @entity1525 :: ('MESH:D004220', 'Chemical') :: ['disulfides'] @entity2804 :: ('MESH:D014238', 'Chemical') :: ['trichloroacetic acid']
@entity1 :: (9606,Species) :: ['human']
