Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.3.5.1 (succinate dehydrogenase)
8,177 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cell sensitivity to a constant magnetic field (CMF) of 100 = 200 Oe was studied on a fibroblast culture using time-lapse microfilming. It was expressed in the phasic development of the motility of cells, intracellular structures and inclusions: a short-term latent phase (10-15 min), an excitation phase (1.5-2 h) and a suppression phase (up to the end of exposure). After field removal the return of cells to the initial state with a slight excess (in 1.5-2 h) was noted. The phasic development, reversibility and compensation of magnetobiological reactions were later on confirmed in studies on the inhibition in CMF of 400-600 Oe of the activity of succinate dehydrogenase and peptidase in isolated surviving rat skeletal muscles, liver and kidney as well as on a model of the reaction of a cytopathogenic effect of lymphocytes from patients with rheumatic fever on human embryonic fibroblasts where a noticeable effect of inhibition with the CMF action on the system of lymphocytes-fibroblasts and, on the contrary, of its activation with adding to fibroblasts lymphocytes preexposed in CMF of 400-600 Oe for 1 and 24 h were revealed and interpreted as supercompensation of the inhibited enzymatic activity of immunocompetent cells. The phasic development, reversibility and compensation of magnetobiological reactions should be necessarily taken into account in working out magnetotherapy.
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PMID:[Cyclicity, reversibility and compensation of magnetobiological reactions in isolated cells and tissues]. 351 10

Mitochondrial diseases are a heterogeneous group of disorders in which a primary mitochondrial dysfunction is proven by morphological, biochemical, and genetic examinations. The mitral valve has important function in the regulation of blood flow from one chamber to another. Often, the mitral valve becomes abnormal with age, in Rheumatic fever or it is abnormal from birth (Congenital) or it can be destroyed by infection i.e. bacterial endocarditis and needs replacement. Myocardial function depends on energy produced by mitochondria and in any of these disease conditions, mitochondrial functions and enzyme activities may be impaired. With this in view, we analyzed the relationship between preoperative clinical conditions (as per New York heart Association) and extent of mitochondrial enzyme activities in damaged Human mitral valve in two types of heart disease such as Rheumatic Heart Disease (RHD) and Bacterial Endocarditis (BE). Thirty nine Patients undergoing cardiopulmonary bypass (CPB) for routine valvular heart surgery were included in the study. Controls included 11 normal porcine mitral valve samples without any evidence of heart disease. Mitochondrial enzymes like cytochrome oxidase (COX), succinate dehydrogenase (SDH), malate dehydrogenase (MDH), citrate synthase (CS) and ATPase were determined. Mitochondrial COX, SDH, CS and Total ATPase activities were significantly decreased in disease condition like BE and RHD when compared with control (P<0.001). On the other hand as per New York Heart Association (NYHA) preoperative clinical classification, all the mitochondrial enzymes were significantly (p<0.05) impaired in class IV as compared with NYHA class I, II and III. Present study shows that impairment in the mitochondrial enzymes activities are more pronounced in bacterial endocarditis (BE). It also indicates that damage to mitochondrial enzymes are most pronounced in NYHA class IV.
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PMID:Defect in mitochondrial functions in damaged human mitral valve. 2310 35