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

The localization of the activities of some selected phosphatases, peptidases and dehydrogenases were studied in cryostat sections of the developing anlage of the suprarenal gland of human embryos from 8 to 20 weeks of the intra-uterine life. In the youngest fetuses under our notice (weeks 8-12), the activity of alkaline phosphatase (AP) on the cellular membranes of the fetal cortex was very low. In contrast, the activity of acid phosphatase (AcP) was comparatively high. Peak activity was found in the cells of the central zone of the fetal cortex. Compared to the activity of the latter, the activity of non-specific esterase (ANE) was somewhat lower. Both its localization and the gradient were identical with those of acid phosphatase. Of the peptidases studied, only dipeptidyl peptidase IV (DPP IV) exhibited slight activity in deeper layers of the primitive fetal cortex after week 8. The other peptidases exhibited only traces of activity. As early as in the first stages followed, the activity of glycero-3-phosphate-dehydrogenase (alpha-GPDH) was very high in all cells of the differentiating fetal cortex. The intensity of the activity of succinate dehydrogenase (SDH) was markedly lower. In older fetuses (weeks 13-20) there was a gradual increase in the activities of most enzymes, seen, after week 15 of the intrauterine life, also in the cells of the so-called definitive cortex. Most pronounced were the increases in the activities of acid phosphatase and non-specific esterase. The relatively low activities of the enzymes under study point to a relatively low degree of cell differentiation of both the primitive and, after week 15, the definitive cortex. Pronounced morphological and functional changes occur after the 20th week of the intrauterine life.
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PMID:Enzyme histochemistry in the developing suprarenal gland of human embryos. 253 Aug 49

In vivo, bicarbonate can affect proximal tubule intermediary metabolism, including gluconeogenesis, ammoniagenesis and maintenance of the mitochondrial substrate supply. In vitro, rabbit proximal tubule cells (RPTC) in primary culture revert from gluconeogenesis to glycolysis and their mitochondrial metabolism remains lower than in vivo. To determine whether the bicarbonate buffer system could have an effect on these deregulations, RPTC in primary culture grown in the absence of insulin and glucose in the culture medium were developed either with the standard sodium bicarbonate buffer with 5% CO2 or with a Hepes hydrogen ion buffer in the presence of 0.5% CO2. Duration of the bicarbonate-free cultures was increased until at least day 17 after seeding, compared with day 11 in bicarbonate-buffered cultures. As could be expected, succinate dehydrogenase activity remained stable as a function of time in bicarbonate-free cultures while an early marked decrease of this activity occurred from seeding in cultures developed in the presence of bicarbonate buffer. Compared to bicarbonate-buffered cells, higher phosphoenolpyruvate carboxykinase activity concomitant with lower intracellular lactate dehydrogenase activity was observed in cultures developed in the absence of bicarbonate, which is indicative of closer carbohydrate metabolism orientation to the in vivo situation for RPTC. Immunofluorescence staining of RPTC with monoclonal antibodies directed to neutral endopeptidase (NEP), and dipeptidyl-peptidase IV (DPP II) showed similar extensive labelling with DPP and NEP in both culture conditions. Confocal microscopy analysis of NEP subcellular distribution, showed exclusive targetting of NEP to the apical plasma membranes. In both models, cAMP production was stimulated by parathyroid hormone and unaffected by arginine vasopressin. In conclusion, bicarbonate withdrawal from the culture medium (without changing the pH of the medium) allows a marked improvement of mitochondrial capacity and carbohydrate metabolism pattern without any loss of differentiated properties.
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PMID:Effects of the medium HCO3-/CO2 buffer system on differentiation and intermediary metabolism properties of rabbit proximal tubule cells in primary culture. 897 88

The mechanisms and myocardial alterations associated with NO-deficient hypertension are still far from clear. The aim of the present study was to focus on the enzyme histochemical and subcellular changes in the heart of L-NAME treated rats, as well as to examine the influence of captopril treatment. Wistar rats were administered either L-NAME (40 mg/kg/day) alone or together with captopril (100 mg/kg/day) for a period of 4 weeks. A significant increase of blood pressure confirmed the reliability of the model. The results showed that long-lasting L-NAME administration was accompanied by a decrease of endothelial NO-synthase activity and by a significant local decrease of the following enzyme activities: capillary-related alkaline phosphatase, 5'-nucleotidase and ATPase (but not dipeptidyl peptidase IV) and cardiomyocyte-related glycogen phosphorylase, succinic dehydrogenase, beta-hydroxybutyrate dehydrogenase and ATPases. No activity of these enzymes was found in the scar, whereas a marked increase of alkaline phosphatase and dipeptidyl peptidase IV activities was found in the foci of fibrotization. Histochemical changes correlated with subcellular changes, which were characterized by 1) apparent fibroblast activation associated with interstitial/perivascular fibrosis, 2) heterogeneous population of the normal, hypertrophic and injured cardiomyocytes, 3) enhancement of the atrial granules and their translocation into the sarcolemma, and 4) impairment of capillaries as well as by induction of angiogenesis. Similar alterations were also found in the heart of captopril co-treated rats, despite of the significant suppression of blood pressure. The results indicate that NO-deficient hypertension is accompanied by metabolic disturbances and ultrastructural alterations of the heart and these changes are probably not induced by the renin-angiotension system only.
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PMID:Chronic disturbances in NO production results in histochemical and subcellular alterations of the rat heart. 1080 8