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)

The enzyme activities of glutathione peroxidase (GPO) with cumenehydroperoxide (cumene-OOH) and H2O2 as substrates, glutathione-S-transferase (GSH-S-T) with 1-chloro-2,4-dinitrobenzene (CDNB) as substrate, phosphofructokinase (PFK) and succinate dehydrogenase (SuDH) were determined for months 1 through 9 of pregnancy in the basal and peripheral sections of the corpora lutea graviditatis of Holstein-Frisean cows. The concentration of reduced glutathione (GSH) was simultaneously measured in these tissue sections. Substantial topographical differences were apparent in the enzyme activities. GPO and GSH-S-T showed activity differences during the course of pregnancy. During the 2nd month of pregnancy, minimal values for the activity of cytoplasmic GPO were observed in the basal areas. The cytoplasmic GPO in the peripheral areas displayed a contrasting dynamic with maximal values during the 6th month. GSH-S-T activities in basal and peripheral tissues appeared similar. GPO activities with H2O2 as substrate, likewise, displayed similar courses of activity in both tissue localizations. SuDH was more active in the peripheral than in the basal area. The activity of PFK displayed just the reverse course. The concentration of GSH in the peripheral area was not higher than in basal area.
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PMID:Biochemical parameters in various sections of bovine corpora lutea graviditatis during the course of pregnancy. 252 8

Brain-derived neurotrophic factor (BDNF) deficiency has been implicated in pathogenesis of Huntington's disease (HD). 3-Nitropropionic acid (3-NP), an irreversible mitochondrial complex II inhibitor, has been commonly used as a pharmacological model recapitulating HD phenotypes in rodents and nonhuman primates. Herein we test whether BDNF may exert neuroprotective effects against mitochondrial dysfunction caused by 3-NP in primary culture of fetal rat cortical neurons. Preconditioning of neuronal cells with BDNF (100 ng/ml for 8h) attenuated 3-NP toxicity (2.5 mM for additional 24h) based on Hoechst and propidium iodide (PI) staining. BDNF effects can be inhibited by the nitric oxide synthase (NOS) inhibitor L-nitroarginine methylester (L-NAME, 100 microM), the cGMP-dependent protein kinase (PKG) inhibitor KT5823 (2 microM), the thioredoxin reductase inhibitor 1-chloro-2,4-dinitrobenzene (DNCB, 5 microM), and a membrane-permeable Bcl-2 inhibitor (12.5 microM). 8-Br-cGMP is a cGMP analogue capable of activating PKG independent of NO. Exogenous application of 8-Br-cGMP (3-30 microM) and purified thioredoxin (3-5 microM) partially mimicked BDNF effects in conferring 3-NP resistance to cortical cells. These results, together with our previous report showing NO donor S-nitrosoglutathione (GSNO)-mediated neuroprotective effects against 3-NP toxicity, suggest that BDNF may protect neurons from mitochondrial dysfunction at least partly via activation of the signaling cascades involving NOS/NO, PKG, thioredoxin and Bcl-2.
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PMID:Protective effects of brain-derived neurotrophic factor against neurotoxicity of 3-nitropropionic acid in rat cortical neurons. 1942 12