Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:2.6.1.44 (
AGT
)
770
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Administration of 1,3-bis(2-chloroethyl)-N-nitrosourea (BCNU) inhibits hepatic activities of
glutathione reductase
(GR) comparably in both adult male Fischer-344 (F344) and Sprague-Dawley (SD) rats in vivo. BCNU pretreatment greatly exacerbates the hepatic necrosis caused by diquat in F344 rats, but does not similarly potentiate liver injury in SD rats. The primary purpose of the present studies was to test the hypothesis that BCNU pretreatment would exhibit differences between the two strains in inhibition of GR activities in hepatic subcellular compartments that would correlate with the differing effects on diquat-induced hepatic necrosis. In the present studies, 16 h after administration of 80 mg/kg of BCNU, GR activities in the hepatic homogenates were 20-30% of activities in vehicle-treated controls. Neither the extents of inhibition nor the GR activities in hepatic cytosol, microsomes. mitochondria, or purified nuclei isolated by differential centrifugation were different between SD and F344 rats treated with BCNU. The results indicate that differences between SD and F344 rats in the effects of BCNU on susceptibilities to diquat-induced hepatic necrosis are not readily attributable to compartmentally selective inhibition of GR. In addition, hepatic O6-alkylguanine-DNA alkyltransferase (
AGT
, MGMT) levels were almost completely depleted in BCNU-treated rats of both strains, thus indicating that MGMT-dependent pathways are unlikely to be critical determinants of the effects of BCNU on this model of acute cell death mediated by reactive oxygen species in vivo.
...
PMID:Compartmental inhibition of hepatic glutathione reductase activities by 1,3-bis(2-chloroethyl)-N-nitrosourea (BCNU) in Sprague-Dawley and Fischer-344 rats. 1510 13
In the present study, we have investigated the analgesic effect of the aqueous extract of the root of Glycine tomentella (
AGT
) using models of acetic acid-induced writhing response and formalin test, the anti-inflammatory effect of
AGT
using model of lambda-carrageenan-induced paw edema. In order to investigate the anti-inflammatory mechanism of
AGT
, we have detected the activities of glutathione peroxidase (GPx) and
glutathione reductase
(GRx) in the liver and the levels of malondialdehyde (MDA) and NO in the edema paw. In the analgesic test,
AGT
(0.5 and 1.0 g/kg) decreased the acetic acid-induced writhing response and the licking time on the late phase in the formalin test. In the anti-inflammatory test,
AGT
(0.5 and 1.0 g/kg) decreased the paw edema at the third, fourth, fifth and sixth hour after lambda-carrageenan administration, and increased the activities of SOD, GPx and GRx in the liver tissue and decreased the MDA level in the edema paw at the third hour after lambda-carrageenan injection. However,
AGT
could not affect the NO level which induced by lambda-carrageenan. These results suggested that
AGT
possessed analgesic and anti-inflammatory effects. The anti-inflammatory mechanism of
AGT
might be related to the decrease in the level of MDA in the edema paw via increasing the activities of SOD, GPx and GRx in the liver.
...
PMID:Analgesic and anti-inflammatory activities of aqueous extract from Glycine tomentella root in mice. 1761 91
Trichosporon asahii is a yeast pathogen implicated in opportunistic infections. Cultures of an isolate collected from industrial wastewater were exposed for 2 days to 100 mg/L sodium arsenite (NaAsO2) and cadmium (CdCl2). Both metals reduced glutathione transferase (GST) activity but had no effect on superoxide dismutase or catalase. NaAsO2 exposure increased
glutathione reductase
activity while CdCl2 had no effect. Protein thiols were labeled with 5-iodoacetamido fluorescein followed by one dimensional electrophoresis which revealed extensive protein thiol oxidation in response to CdCl2 treatment but thiol reduction in response to NaAsO2. Two dimensional electrophoresis analyses showed that the intensity of some protein spots was enhanced on treatment as judged by SameSpots image analysis software. In addition, some spots showed decreased IAF fluorescence suggesting thiol oxidation. Selected spots were excised and tryptic digested for identification by MALDI-TOF/TOF MS. Twenty unique T. asahii proteins were identified of which the following proteins were up-regulated in response to NaAsO2: 3-isopropylmalate dehydrogenase, phospholipase B,
alanine-glyoxylate aminotransferase
, ATP synthase alpha chain, 20S proteasome beta-type subunit Pre3p and the hypothetical proteins A1Q1_08001, A1Q2_03020, A1Q1_06950, A1Q1_06913. In addition, the following showed decreased thiol-associated fluorescence consistent with thiol oxidation; aconitase; aldehyde reductase I; phosphoglycerate kinase; translation elongation factor 2; heat shock protein 70 and hypothetical protein A1Q2_04745. Some proteins showed both increase in abundance coupled with decrease in IAF fluorescence; 3-hydroxyisobutyryl-CoA hydrolase; homoserine dehydrogenase Hom6 and hypothetical proteins A1Q2_03020 and A1Q1_00754. Targets implicated in redox response included 10 unique metabolic enzymes, heat shock proteins, a component of the 20S proteasome and translation elongation factor 2. These data suggest extensive proteomic alterations in response to metal-induced oxidative stress in T. asahii. Amino acid metabolism, protein folding and degradation are principally affected.
...
PMID:Redox proteomics changes in the fungal pathogen Trichosporon asahii on arsenic exposure: identification of protein responses to metal-induced oxidative stress in an environmentally-sampled isolate. 2506 82
The article deals with studying of enzyme activity of first and second lines of anti-oxidant defense in adolescents with arterial hypertension and establishing role of genetic component in realization of mechanism of development of this pathology. The main group included 20 adolescents aged from 13 to 16 years with diagnosis of arterial hypertension stage I (risk). The control group consisted of 20 healthy adolescents of corresponding age. The study was carried out to detect activity of superoxide dismutase [EC 1.15.1.1], catalase [EC 1.11.1.6], glutathione peroxidase [EC 1.11.1.9], glucose-6-phosphate dehydrogenase [EC 1.1.1.49]. The concentration of reduced glutathione was established using photoelectrocolorimeter KFK-2MP (Russia). The activity of
glutathione reductase
[
EC 1.8.1.7
] was evaluated using spectrophotometer CF-46 (LOMO, Russia). The content of nitrogen oxide was detected using V.A. Metelskaia and N.G. Gumanova technique (2005). The detection of genetically mediated risk of development of arterial hypertension and identification of gene-gene dependencies (ACE,
AGT
, NOS3) was implemented using technique of PCR-RFLP diagnostic ("DNA-technology", Russia). The genetic analysis identified in main group the following gene-candidates: deletion genotype DD for ACE, polymorphism M235T T->C gene
AGT
, version 786 C/C gene NOS3. All of then can be applied in diagnostic of arterial hypertension. In adolescents with arterial hypertension imbalance of molecular mechanisms of anti-oxidant defense was revealed. This condition is manifested by imbalance in functioning of enzymes of first line of anti-oxidant defense and accumulation of H2O2, increasing of activity of glutathione peroxidase and depressing of activity of the rest of glutathione depending enzymes. Against this background, decreasing of content of nitrogen oxide results in development of endothelial dysfunction.
...
PMID:[The genetic biochemical markers of arterial hypertension in Adolescents.] 3156 70