Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.5.1.18 (glutathione S-transferase)
 22,582 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Activity of microsomal UDP-glucuronosyl transferase and cytosol glutathione transferase was studied in the liver and small intestine mucosa of rats which received rations with 5.18 and 33% of protein, during 2 months. Activity of UDP-glucuronosyl transferase GT1-isoform both in native and in detergent-activated microsomes of the liver increased with protein deficiency in the ration, while GT2-isoform activity and that of three glutathione transferase forms decreased. Excess of protein in the ration led to a growth of conjugation enzyme activity in the liver. The food protein level influenced the degree of GT1 and GT2 induction by benzyl but it did not change the capacity for induction of glutathione transferase. Activity of conjugation enzymes in the small intestine mucosa of rats to a lesser degree depended on the protein level in the ration.
 ...
PMID:[Dietary protein as a modulator of the activity of enzymes metabolizing xenobiotics. UDP glucuronosyltransferase and glutathione transferase]. 212 26

Pregnant rhesus monkeys (Macaca mulatta) were fed either selenium (Se) deficient or Se supplemented diets with adequate vitamin E. Except for some cardiac irregularities in the first babies born to these females, no physiological disorders due to Se deficiency were seen in a subsequent offspring. Plasma and erythrocyte glutathione peroxidase activities and blood Se levels increased in the Se supplemented monkeys but decreased in the deficient ones. The data indicated that hair Se levels reflect long term exposure to this element. In a very preliminary experiment, evidence was obtained to indicate that dietary protein deficiency along with Se deficiency will generate cardiomyopathic lesions characteristic of Se deficiency. It is hypothesized that, in addition to Se deficiency, another dietary deficiency (or abnormality) is necessary to produce Se deficiency lesions in higher primates. Higher glutathione transferase (or non-Se glutathione peroxidase) activity in tissues of rhesus monkeys may account for this resistance.
 ...
PMID:Effects of feeding selenium deficient diets to rhesus monkeys (Macaca Mulatta). 334 74

Protein deficiency was produced by feeding synthetic 8%-protein diet. Lithium carbonate at the dose level of 1.1g/kg diet was administered to normal and protein-deficient rats for a period of one mo. A significant inhibition in the levels of cytochrome (cyt) P450, cyt b5, glutathione (GSH), glutathione S-transferase (GST) and glutathione peroxidase (GPx), but an increase in gamma-glutamyl transpeptidase (gamma-GT), was observed in low-protein LP-fed rats. Lithium treatment to normal rats caused no significant change in the activities of cyt P450, cyt b5, GST, and GSH levels, whereas there was elevation in the activities of gamma-GT and GPx and suppression in glutathione reductase (GRd) activity. Lithium administration to LP-fed rats resulted in significant increases in the hepatic gamma-GT and GPx activities.
 ...
PMID:Effect of lithium on hepatic drug-metabolizing enzymes of protein-deficient rats. 952 58

This study was designed to evaluate the protective effects of zinc on the liver activities of antioxidant enzymes in protein-deficient rats. Zinc sulfate at a dose level of 227 mg/l in drinking water was administrated to Sprague Dawley normal control as well as to protein-deficient rats for a total duration of eight weeks. The effects of zinc treatment and protein deficiency alone as well as combined were studied on rat liver antioxidant enzymes which included catalase, glutathione peroxidase (GPX), glutathione reductase (GR), superoxide dismutase (SOD), and glutathione S-transferase (GST). Protein deficiency in normal rats resulted in a significant increase in hepatic lipid peroxidation and in catalase, Gpx, GR and GST activity. A significant inhibition in the levels of SOD activity and reduced glutathione (GSH) was observed following protein deficiency in normal rats. Zn treatment to protein deficient animals lowered lipid peroxidation and catalase, Gpx and GST activities, and also resulted in a significant elevation in the levels of GSH and SOD activity. The concentration of zinc decreased significantly in protein deficient animals but returned to normal levels when zinc was administered.
 ...
PMID:Protective effects of zinc on oxidative stress enzymes in liver of protein deficient rats. 1567 49