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

Hexachlorobutadiene (HCBD) is a potent nephrotoxin in rodents that can cause degeneration, necrosis and regeneration in renal tubular epithelial cells. Its toxicity is due to its conjugation by glutathione (GSH) to form glutathione S-conjugate, by the enzyme glutathione S-transferase and finally to the related cysteine-conjugate. This metabolite is then actively taken up by kidney and cleared in the renal tubular epithelial cells, rich in beta-lyase, to a reactive thiol derivative that covalently binds to the macromolecules. In this study, different groups of 28-day male Wistar albino (W/A) rats were dosed daily with 25 mg/kg HCBD for 2, 3, 4 and 7 days; control group dosed with corn oil. Data showed that in the 2- and 3-day treated groups there was substantial necrosis to the straight portion of the proximal tubules (pars recta or S3 segment), rich in glutamine transaminase K (GTK/beta-lyase). In the 4-day treated group, the renal proximal tubules had regenerated and showed a basophilic appearance. In animals treated for 7 days, it was observed that the kidney appeared to have returned to normal and had become resistant to further doses of HCBD. To define the time for the kidney to regain susceptibility to HCBD, 18- and 25-day studies with both low (25 mg/kg) and high (100 mg/kg) doses of HCBD (following two initial doses of 25 mg/kg) were performed. In the 18-day study, histopathological examination of the kidneys in animals of this group and also animals in the 25-day study, which received two further doses of HCBD, showed that the severity of kidney damage is much less than in the 2-day treated animals, a clear indication that the tubular cells were still resistant to the low dose of HCBD. Concentration of blood urea nitrogen, as a marker of kidney damage, in these two groups also confirmed the results. In animals re-exposed to the high dose of HCBD, data showed that the susceptibility to HCBD was starting to return.
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PMID:Development of resistance against hexachlorobutadiene in the proximal tubules of young male rat. 1501 8

For a long time, aluminium (Al) has been considered an indifferent element from a toxicological point of view. In recent years, however, Al has been implicated in the pathogenesis of several clinical disorders, such as dialysis dementia, the fulminant neurological disorder that can develop in patients on renal dialysis. Therefore, the present experiment was carried out to determine the effectiveness of l-ascorbic acid (AA) in alleviating the toxicity of aluminium chloride (AlCl3) on certain hemato-biochemical parameters, lipid peroxidation and enzyme activities of male New Zealand white rabbits. Six rabbits per group were assigned to 1 of 4 treatment groups: 0mg AA and 0mg AlCl3/kg body weight (BW) (control); 40 mg AA/kg BW; 34 mg AlCl3/kg BW (1/25 LD50); 34 mg AlCl3 plus 40 mg AA/kg BW. Rabbits were orally administered their respective doses every other day for 16 weeks. Evaluations were made for lipid peroxidation, enzyme activities and hemato-biochemical parameters. Results obtained showed that AlCl3 significantly (P<0.05) induced free radicals and decreased the activity of glutathione S-transferase (GST) and the levels of sulfhydryl groups (SH groups) in rabbit plasma, liver, brain, testes and kidney. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (AlP), acid phosphatase (AcP), and phosphorylase activities were significantly decreased in liver and testes due to AlCl3 administration. While, plasma, liver, testes and brain lactate dehydrogenase (LDH) activities were significantly increased. Contrariwise, the activity of acetylcholinesterase (AChE) was significantly decreased in brain and plasma. Aluminium treatment caused a significant decrease in plasma total lipids (TL), blood haemoglobin (Hb), total erythrocytic count (TEC) and packed cell volume (PCV), and increased total leukocyte count (TLC) and the concentrations of glucose, urea, creatinine, bilirubin and cholesterol. Ascorbic acid alone significantly decreased the levels of free radicals, TL, cholesterol, glucose and creatinine, and increased the activity of GST, SH groups, Hb, TEC and PCV. While, the rest of the tested parameters were not affected. Also, the present study showed that ascorbic acid can be effective in the protection of aluminium-induced toxicity.
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PMID:Aluminium-induced changes in hemato-biochemical parameters, lipid peroxidation and enzyme activities of male rabbits: protective role of ascorbic acid. 1512 98

Vitronectin (VN) is one of the primary adhesive proteins in serum and serves to promote the attachment and spreading of a wide variety of cell types to tissue culture plastic. In this study, the pGEX2t expression vector was used to express full-length human VN as a GST-tagged fusion protein in Escherichia coli. GST/VN production was induced with IPTG and the protein was found to localize to inclusion bodies. The inclusion bodies were isolated from cell lysates, washed once with 2 M urea and Triton X-100, and then solubilized with 8 M urea in the presence of a reducing compound. Solubilized GST/VN was purified by heparin affinity chromatography and refolded by dialysis against phosphate buffered saline. Approximately 40 mg of GST/VN was recovered from 1L of bacterial culture. Purified GST/VN migrated at the predicted molecular mass on SDS-PAGE and was recognized by both anti-GST and anti-VN antibodies. GST/VN bound to heparin and promoted cell adhesion, spreading, and growth to a similar extent as that observed with plasma-derived VN. As such, the production of recombinant VN in bacteria represents a rapid and convenient method to produce large quantities of VN for cellular studies.
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PMID:Expression, production, and characterization of full-length vitronectin in Escherichia coli. 1517 94

Role of alpha-tocopherol (vitamin E), beta-carotene and/or their combination as antioxidants against the toxicity of fenvalerate on blood hematology, free radicals, biochemical parameters, and semen quality were studied in male rats. Fenvalerate (20 mg/kg BW), vitamin E (100 mg/kg BW), beta-carotene (10 mg/kg BW), and vitamin E plus beta-carotene (100 + 10 mg/kg BW, respectively) were given alone or in combination with fenvalerate. The tested doses were given to rats every other day for 30 days. Results obtained showed that fenvalerate significantly (P < 0.05) induced free radicals in plasma and brain and insignificantly in liver and testes. While, vitamin E, beta-carotene alone and/or in combination decreased the levels of free radicals in plasma, liver, testes, and brain. The activities of glutathione S-transferase (liver), alkaline phosphatase (plasma and liver), aspartate aminotransferase (plasma, liver, and testes) and alanine aminotransferase (plasma and liver) were significantly (P < 0.05) increased due to fenvalerate administration. The activity of acetylcholinesterase was significantly (P < 0.05) decreased in brain and plasma, while plasma glucose, urea, creatinine, and bilirubin concentrations were significantly (P < 0.05) increased in rats treated with fenvalerate. Also, results showed a significant (P < 0.05) alterations in plasma proteins, hematological parameters, body weight, and relative weights of organs. Sperm concentration and motility (%) were significantly (P < 0.05) decreased, while dead and abnormal sperm increased in rats exposed to fenvalerate. Vitamin E, beta-carotene alone and/or in combination did not cause any changes in the investigated parameters, but improved semen quality and minimized the toxic effect of fenvalerate. The obtained results demonstrated the beneficial influences of vitamin E, beta-carotene alone and/or in combination in reducing the harmful effects of fenvalerate.
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PMID:Role of alpha-tocopherol and beta-carotene in ameliorating the fenvalerate-induced changes in oxidative stress, hemato-biochemical parameters, and semen quality of male rats. 1518 33

Cadmium is a well-known human carcinogen and a potent nephrotoxin. Lipid peroxidation is involved in cadmium-related toxicity. Vitamin E and beta-carotene are effective antioxidants and free radical scavengers. Therefore, the present study was carried out to investigate the potential protective effects of vitamin E and beta-carotene alone or in combination against cadmium (Cd) toxicity. Cadmium chloride (CdCl2, 5 mg/kg BW, 1/15 LD50), vitamin E (100 mg/kg BW), beta-carotene (10 mg/kg BW), and vitamin E with beta-carotene (100 + 10 mg/kg BW, respectively) were orally administered by gavage alone or in combination. The tested doses were given to rats every other day (15 times). Results obtained showed that CdCl2 significantly (P < 0.05) induced free radicals in plasma, liver and brain. The activities of glutathione S-transferase (GST) (plasma and liver), alkaline phosphatase (AlP) (plasma and liver), aspartate aminotransferase (AST), alanine aminotransferase (ALT) (liver) and acetylcholinesterase (AChE) (plasma and brain) were significantly (P < 0.05) decreased due to CdCl2 administration, whereas, the activities of AST and ALT were increased in plasma. Treatment with CdCl2 caused a significant (P < 0.05) increase in glucose, urea, creatinine and bilirubin in plasma. On the other hand, results showed that CdCl2 significantly (P < 0.05) decreased plasma total protein (TP), albumin (A), blood hemoglobin (Hb), total erythrocytic count (TEC) and packed cell volume (PCV), while total leukocyte count (TLC) increased. Treatment with CdCl2 caused a significant (P < 0.05) decrease in sperm concentration, motility (%), weight of testes and epididymis, and increase in dead and abnormal sperm. Results demonstrated the beneficial influences of vitamin E, -carotene alone and/or in combination in reducing the harmful effects of CdCl2.
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PMID:Cadmium-induced changes in lipid peroxidation, blood hematology, biochemical parameters and semen quality of male rats: protective role of vitamin E and beta-carotene. 1530 3

Adipocyte differentiation-related protein (ADRP) is a member of PAT proteins existing in lipid droplets (LDs). By yeast two-hybrid screening, we identified ADP-ribosylation factor 1 (ARF1) as a binding partner of ADRP. The interaction of ADRP and ARF1 was verified by GST pull-down and co-immunoprecipitation experiments. Interestingly, ADRP precipitated the GDP-bound ARF1 preferentially to the GTP-bound ARF1. Consistent with this, either brefeldin A (BFA), a fungal metabolite to inhibit ARF-GEF, or a dominant-negative mutant of ARF1 caused dissociation of ADRP from LD. On the other hand, overexpression of wild-type ARF1 did not promote the ADRP dissociation or new LD formation. By using deletion mutants, a central domain of ADRP, which is dispensable for LD binding, was shown to bind to ARF1. The present study showed that the GDP-bound ARF1 induces dissociation of ADRP from the LD surface, and that LD is a target of BFA action.
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PMID:ADRP is dissociated from lipid droplets by ARF1-dependent mechanism. 1533 57

Acute renal failure (ARF) usually develops in 5% to 30% of patients undergoing heart surgery and is associated with a more complicated clinical evolution course and with an excessive mortality of up to 80%. The objective of this study was to verify the frequency of ARF in postoperative coronary artery bypass surgery with and without cardiopulmonary bypass, by the evaluation of renal function markers' performance [plasma creatinine, plasma urea, urinalysis, fractional excretion of sodium, creatinine clearance and Alpha-glutathione S-transferase (alpha-GST)], besides to verify possible relations between clinical variables involved in postoperative heart surgery and the occurrence of renal insufficiency.
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PMID:Does urinalysis predict acute renal failure after heart surgery? 1546 6

Porcine interleukin-6 (PIL-6) protein without signal peptide was expressed as a glutathione S-transferase (GST) fusion protein in Escherichia coli. The fusion protein was expressed in an insoluble fraction, however, it was solubilized by refolding procedure using urea. From the solubilized protein, the recombinant PIL-6 (rPIL-6) was purified by a batch method using glutathione sepharose 4B and PreScission protease cleavage. By the B3B1 hybridoma cell proliferation assay, biological activity of the purified rPIL-6 was confirmed. Three monoclonal antibodies (MAbs) named 2B-1, 5A-8 and 4C-3 were generated by using the rPIL-6 as an immunogen. Immunoglobulin isotypes of the MAbs were IgG2a (4C-3) and IgG2b (2B-1 and 5A-8). For the epitope analysis, additive enzyme-linked immunosorbent assay and immunoblot analysis using deletion mutants of PIL-6 were performed. These experiments revealed that the two MAbs (2B-1 and 5A-8) recognize an overlapped epitope and the other (4C-3) recognizes a distinct epitope, and all epitopes reside in the region of aa26-64 of PIL-6.
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PMID:Generation of monoclonal antibodies to porcine interleukin 6 (PIL-6) using the recombinant PIL-6 expressed in Escherichia coli. 1547 67

Vaccination with a membrane-bound thiol Sepharose-binding fraction (TSBP) of adult Haemonchus contortus has been shown to confer significant levels of protection against homologous challenge in sheep. This fraction is greatly enriched for cysteine proteinase activity. Following fractionation of TSBP by anion-exchange chromatography on MonoQ, protection was found to partition with those fractions further enriched for cysteine proteinase activity. In this study, the cysteine proteinases of adult H. contortus TSBP were specifically purified by affinity chromatography using recombinant H. contortus cystatin, a potent cysteine proteinase inhibitor. Although only 1-1.5% of total TSBP bound to cystatin-Sepharose, this fraction contained 100% of the cysteine proteinase activity, as determined by gelatin substrate gel analysis. When used to immunise sheep, less than 3microg per dose of this cysteine proteinase fraction was found to confer a substantial and repeatable level of protection against homologous challenge infection, reducing faecal egg counts by 48 and 28% and worm burdens by 44 and 46% over two trials. Host serum immunoglobulin levels and abomasal mast cell and eosinophil numbers were evaluated, although no correlation with protection was observed. Three cathepsin B-like cysteine proteinases present in TSBP (hmcp1, 4 and 6) have been identified previously by cDNA library immunoscreening. The predicted mature forms of these three cysteine proteinases were expressed in bacteria as insoluble, GST-fusion proteins. Following solubilisation in urea/DTT, the protective capacity of a cocktail of recombinant proteins was evaluated in sheep. Although no reduction in faecal egg counts was observed, sheep vaccinated with recombinant cysteine proteinases showed a highly significant 38% reduction (P <0.01) in worm burdens.
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PMID:Protection studies in sheep using affinity-purified and recombinant cysteine proteinases of adult Haemonchus contortus. 1547 16

Aluminium has the potential to be neurotoxic in humans and animals, and is present in many manufactured foods and medicines and is also added to drinking water for purification purposes. Therefore, the present study was carried out to investigate (1) the alterations in biochemical parameters, free radicals and enzyme activities induced by aluminium chloride (AlCl3) in plasma and different tissues of male rats, and (2) the role of vitamin E (VE) and selenium in alleviating the negative effects of aluminium. VE plays an important role as an antioxidant and is consequently expected to protect tissues from damage caused by reactive oxygen metabolites. Selenium is also generally recognized to be a trace mineral of great importance for human health, protecting the cells from the harmful effects of free radicals. Seven rats per group were assigned to one of six treatment groups: 0 mg VE, 0 mg Se and 0 mg AlCl3/kg body weight (BW) (control); 100 mg VE/kg BW; 200 microg Se kg BW; 34 mg AlCl3/kg BW (1/25 LD50); 34 mg AlCl3 plus 100 mg VE/kg BW; 34 mg AlCl3 plus 200 microg Se/kg BW. Rats were orally administered their respective doses every other day for 30 days. Evaluations were made for lipid peroxidation, enzyme activities and biochemical parameters. Results obtained showed that AlCl3 significantly (p<0.05) induced free radicals (thiobarbituric acid-reactive substances) and decreased the activity of glutathione S-transferase (GST) and the levels of sulphydryl groups (SH groups) in rat plasma, liver, brain, testes and kidney. Aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, acid phosphatase, and phosphorylase activities were significantly decreased in liver and testes due to AlCl3 administration, while the activities of these enzymes were significantly increased in plasma. In addition, plasma, liver, testes and brain lactate dehydrogenase activities were significantly increased. On the contrary, the activity of acetylcholinesterase was significantly decreased in brain and plasma. Al treatment caused a significant decrease in plasma total protein (TP), albumin and total lipids (TL), and increased the concentrations of glucose, urea, creatinine, bilirubin and cholesterol. VE or Se alone significantly decreased the levels of free radicals, TL, cholesterol, urea and bilirubin, and increased the activity of GST, and SH groups, TP and albumin, while the rest of the tested parameters were not affected. VE or Se in combination with Al partially or totally alleviated its toxic effects on the studied parameters. In conclusion, VE and Se have beneficial effects and could be able to antagonize Al toxicity.
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PMID:Antioxidant effect of vitamin E and selenium on lipid peroxidation, enzyme activities and biochemical parameters in rats exposed to aluminium. 1548 71


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