1,721,120 research outputs found
Purification and characterization of glutathione transferases from the sea bass (Dicentrarchus labrax) liver
No full textTwo forms of glutathione transferase were purified from liver cytosol of the sea bass (Dicentrarchus labrax) by GSH-Sepharose affinity chromatography followed by chromatofocusing. The major enzyme (DL-GST-6.7; 75% of total activity bound to the column) has a pI value of 6.7 and is composed of two subunits of apparent molecular mass 26.5 kDa. The minor enzyme (DL-GST-8.2; 25% of total activity bound to the column) has a pI value of 8.2 and is composed of two subunits of molecular mass 23.5 kDa. Both isoenzymes appear to have blocked N-terminal. The purified proteins were characterized with respect to substrate specificity, CD spectra, TNS binding properties (with 2-toluidinylnaphthalene 6-sulfonate), and immunological reactivity. Partial internal amino acid sequence was also determined for each isoenzyme. The results obtained suggest that DL-GST-6.7 and DL-GST8.2 are novel GSTs belonging, respectively, to theta and alpha classes
Induction of rat liver glutathione transferase subunit 7 by lead nitrate.
No full textThe effect of a single dose of lead nitrate (10 microM/100 g body wt), a hepatic mitogen, on rat liver glutathione transferase (GST) subunit expression was investigated. Using SDS-polyacrylamide gel electrophoresis and Western blot technique evidence for the induction of GST 7-7 is shown. This occurrence is identical to that observed in preneoplastic nodules generated in rat liver by different models of chemical carcinogenesis, suggesting that lead nitrate may be a very simple model for investigation of the mechanism of glutathione transferase 7-7 gene expression in chemical hepatocarcinogenesis
A conserved hydrogen-bond network stabilizes the structure of Beta class glutathione S-transferases.
No full textThe prooxidant properties of captopril
No full textAbstract- The thiol drug captopril has been reported to possess reducing and transition metal-binding properties, which could result in specific changes in iron and copper prooxidant capacity. Thus, the effects of captopril on iron- and copper-induced oxidative injury were evaluated using deoxyribose as the oxidizable substrate in the presence of physiological phosphate concentrations but in the absence of the non-physiological chelator EDTA. In an iron(III)/H2O2/ascorbate oxidant system, captopril enhanced deoxyribose oxidation only when it was pre-mixed with iron, whereas it did not influence sugar degradation when not pre-mixed with the metal or when ascorbate was omitted. The physiological thiol GSH acted in a similar manner, whereas the SH-lacking angiotensin-converting enzyme inhibitor ramiprilat did not influence iron-induced deoxyribose oxidation, indicating that the thiol group is crucial in favouring enhanced iron reactivity due to 'malignant' chelation. Further specific experiments designed to evaluate possible thiol-dependent iron(III) reduction failed to demonstrate ferric to ferrous reduction by either captopril or reduced glutathione (GSH). When iron(III) was replaced by copper(II) to induce deoxyribose oxidation, captopril was prooxidant both in the presence and absence of ascorbate, and when pre-mixed or not with copper. On the other hand, GSH was prooxidant up to 2:1 molar ratio with respect to copper but markedly inhibited copper-dependent sugar oxidation beginning at molar ratio of 4:1. Ramiprilat did not significantly influence copper-induced deoxyribose oxidation. Moreover, unlike the experiments performed with iron, captopril, as well as GSH, readily reduced copper(II) to copper(I). Hence, captopril can act as prooxidant in the presence of iron or copper. In the former case, only 'malignant' iron chelation by the drug is involved in oxidant injury, whereas in the latter both copper chelation and reduction are operative, although specific chelating mechanisms are crucial in enhancing copper-induced oxidant injury. Captopril, therefore, cannot be considered simply as an 'antioxidant drug', and its catalytic transition metal-related prooxidant capacity should be taken into account in experimental and clinical investigations
Effects of glutathione on kinetics and structural properties of amphibian BbGSTP1-1
No full textEffects of glutathione on the kinetics and structural properties of BbGSTP1-1 were investigated. The liganded state BbGSTP1-1 acquires the capacity to bind the hydrophobic molecules more avidly. Thus, GSH-binding produces significant conformational changes on BbGSTP1-1 which are transmitted to the hydrophobic binding site. Fluorescent experiments carried out with glutathione-analog S-methylglutathione suggest that the -SH group of tripeptide is essential for triggering protein conformational changes. It is argued that the capacity of BbGSTP1-1 to be modulated by GSH concentration allows it to play an efficient detoxication action in both aquatic and terrestrial environment
High levels of antioxidant enzymatic defence assure good protection against hypoxic stress in spontaneously diabetic rats
No full textRecent data from literature report that reactive oxygen species (ROS) seem to play a crucial role in the etiology of both types
I and II diabetes. This may render diabetic individuals more prone to oxidative injury when challenged with hypoxic stress. It is
in fact well known that many diabetic complications cause ischaemic episodes, with a consequent reduction in oxygen supply to
various tissues and organs.
To check this hypothesis, in this work we tested type I diabetic individuals’ antioxidant capability towards a hypoxic-mediated
oxidative challenge. In particular, spontaneously diabetic and age-matched non-diabetic biobreeding (BB)Wistar rats were submitted
to chronic normobaric hypoxia, and the response of antioxidant enzymes, as well as redox-sensitive transcription factor NF-B and
p53, were monitored.
Results show that diabetic subjects present a dramatic enhancement in the major antioxidant enzymes activities, thus supporting
the notion of diabetes-related changes in cellular redox status. This allows diabetic individuals to counteract hypoxia-mediated
oxidative challenge better than the non-diabetic counterpart.
Also the behaviour of both the redox-sensitive nuclear transcription factor NF-B and p53 protein in response to hypoxic
stimulation seems to support the hypothesis of a better ROS scavenging efficiency in diabetics under hypoxic conditions.
In conclusion, high levels of antioxidant enzymatic defences in diabetic BB rats reflect a positive adaptive response able to assure
an efficient protection not only against chronic, diabetes-mediated reactive oxygen species (ROS) overproduction, but also versus
further oxidative damage.
© 2006 Elsevier Ltd. All rights reserved
Late-onset running biphasically improves redox balance, energy- and methylglyoxal-related status, as well as SIRT1 expression in mouse hippocampus
No full text"Despite the active research in this field, molecular mechanisms underlying exercise- induced beneficial effects on brain physiology and functions are still matter of debate, especially with regard to biological processes activated by regular exercise affecting the onset and progression of hippocampal aging in individuals unfamiliar with habitual physical activity. Since such responses seem to be mediated by changes in antioxidative, antiglycative and metabolic status, a possible exercise-induced coordinated response involving redox, methylglyoxal- and sirtuin-related molecular networks may be hypothesized.. In this study, hippocampi of CD1 mice undergoing the transition from mature to middle age were analyzed for redox-related profile, oxidative and methylglyoxal-dependent damage patterns, energy metabolism, sirtuin1 and glyoxalase1 expression after a 2- or 4-mo treadmill running program. Our findings suggested that the 4-mo regular running lowered the chance of dicarbonyl and oxidative stress, activated mitochondrial catabolism and preserved sirtuin1-related neuroprotection. Surprisingly, the same cellular pathways were negatively affected by the first 2 months of exercise, thus showing an interesting biphasic response.. In conclusion, the duration of exercise caused a profound shift in the response to regular running within the rodent hippocampus in a time-dependent fashion. This research revealed important details of the interaction between exercise and mammal hippocampus during the transition from mature to middle age, and this might help to develop non-pharmacological approaches aimed at retarding brain senescence, even in individuals unfamiliar with habitual exercise.
Glutathione S-transferase, similar to sigma class, from skin secretion of Xenopus laevis
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Antioxidant and GSH-related enzyme response to a single teratogenic exposure to the anticonvulsant phenytoin: temporospatial evaluation
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