Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.1.1.49 (glucose-6-phosphate dehydrogenase)
 7,794 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study examined the in vivo antioxidant and/or prooxidant effect of short-term dehydroepiandrosterone (DHEA) injection and the effect of dietary vitamin E. Male Sprague-Dawley rats (4 wk old) were fed vitamin E-deficient or vitamin E-adequate (30 mg DL-alpha-tocopheryl acetate/kg) diet for 4 weeks followed by intraperitoneal injection of DHEA for 1 week. The results showed that DHEA injection caused a dose-dependent decrease in body weight, and this effect was more pronounced in vitamin E-deficient rats. In contrast, DHEA injection significantly increased liver, kidney and adrenal weights. Hepatic vitamin E content was significantly lowered by vitamin E deficiency, which led to significantly increased ex vivo and iron-induced lipid peroxidation. DHEA injection did not affect hepatic vitamin E content but significantly decreased ex vivo and iron-induced lipid peroxidation in vitamin E-deficient rats. Hepatic total sulfhydryl (SH) groups and non-protein SH contents were not affected by vitamin E but were significantly increased by DHEA injection, which at 100 mg/kg was not more effective than at 50 mg/kg. Hepatic glutathione S-transferase (GST) activity was significantly decreased by DHEA, but vitamin E alleviated such a decrease. DHEA injection significantly increased hepatic glucose 6-phosphate dehydrogenase (G6PD) activity, and the effect was dose dependent in vitamin E-deficient rats. Thus, DHEA may compensate for vitamin E deficiency in vivo, and this effect is masked when dietary vitamin E is adequate. The antioxidant effect of DHEA is accompanied by decreased body weights, enlarged (fat-laden) tissues and altered activities of hepatic GST and G6PD.
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PMID:Toxicological and antioxidant effects of short-term dehydroepiandrosterone injection in young rats fed diets deficient or adequate in vitamin E. 1045 78

High frequencies of both thalassemia trait (5.2%) and glucose 6-phosphate dehydrogenase (G6PD) deficiency for only males (1.3%) have been observed in the Calabrian population. The G6PD activity measurement was carried out on 1239 samples of whole blood from Calabrian subjects of both sexes (age range 10-55) by a differential pH-metry technique which was quite suitable to determine the G6PD deficiency in mass screenings. The analyzed subjects showed: only the thalassemia trait; or only the G6PD deficiency; or only the total iron serum deficiency; or G6PD deficiency associated with the thalassemia trait or with the total iron serum deficiency. The G6PD heterozygous subjects have an enzymatic activity which is masked by both the thalassemia trait and the total iron serum deficiency. In a population showing high frequencies of both thalassemia trait and G6PD deficiency, the comparison of G6PD activity of heterozygous subjects also affected with the thalassemia trait is more reliable if referred to the enzymatic activity of the carriers of the latter inherited anomaly rather than to G6PD activity of normal subjects.
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PMID:Identification of glucose 6-phosphate dehydrogenase deficiency in a population with a high frequency of thalassemia. 1064 29

The influence of occupational exposure to mercury vapours on the activity of the red cell enzymes [glucose-6-phosphate dehydrogenase (G-6PD), acetylcholinesterase (AChE), glutathione reductase (GR) and superoxide dismutase (SOD)], as well as on peripheral blood indices [erythrocyte number (RBC), HCT, Hb, MCHC] and on serum concentrations of iron, ferritin, transferrin and total iron binding capacity (TIBC), was assessed. Studies were carried out on 46 men aged between 21 and 56 years (X = 39 +/- 10.4) exposed to mercury vapours during their work from 7 months to 32 years (= 14.7 +/- 10.8). The control group consisted of 35 healthy workers aged between 20 and 54 years (X = 33.6 +/- 9.8) not exposed to chemical nor physical agents. In both groups studied, there were 50% and 34.3% smokers, respectively. The activity of studied red cell enzymes--G-6PD, AChE, GR and SOD--was estimated according to the colorimetric methods described by Beutler and expressed as international units per gram of hemoglobin (IU g Hb(-1)). Peripheral blood cell parameters were determined using an automatic cell counter. The concentration of serum iron and TIBC was determined using colorimetric methods (Beckman), while that of ferritin and transferrin by nephelometric methods. The time-weighted average (TWA) of mercury concentration in the air determined before the study was 0.0028 mg m(-3). Statistical analysis of the data was performed using either the Cochran and Cox C-test or the Student's t-test. The medium mercury concentration in the urine was 77.44 +/- 48.15 microg l(-1). In the group exposed to mercury vapours, a significant decrease was found in G-6PD activity (23.9%, P<0.001), GR (18.8%, P<0.001), and SOD (5%, P<0.001) with a concomitant increase in AChE activity (35.9%, P<0.001) was found. Moreover, a statistically significant increase occurred in HCT and RBC, and a decrease in MCV and MCHC as well as increases of ferritin (130.9%, P<0.001), transferrin (118.4%, P<0.001) and TIBC (11.2%, P<0.05). Our results indicate that long-term exposure to mercury vapours induces changes in the activity of red cell enzymes--G-6PD, AChE, GR and SOD--and may also influence other important hematological parameters of the peripheral blood.
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PMID:The activity of erythrocyte enzymes and basic indices of peripheral blood erythrocytes from workers chronically exposed to mercury vapours. 1079 23

In recent years, considerable efforts have been made to identify new chemopreventive agents which could be useful for man. Myrica nagi, a subtropical shrub, has been shown to possess significant activity against hepatotoxicity and other pharmacological and physiological disorders. We have shown a chemopreventive effect of Myrica nagi on cumene hydroperoxide-induced cutaneous oxidative stress and toxicity in mice. Cumene hydroperoxide treatment at a dose level of 30 mg/animal/0.2 ml acetone enhances susceptibility of cutaneous microsomal membrane for iron-ascorbate-induced lipid peroxidation and induction of xanthine oxidase activity which are accompanied by decrease in the activities of cutaneous antioxidant enzymes such as catalase, glutathione peroxidase, glutathione reductase, glucose-6-phosphate dehydrogenase and depletion in the level of cutaneous glutathione. Parallel to these changes a sharp decrease in the activities of phase II metabolizing enzymes such as glutathione S-transferase and quinone reductase has been observed. Application of Myrica nagi at doses of 2.0 mg and 4.0 mg/kg body weight in acetone prior to that of cumene hydroperoxide (30 mg/animal/0.2 ml acetone) treatment resulted in significant inhibition of cumene hydroperoxide-induced cutaneous oxidative stress and toxicity in a dose-dependent manner. Enhanced susceptibility of cutaneous microsomal membrane for lipid peroxidation induced by iron ascorbate and xanthine oxidase activities were significantly reduced (P<0.05). In addition the depleted level of glutathione, the inhibited activities of antioxidants, and phase II metabolizing enzymes were recovered to a significant level (P<0.05). The protective effect of Myrica nagi was dose-dependent. In summary our data suggest that Myrica nagi is an effective chemopreventive agent in skin and capable of ameliorating cumene hydroperoxide-induced cutaneous oxidative stress and toxicity.
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PMID:Myrica nagi attenuates cumene hydroperoxide-induced cutaneous oxidative stress and toxicity in Swiss albino mice. 1086 2

The effects of iron deficiency and iron resupply on the metabolism of leaf organic acids have been investigated in hydroponically grown sugar beet. Organic acid concentrations and activities in leaf extracts of several enzymes related to organic acid metabolism were measured. Enzymes assayed included phosphoenol pyruvate carboxylase (PEPC; EC 4.1.1.31), different Krebs cycle enzymes: malate dehydrogenase (MDH; EC 1.1.1.37), aconitase (EC 4.2.1.3), fumarase (EC 4.2.1.2), citrate synthase (CS; EC 4.1.3.7) and isocitrate dehydrogenase (ICDH; EC 1.1.1.42), glucose-6-phosphate dehydrogenase (G6PDH; EC 1.1.1.49) and two enzymes related to anaerobic metabolism (lactate dehydrogenase [LDH]; EC 1.1.1.27, and pyruvate decarboxylase [PDC]; EC 4.1.1.1). Iron concentration in leaves was severely decreased by iron deficiency. Iron resupply caused an increase in iron concentrations, reaching levels similar to the controls in 96 h. Iron deficiency induced a 2.3-fold (from 16 to 37 mmol m-2) increase in leaf total organic acid concentration. Organic anion concentrations were still 4-fold higher than the controls 24 h after resupply and decreased to values similar to those found in the controls after 96 h. All measured enzymes had increased activities in extracts of iron-deficient leaves when compared to the controls and generally decreased to control values 24 h after iron addition. These data provide evidence that organic acid accumulation in iron-deficient leaves is likely not due to an enhancement in leaf carbon fixation. Instead, this accumulation could be associated with organic acid export from the roots to the leaves via xylem.
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PMID:Changes induced by Fe deficiency and Fe resupply in the organic acid metabolism of sugar beet (Beta vulgaris) leaves. 1131 12

In an earlier communication, we have shown that Tephrosia purpurea ameliorates benzoyl peroxide-induced oxidative stress in murine skin (Saleem et al. 1999). The present study was designed to investigate a chemopreventive efficacy of T purpurea against N-diethylnitrosamine-initiated and potassium bromate-mediated oxidative stress and toxicity in rat kidney. A single intraperitoneal dose of N-diethylnitrosamine (200 mg/kg body weight) one hr prior to the dose of KBrO3 (125 mg/kg body weight) increases microsomal lipid peroxidation and the activity of xanthine oxidase and decreases the activities of renal antioxidant enzymes viz., catalase, glutathione peroxidase, glutathione reductase and glucose-6-phosphate dehydrogenase, phase II metabolizing enzymes such as glutathione-S-transferase and quinone reductase and causes depletion in the level of renal glutathione content. A sharp increase in blood urea nitrogen and serum creatinine has also been observed. Prophylactic treatment of rats with T. purpurea at doses of 5 mg/kg body weight and 10 mg/kg body weight prevented N-diethylnitrosamine-initiated and KBrO3 promoted renal oxidative stress and toxicity. The susceptibility of renal microsomal membrane for iron ascorbate-induced lipid peroxidation and xanthine oxidase activities were significantly reduced (P<0.01). The depleted levels of glutathione, the inhibited activities of antioxidant enzymes, phase II metabolizing enzymes and the enhanced levels of serum creatinine and blood urea nitrogen were recovered to a significant level (P<0.01). All the antioxidant enzymes were recovered dose-dependently. Our data indicate that T purpurea besides a skin antioxidant can be a potent chemopreventive agent against renal oxidative stress and carcinogenesis induced by N-diethylnitrosamine and KBrO3.
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PMID:Tephrosia purpurea ameliorates N-diethylnitrosamine and potassium bromate-mediated renal oxidative stress and toxicity in Wistar rats. 1145 68

The cytotoxicity of asbestos has been related to its ability to increase the production of reactive oxygen species (ROS), via the iron-catalyzed reduction of oxygen and/or the activation of NADPH oxidase. The pentose phosphate pathway (PPP) is generally activated by the cell exposure to oxidant molecules. Contrary to our expectations, asbestos (crocidolite) fibers caused a dose- and time-dependent inhibition of PPP and decreased its activation by an oxidative stress in human lung epithelial cells A549. In parallel, the intracellular activity of the PPP rate-limiting enzyme, glucose 6-phosphate dehydrogenase (G6PD), was significantly diminished by crocidolite exposure. This inhibition was selective, as the activity of other PPP and glycolysis enzymes was not modified, and was not attributable to a decreased expression of G6PD. On the opposite, the incubation with glass fibers MMVF10 did not modify PPP and G6PD activity. PPP and G6PD inhibition did not correlate with the increased nitric oxide (NO) production elicited by crocidolite in A549 cells. Experiments with the purified enzyme suggest that crocidolite inhibits G6PD by directly interacting with the protein. We propose here a new mechanism of asbestos-evoked oxidative stress, wherein fibers increase the intracellular ROS levels also by inhibiting the main antioxidant pathway of the cell.
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PMID:Crocidolite asbestos inhibits pentose phosphate oxidative pathway and glucose 6-phosphate dehydrogenase activity in human lung epithelial cells. 1197 96

Ascorbate deficiency in the Arabidopsis thaliana vtc1 mutant had no effect on photosynthesis, but modified defense pathways. The ascorbate content of vtc1 leaves was increased 14-fold after 10 mM ascorbate was supplied, without a concomitant change in redox state. High ascorbate modified the abundance of 495 transcripts. Transcripts encoding dehydroascorbate reductase, pathogenesis-related protein 1, and a peroxiredoxin were decreased, whereas those encoding salicylate induction-deficient protein 1, Cu,Zn superoxide dismutase, iron superoxide dismutase, metallothionein, and glutathione transferases were increased. Catalase transcripts were unaffected, but ascorbate peroxidase isoforms APX1 and tAPX were slightly decreased and sAPX transcripts increased. A number of nuclear encoded transcripts for photosynthetic electron transport components were repressed as a result of ascorbate accumulation, whereas those that were chloroplast-encoded were increased. High ascorbate caused decreases in mRNAs encoding chloroplast enzymes such as fructose-1,6-bisphosphatase and sedoheptulose-1,7-bisphosphatase that are activated by reduced thioredoxin. In contrast, others, such as glucose 6-phosphate dehydrogenase, whose activity is inactivated by reduced thioredoxin, were repressed. Together, these results show that ascorbate is involved in metabolic cross-talk between redox-regulated pathways. The abundance of this antioxidant provides information on redox buffering capacity that coordinates redox processes associated with the regulation of photosynthesis and plant defense.
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PMID:Effects of leaf ascorbate content on defense and photosynthesis gene expression in Arabidopsis thaliana. 1262 14

CDKN2A is regarded as a major melanoma susceptibility gene. A 19 bp deletion has been detected within Dutch families with familial atypical multiple mole-melanoma syndrome. Genetic analysis revealed two individuals with germline deletions in both copies of CDKN2A. One of them did not develop atypical naevi or melanoma, but died of adenocarcinoma at the age of 54 years. This report describes the results of the investigation of the second p16-null individual, who was also found to have glucose-6-phosphate dehydrogenase (G-6-PD) deficiency and who has developed many atypical naevi and seven melanomas. Using electron microscopic techniques, striking alterations in melanosomal structures and deviations in their sulphur, iron and calcium composition indicating a strong preference for phaeomelanogenesis and increased oxidative stress were found in the naevus cells of the patient. Using an in vitro model, we demonstrated that leaking melanin precursors may strongly enhance oxidative DNA damage through iron release from ferritin. We conclude that the homozygous p16 deletion is not sufficient for the development of a dysplastic naevus phenotype and melanoma. However, when an additional modifying factor, such as G-6-PD deficiency, increases the level of oxidative DNA damage in melanin-producing cells, the risk of developing atypical naevi and their malignant transformation may increase significantly.
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PMID:Homozygous germline mutation of CDKN2A/p16 and glucose-6-phosphate dehydrogenase deficiency in a multiple melanoma case. 1269 Mar 1

Advantage is taken in many sterilization processes, especially for food packaging materials, of the synergy between H2O2 and UV irradiation for spore killing. The nature of the synergy is currently not well defined in terms of targets and mechanisms. We found that under some experimental conditions, the synergistic killing of spores of Bacillus megaterium ATCC 19213 appeared to be mainly UV-enhanced peroxide killing, while under other conditions, it appeared to be mainly peroxide-enhanced UV killing. Lethal combinations of H2O2 and UV irradiation for spores resulted in only modest increases in auxotrophic mutations among survivors, indicative of little DNA damage, in contrast to higher mutation levels after dry-heat damage at 115 degrees C. However, the combination of UV light and peroxide did lead to major inactivation of glucose 6-phosphate dehydrogenase, an enzyme that was used to monitor the damage to bacterial protein. Synergistic UV-H2O2 killing was reduced by agents such as pyruvate, thiosulfate, and iron or copper cations, which appeared to act at least in part by reacting chemically with H2O2, and was only slightly affected by the use of UV light at a wavelength of 222 nn rather than 254 nm. Hydrogen peroxide treatment can precede UV irradiation for synergistic killing by some hours with an interim of drying for spores of Bacillus subtilis A, a spore type used commonly for the validation of aseptic processes. Synergistic killing of dried spores or those in suspensions was accelerated at higher temperatures (50 degrees C) rather than at lower temperatures (25 degrees C).
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PMID:Characterization of UV-peroxide killing of bacterial spores. 1287 Jul 58


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