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

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Query: EC:1.4.1.2 (glutamate dehydrogenase)
4,380 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Changes in oxidative metabolism were studied in hepatopancreas, muscle, and hemolymph of the edible crab Scylla serrata, exposed to a sublethal concentration (2.5 ppm) of cadmium chloride. A significant decrease in glycogen, total carbohydrates, and pyruvate and an increase in lactate levels in hepatopancreas and muscle were observed. Hemolymph sugar levels were increased in experimental crabs. An increase in phosphorylase suggested increased glycogenolysis during cadmium toxicity. The decrease in lactate dehydrogenase activity and the increase in lactate content indicated reduced mobilization of pyruvate into the citric acid cycle. Krebs cycle enzymes such as succinate dehydrogenase and malate dehydrogenase were found to be decreased, suggesting impairment of mitochondrial oxidative metabolism as a consequence of cadmium toxicity. Glucose-6-phosphate dehydrogenase activity was increased, suggesting enhanced oxidation of glucose by the HMP pathway. Cytochrome-c oxidase and Mg2+ ATPase activity levels decreased, indicating impaired energy synthesis during cadmium stress. Acid and alkaline phosphatase activities increased, suggesting enhanced breakdown of phosphates to release energy in view of impaired ATPase system during cadmium exposure. A significant decrease in protein and free amino acid and an increase in ammonia, urea, and glutamine levels were observed in the tissues during exposure. An increase in protease, alanine aminotransaminase, and aspartate aminotransaminase suggested increased proteolysis and transamination of amino acids. The increase in glutamate dehydrogenase, AMP deaminase, and adenosine deaminase indicated increased ammonia production. The increased arginase and glutamine synthetase suggested the detoxification or mobilization of ammonia toward the production of urea and glutamine. These results suggest that cadmium affects oxidative metabolism and induces hyperammonemia, and crabs switch over their metabolic profiles toward compensatory mechanisms for the survivability in cadmium-polluted habitats.
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PMID:Changes in oxidative metabolism in selected tissues of the crab (Scylla serrata) in response to cadmium toxicity. 753 86

Studies on the effect of various Cd2+ concentrations on substrate oxidation by whole cells of cadmium-sensitive Staphylococcus aureus 17810S showed that oxidation of glutamate or pyruvate was highly sensitive to low Cd2+ concentrations (5 microM), whereas L-lactate oxidation was insensitive even to high Cd2+ concentrations (100 microM). Location of the cadmium-sensitive targets in the enzyme systems involved in oxidation of these substrates was studied in subcellular fractions prepared from cells pretreated with 5 or 100 microM Cd2+. Activities of the cytoplasmic 2-oxoglutarate dehydrogenase complex (ODHC)') and pyruvate dehydrogenase complex (PDHC) were strongly inhibited with 5 microM Cd2+, while with 100 microM Cd2+ the inhibition was almost complete. In contrast, activities of the cytoplasmic NAD-dependent glutamate dehydrogenase (NAD-GDH), the membrane-bound NADH dehydrogenase (NDH) and HQNO-sensitive NADH oxidase were not sensitive to 100 microM Cd2+. These data indicate that the accessible, cadmium-sensitive targets are located only in the cytoplasmic ODHC and PDHC. It is postulated that two vicinal dithiols present in ODHC and PDHC may be regarded as the primary cadmium-sensitive targets in the systems oxidizing glutamate or pyruvate. Since activities of the membrane-bound NAD-independent L-lactate dehydrogenase (iLDH) and HQNO-sensitive L-lactate oxidase were not affected by 100 microM Cd2+, this indicates that the L-lactate oxidizing system lacks the accessible, cadmium-sensitive targets. The mechanism of Cd2+ toxicity to energy conservation with glutamate, pyruvate or L-lactate in S. aureus is discussed.
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PMID:Cadmium-sensitive targets in the aerobic respiratory metabolism of Staphylococcus aureus. 895 92

The specific activities of D-3-hydroxybutyrate dehydrogenase (BDH) and glutamate dehydrogenase (GDH) are reduced in the liver and kidney of rats intoxicated with 2.5 mg Cd/kg body wt and sacrificed after 24 h; conversely ketone-body concentration is strongly increased in both of these organs and blood. In the same animals a great stimulation of antioxidant enzymes glutathione reductase and glutathione peroxidase occurs. The prooxidant state induced by cadmium in liver mitochondria and microsomes is unaffected by superoxide dismutase, catalase, or mannitol, whereas it is completely blocked by vitamin E thus excluding the involvement of reactive oxygen species in this process. The mechanism by which cadmium induces lipid peroxidation has been investigated by measuring the effect of this metal on liposomes. Ninety-minute treatment of liposomes with CdCl2 does not induce any lipid peroxidation. In contrast, Fe2+ ions under the same conditions cause strong liposome peroxidation. It has also been observed that cadmium promotes a time-dependent iron release from biological membranes. When lipid peroxidation is induced by a low concentration (5 microM) of FeCl2, in place of CdCl2, the characteristics of this process and the sensitivity to the various antioxidants used are similar to those observed with Cd. From these results we conclude that the prooxidative effect of cadmium is an indirect one since it is mediated by iron. With regard to the inhibitory effect on BDH and GDH following cadmium intoxication, it does not appear to be imputable to lipid peroxidation since in vitro investigations indicate that the presence of vitamin E does not remove the inhibition at all.
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PMID:Enzyme activity alteration by cadmium administration to rats: the possibility of iron involvement in lipid peroxidation. 934 63

Twelve male and female Wistar rats each received cadmium (as CdCl2) in their diet at concentrations of 0, 10, 50, and 250 ppm for 72 weeks. After 1, 4, 8, 13, 18, 26, 32, 45, 57, and 68 weeks a total of 8 enzymes from different cellular compartments of the nephron were measured. At the end of the study period, the kidneys were examined histopathologically. Concentrations up to and including 50 ppm did not induce any adverse effect. At 250 ppm, growth of male and female animals was markedly retarded. Significantly increased activities of the cytosolic phosphohexose isomerase were excreted by males and females receiving 250 ppm at all timepoints from week 13. The values of the mitochondrial glutamate dehydrogenase were mostly elevated from week 1 to 57, however, due to a wide scatter range, were only occasionally significantly different from control values. The brush border enzymes (gamma-glutamyl transferase, alkaline phosphatase and leucine arylamidase) were not changed in a relevant manner in female rats, while in 250 ppm males the excreted activity of ALP and LAP from week 1 to week 18, and that of GGT during the entire study period were significantly lower than the control values. Excretion of the lysosomal enzymes aryl sulfatase A, beta-galactosidase, and beta-N-acetyl-D-glucosaminidase was at no time influenced in a noteworthy manner. Histopathology after 72 weeks revealed chronic but also acute degenerative changes in the kidneys of 250 ppm males and females. A comparison of published data on persons having undergone high cadmium exposure with the results presented here shows remarkable differences.
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PMID:Time course of chronic oral cadmium nephrotoxicity in Wistar rats: excretion of urinary enzymes. 1053 56

A 44-year-old patient died from amyotrophic lateral sclerosis (ALS) after nine years of heavy exposure to cadmium (Cd) in a nickel cadmium (Ni-Cd) battery factory. Two years after starting work he and co-workers had experienced pruritus, loss of smell, nasal congestion, nosebleeds, cough, shortness of breath, severe headaches, bone pain, and proteinuria. Upper back pain and muscle weakness progressed to flaccid paralysis. EMG findings were consistent with motor neuron disease. Cd impairs the blood-brain barrier, reduces levels of brain copper-zinc (Cu-Zn) superoxide dismutase (SOD), and enhances excitoxicity of glutamate via up-regulation of glutamate dehydrogenase and down-regulation of glutamate uptake in glial cells. High levels of methallothionein, a sign of exposure to heavy metals, have been found in brain tissue of deceased ALS patients. The effects of Cd on enzyme systems that mediate neurotoxicity and motor neuron disease suggest a cause effect relationship between Cd and ALS in this worker.
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PMID:Amyotrophic lateral sclerosis in a battery-factory worker exposed to cadmium. 1137 40

The effect of cadmium (Cd) was investigated on the in vitro activities of leaf and root enzymes involved in carbon (C) and nitrogen (N) metabolism of bean (Phaseolus vulgaris L. cv. Morgane). Cd induced a high increase in maximal extractable activity of glutamate dehydrogenase (NADH-GDH, EC 1.4.1.2). Cd promoted ammonium accumulation in leaves and roots, and a tight correlation was observed between ammonium amount and GDH activity. Changes in GDH activity appear to be mediated by the increase in ammonium levels by Cd treatment. Cd stress also enhanced the activities of phosphoenolypyruvate carboxylase (PEPC, EC 4.1.1.31) and NADP(+)-isocitrate dehydrogenase (NADP(+)-ICDH, EC 1.1.1.42) in leaves while they were inhibited in roots. Immuno-titration, the PEPC sensitivity to malate and PEPC response to pH indicated that the increase in PEPC activity by Cd was due to de novo synthesis of the enzyme polypeptide and also modification of the phosphorylation state of the enzyme. Cd may have modified, via a modulation of PEPC activity, the C flow towards the amino acid biosynthesis. In leaves, Cd treatments markedly modified specific amino acid contents. Glutamate and proline significantly accumulated compared to those of the control plants. This study suggests that Cd stress is a part of the syndrome of metal toxicity, and that a readjustment of the co-ordination between N and C metabolism via the modulation of GDH, PEPC and ICDH activities avoided the accumulation of toxic levels of ammonium.
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PMID:Effects of cadmium on the co-ordination of nitrogen and carbon metabolism in bean seedlings. 1275 16

In order to better understand the effects of heavy metals on the growth of plants, we decided to perform recovering experiments by following both chemical and physiological parameters in cadmium pre-stressed tomato seedlings after cadmium had been removed from the nutrient solution. The work shows that cadmium suppression results in resumption of growth activity. The biomass of leaves and stems rose steadily. The increase in root biomass exceeded those of leaves and stems. At the same time, nitrate content was increased to reach the level obtained with unstressed controls. In all the organs studied, the activities of the enzymes involved in the anabolic nitrogen primary assimilation pathways (nitrate reductase (NR), nitrite reductase (NiR) and glutamine synthetase (GS) soared after that cadmium had been removed. While NAD(+)-dependent glutamate dehydrogenase (GDH-NAD+) activity also rose progressively during the recovering time, the cognate NADH-dependent glutamate dehydrogenase (GDH-NADH) activity decreased. This result allows us to propose that the ammonia produced by the stress-induced protein catabolism is detoxified and re-assimilated by the GDH-NADH isoenzyme. On the basis of these results, we will discuss the ability of the plant to dilute the effects of pollutants during the recovering period. An important outcome of this work is that a transient contamination of the culture medium by pollutants is not necessarily followed by a significant depreciation in product yield or quality.
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PMID:[Reversibility of the effects of cadmium on the growth and nitrogen metabolism in the tomato(Lycopersicon esculentum)]. 1289 45

Toxic doses of zinc and cadmium inhibit shoot growth but increase the capacity of several leaf enzymes in dwarf beans (Phaseolus vulgaris L.). Both effects were studied as a function of the metal concentration applied to the plant. There was a linear relationship between the metal content of the primary leaf and the nutrient solution. When leaf metal content exceeded a toxic threshold value, shoot growth became inhibited and an increase in capacity of the following enzymes was measured in the leaf: glucose-6-phosphate dehydrogenase, glutamate dehydrogenase, isocitrate dehydrogenase, malic enzyme, glutamate-oxaloacetate transminase, peroxidase. The threshold values were similar for growth inhibition as well as for enzyme capacity induction. Both effects were strongly correlated to each other, especially under conditions of toxic zinc treatment. Measurement of enzyme capacity might therefore provide a useful criterion for the evaluation of the phytotoxicity of soils, contaminated by zinc and/or cadmium.
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PMID:Induction of enzyme capacity in plants as a result of heavy metal toxicity: dose-response relations in Phaseolus vulgaris L., treated with zinc and cadmium. 1509 10

The interactions between sulphur nutrition and Cd exposure were investigated in maize (Zea mays L.) plants. Plants were grown for 12 days in nutrient solution with or without sulphate. Half of the plants of each treatment were then supplied with 100 microM Cd. Leaves were collected 0, 1, 2, 3, 4 and 5 days from the beginning of Cd application and used for chemical analysis and enzyme assays. Cd exposure produced symptoms of toxicity (leaf chlorosis, growth reduction) and induced a noticeable accumulation of non-protein SH compounds. As phytochelatins are glutamate- and cysteine-rich peptides, the effect of cadmium on some enzyme activities involved in N and S metabolism of maize leaves was studied in relation to the plant sulphur supply. In vivo Cd application to S-sufficient plants resulted in a drop of all measured enzyme activities. On the other hand, S-deficient plants showed a decrease in nitrate reductase (NR; EC 1.6.6.1) and glutamine synthetase (GS; EC 6.3.1.2) activity, and an increase in NAD-dependent glutamate dehydrogenase (GDH; EC 1.4.1.2) and phosphoenolpyruvate carboxylase (PEPc; EC 4.1.1.31) activity as a result of the Cd treatment. Furthermore, in the same plants ATP sulphurylase (ATPs; EC 2.7.7.4) and O-acetylserine sulphydrylase (OASs; EC 4.2.99.8) showed a particular pattern as both enzymes exhibited a transient maximum value of activity after 4 days from the beginning of Cd exposure. Results provide evidence that the increase of ATPs, OASs, GDH and PEPc activities, observed exclusively in S-deficient Cd-treated plants, may be part of the defence mechanism based on the production of phytochelatins.
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PMID:Role of sulphur availability on cadmium-induced changes of nitrogen and sulphur metabolism in maize (Zea mays L.) leaves. 1531 68

Tomato (Lycopersicon esculentum) seedlings were grown in the presence of cadmium. After 1 week of Cd treatment, a sharp decline in biomass accumulation in the leaves and roots was observed, together with a decrease in the rate of photosynthetic activity due to both Rubisco and chlorophyll degradation and stomata closure. Cadmium induced a significant decrease in nitrate content and inhibition of the activities of nitrate reductase, nitrite reductase, glutamine synthetase (GS) and ferredoxin-glutamate synthase. An increase in NADH-glutamate synthase and NADH-glutamate dehydrogenase activity was observed in parallel. The accumulation of ammonium into the tissues of treated plants was accompanied by a loss of total protein and the accumulation of amino acids. Gln represented the major amino acid transported through xylem sap of Cd-treated and control plants. Cadmium treatment increased the total amino acid content in the phloem, maintaining Gln/Glu ratios. Western and Northern blot analysis of Cd-treated plants showed a decrease in chloroplastic GS protein and mRNA and an increase in cytosolic GS and glutamate dehydrogenase transcripts and proteins. An increase in asparagine synthetase mRNA was observed in roots, in parallel with a strong increase in asparagine. Taken together, these results suggest that the plant response to Cd stress involved newly induced enzymes dedicated to coordinated leaf nitrogen remobilization and root nitrogen storage.
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PMID:Cadmium toxicity induced changes in nitrogen management in Lycopersicon esculentum leading to a metabolic safeguard through an amino acid storage strategy. 1557 44


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