Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.7.1.2 (nitrate reductase)
 3,861 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Starved cells of a glucose-grown strain of Staphylococcus aureus are resistant to the action of staphylococcin 1580. Reinitiation of sensitivity is readily obtained upon the addition of glucose, but only weakly with L-lactate, although the latter induces higher ATP levels and supports L-glutamic acid uptake better than glucose does. The NADH/NAD+ ratio correlates with the staphylococcin sensitivity. 2. Starved pyruvate-grown cells remain partially susceptible and full sensitivity is restored both in the presence of glucose and L-lactate. 3. Arsenate but not dicyclohexylcarbodiimide (DCCD) blocks the reinitiation of sensitivity in the presence of glucose. Both arsenate and DCCD block sensitivity in the presence of L-lactate. 4. Aerobically grown cells are sensitive to staphylococcin 1580 under anaerobic conditions. Anaerobically grown cells are less susceptible, but sensitivity can be restored by glucose and also by L-lactate plus nitrate when cells are previously induced for nitrate reductase. 5. Starved cells of a mutant strain defective in the maintenance of a high-energy state of the membrane are normally sensitive in the presence of glucose, but resistant in the presence of L-lactate. A strain lacking a functional respiratory chain (men-) is also sensitive with glucose but resistant in the presence of L-lactate. 6. It is concluded that the initiation of the staphylococcin 1580 action is under control of a mechanism regulating the energy flow in the cell, and involving the presence of a high-energy phosphorylated compound.
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PMID:Energy requirements for the action of staphylococcin 1580 in Staphyloccus aureus. 20 62

1. Starved cells of a strain of Escherichia coli and its mutant uncA, treated with colicin K, E2 or E3, remained fully rescuable upon trypsin treatment (stage I in colicin action). The transition to stage II in colicin action (cells no longer rescuable by trypsin) was promoted by the addition of either glucose or D-lactate. 2. Aerobically glucose-grown cells of the normal strain were irreversibly killed by colicin K, E2 or E3 under anerobic conditions, while similarly treated cells ot its mutant uncA remained fully rescuable. The stage I-stage II transition in colicin action was blocked in normal cells under anaerobic conditions when succinate was the sole carbon source. 3. Arsenate alone had little effect on the progression of the stage I-stage II transition in normal cells, treated with colicin K. However, this transition was abolished in the presence of both arsenate and anaerobic conditions. 4. The initiation of colicin action could be coupled to the anaerobic electron transfer systems formate dehydrogenase-nitrate reductase and alpha-glycerophosphate dehydrogenase-fumarate reductase. 5. These results indicate that an energized state of the cytoplasmic membrane is required for the initiation of colicin action and that no high-energy phosphorylated compounds are necessary.
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PMID:Energy requirement for the initiation of colicin action in Escherichia coli. 109 62

Metal toxicity in crop plants is a matter of scientific concern. Therefore, in recent years efforts have been made to minimize metal toxicity in crop plants. Out of various strategies, priming of seedlings with certain chemicals, like e.g. donors of signaling molecules, nutrients, metabolites or plant hormones has shown encouraging results. However, mechanisms related with the priming-induced mitigation of metal toxicity are still poorly known. Hence, we have tested the potential of 2-oxoglutarate (2-OG) priming in enhancing the arsenate (AsV ) toxicity tolerance in tomato seedlings along with deciphering the probable role of nitric oxide (NO) in accomplishing this task. Arsenate decreased growth, endogenous NO and nitric oxide synthase-like activity but enhanced the accumulation of As, which collectively led to root cell death. Arsenate toxicity also decreased some photosynthetic characteristics (i.e. Fv /Fm, qP, Fv /F0 and Fm /F0 , and total chlorophyll content) but enhanced NPQ. However, priming with 2-OG alleviated the toxic effect of AsV on growth, endogenous NO, cell death and photosynthesis. Moreover, arsenate inhibited the activities of enzymes of nitrogen metabolism (i.e. nitrate reductase, nitrite reductase, glutamine synthetase and glutamine 2-oxoglutarate aminotransferase) but increased the activity of glutamate dehydrogenase and NH4 + content. Superoxide radicals, hydrogen peroxide, lipid peroxidation, protein oxidation and membrane damage increased upon AsV exposure, but the antioxidant enzymes (i.e. superoxide dismutase, catalase and glutathione-S-transferase) showed differential responses. Overall, our results showed that 2-OG is capable of alleviating AsV toxicity in tomato seedlings but the involvement of endogenous NO is probably required.
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PMID:Priming of tomato seedlings with 2-oxoglutarate induces arsenic toxicity alleviatory responses by involving endogenous nitric oxide. 3265 64