Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vibrio cholerae, the causative agent of Asiatic cholera, has been reported to make large quantities of polyphosphate. Inorganic polyphosphate is a ubiquitous molecule with a variety of functions in prokaryotic and eukaryotic cells. We constructed a V. cholerae mutant with a deletion in the polyphosphate kinase (ppk) gene. The mutant was defective in polyphosphate biosynthesis. Deletion of ppk had no significant effect on production of cholera toxin, hemagglutinin/protease, motility, biofilm formation, and colonization of the suckling mouse intestine. The wild type and mutant had similar growth rates in rich and minimal medium and exhibited similar phosphate uptake and alkaline phosphatase induction. In contrast to ppk mutants from other gram-negative bacteria, the V. cholerae mutant survived prolonged starvation in LB medium and artificial seawater basal salts. The ppk mutant was significantly more sensitive to low pH, high salinity, and oxidative stress when it was cultured in low-phosphate minimal medium. The ppk mutant failed to induce catalase when it was downshifted to phosphorus-limiting conditions. Furthermore, the increased sensitivity of the ppk mutant to environmental stressors in phosphate-limited medium correlated with a diminished capacity to synthesize ATP from intracellular reservoirs. We concluded that polyphosphate protects V. cholerae from environmental stresses under phosphate limitation conditions. It has been proposed that toxigenic V. cholerae can survive in estuaries and brackish waters in which phosphorus and/or nitrogen can be a limiting nutrient. Thus, synthesis of large polyphosphate stores could enhance the ability of V. cholerae to survive in the aquatic environment.
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PMID:Polyphosphate stores enhance the ability of Vibrio cholerae to overcome environmental stresses in a low-phosphate environment. 1695 Aug 99

Peroxisome proliferator-activated receptor gamma (PPARgamma) is a metabolic regulator that plays an important role in sensitizing tissues to the action of insulin and in normalizing serum glucose and free fatty acids in type 2 diabetic patients. The receptor has also been implicated in the modulation of inflammatory responses, and ligands of PPARgamma have been found to induce apoptosis in lymphocytes. However, apoptosis induction may not depend on the receptor, because high doses of PPARgamma agonists are required for this process. Using cells containing or lacking PPARgamma, we reported previously that PPARgamma attenuates apoptosis induced by cytokine withdrawal in a murine lymphocytic cell line via a receptor-dependent mechanism. PPARgamma exerts this effect by enhancing the ability of cells to maintain their mitochondrial membrane potential during cytokine deprivation. In this report, we demonstrate that activation of PPARgamma also protects cells from serum starvation-induced apoptosis in human T lymphoma cell lines. Furthermore, we show that the survival effect of PPARgamma is mediated through its actions on cellular metabolic activities. In cytokine-deprived cells, PPARgamma attenuates the decline in ATP level and suppresses accumulation of reactive oxygen species (ROS). Moreover, PPARgamma regulates ROS through its coordinated transcriptional control of proteins and enzymes involved in ROS scavenging, including uncoupling protein 2, catalase, and copper zinc superoxide dismutase. Our studies identify cell survival promotion as a novel activity of PPARgamma and suggest that PPARgamma may modulate cytokine withdrawal-induced activated T cell death.
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PMID:Peroxisome proliferator-activated receptor gamma promotes lymphocyte survival through its actions on cellular metabolic activities. 1695 34

In a previous study we analysed the effect of diesel seawater contamination in the digestive gland of the Antarctic limpet Nacella concinna. We observed that antioxidant enzyme activities decreased after one-week starvation prior to the experiment, and this was considered in the analysis of the obtained results. To know whether the digestive gland oxidant-antioxidant status may be altered by starvation and experimental conditions, we evaluated the food deprivation effect in limpets from the nearshore shallow waters of Potter Cove, Antarctica. Organisms were acclimated to laboratory conditions and were divided in fed and starved groups, and maintained in these conditions during one month. Every week 20 limpets were sampled from each group. Digestive glands were dissected and kept frozen until they were processed. Superoxide dismutase (SOD), catalase (CAT) and glutathione S-transferase (GST) activities, as well as lipid peroxidation (LPO) measured as thiobarbituric reactive substances (TBARS), protein oxidation (PO) and reduced glutathione (GSH) were measured. For both groups of limpets, SOD increased its activity in the first week of the exposure period, with a maximum in the second week. CAT activity increased significantly in the second week, only for the starved group. Similarly, GST activity also increased for starved group in the second week; but maintained this tendency for both groups until the fourth week. In fed and starved limpets, TBARS values increased significantly, during the first week and then returned to normal values. The PO levels in the starved group increased only during the first week. The GSH content, for the fed group, increased significantly after the third week. The obtained results indicate that biochemical or physiological studies conducted with N. concinna should consider the effects of food deprivation and time spent under experimental conditions.
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PMID:Does starvation influence the antioxidant status of the digestive gland of Nacella concinna in experimental conditions? 1719 86

The antioxidant properties of rhapontigenin and rhaponticin isolated from Rheum undulatum were investigated. Rhapontigenin was found to scavenge intracellular reactive oxygen species (ROS), the 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical, and hydrogen peroxide (H2O2). The radical scavenging effect of rhapontigenin was more effective than rhaponticin. Rhapontigenin protected against H2O2-induced membrane lipid peroxidation and cellular DNA damage, which are the main targets of oxidative stress-induced cellular damage. The radical scavenging activity of rhapontigenin protected Chinese hamster lung fibroblast (V79-4) cells exposed to H2O2 by inhibiting apoptosis. Rhapontigenin inhibited cell damage induced by serum starvation and was also found to increase the activity of catalase and its protein expression. Further, rhapontigenin increased phosphorylation of extracellular signal-regulated kinase (ERK) and inhibited the activity of activator protein 1 (AP-1), a redox-sensitive transcription factor. In summary, these results suggest that rhapontigenin protects V79-4 cells against oxidative damage by enhancing the cellular antioxidant activity and modulating cellular signal pathways.
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PMID:Rhapontigenin from Rheum undulatum protects against oxidative-stress-induced cell damage through antioxidant activity. 1755 11

Dps (DNA protection during starvation) is a member of the iron-binding protein family in prokaryotes. It has been shown previously that Dps possesses ferroxidase activity and the ability to sequester iron that seems to protect DNA from oxidative damage. Based on the method of Polymerase Chain Reaction and homologous genetic recombination in vivo, the gene (DRB0092) encoding a Dps protein homology in the extremely radioresistant bacterium Deinococcus radiodurans was deleted from the wild type strain R1 genome. The obtained mutant was designated as Kdps and further verified by PCR and sequencing. Survival rates of the mutant and wild type strain were investigated after challenged with different doses of hydrogen peroxide (H2O2). Results showed that the survival rate of dps mutant reduced rapidly under the low concentration of H2O2 (< or = 10mmol/L), while the wild type strain showed no sudden decrease. When the H2O2 concentration was higher than 30mmol/L, the difference of the survival rates between the mutant and wild type was more than 50-folds. The result demonstrated that the loss of dps gene in D. radiodurans made cells become more sensitive to oxidative damage. An iron staining method was used to determinate catalase activity in native polyacrylamide electrophoresis gels. The result displayed that two catalases in dps mutant were enhanced about 2-folds than that of wild type. The soluble Dps protein was obtained after construction of expression plasmid and inducement in E. coli transformant. The Dps protein showed the capacity of DNA binding and protected DNA from hydroxyl free radical cleavage in vitro. This study demonstrates that Dps protein of D. radiodurans plays an important role in its antioxidant system, which may contribute to its extreme resistance of this bacterium.
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PMID:[Construction of a dps mutant and its functional analysis in Deinococcus radiodurans]. 1794 59

We determined the global protein turnover profiles for Mycobacterium smegmatis under acid shock and iron starvation conditions using a simple (15)N isotope doping technique and a complete medium replacement method for chasing. We used a high-resolution hybrid-linear ion trap-Fourier transform mass spectrometer coupled with nanoliquid chromatography separation to measure protein turnover values for 151 proteins over a dynamic range of 3 orders of magnitude ranging from about 0.2 to 500. Of these 151 proteins, 31 had significant protein turnover changes (p <0.05) at both stress conditions and had protein turnover values increased or decreased by more than 2-fold under at least one stress condition. Protein turnover increased under acid shock for 28 of the 31 proteins but decreased under iron starvation for all the 31 proteins. Only two proteins had protein turnover lowered by more than 2-fold (p <0.05) under both stress conditions, including an ATP synthase F1 beta subunit (MSMEG4921; AtpD) and a catalase/peroxidase (MSMEG6346; KatG). KatG is required for in vivo activation of isoniazid to be bacterialcidal. Decrease of KatG protein turnover under both stress conditions supports the view that isoniazid may induce a dormancy program in mycobacteria, which in turn limits the efficacy of this drug against dormant subpopulation of mycobacteria. Thus, measuring protein turnover in stressed Mycobacterium cells has implications in understanding drug action and resistance mechanisms.
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PMID:Determination of global protein turnover in stressed mycobacterium cells using hybrid-linear ion trap-fourier transform mass spectrometry. 1808 50

Physiological costs of compensatory growth are poorly understood, yet may be the key components in explaining why growth rates are typically submaximal. Here we tested the hypothesized direct costs of compensatory growth in terms of oxidative stress. We assessed oxidative stress in a study where we generated compensatory growth in body mass by exposing larvae of the damselfly Lestes viridis to a transient starvation period followed by ad libitum food. Compensatory growth in the larval stage was associated with higher oxidative stress (as measured by induction of superoxide dismutase and catalase) in the adult stage. Our results challenge two traditional views of life-history theory. First, they indicate that age and mass at metamorphosis not necessarily completely translate larval stress into adult fitness and that the observed physiological cost may explain hidden carry-over effects. Second, they support the notion that costs of compensatory growth may be associated with free-radical-mediated trade-offs and not necessarily with resource-mediated trade-offs.
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PMID:Compensatory growth and oxidative stress in a damselfly. 1818 73

In most medical facilities in Japan, either uricase-catalase or uricase-peroxidase method has been adopted as a sensitive determination of serum uric acid concentration. However, the values obtained from the same patients at different time points are often variable with those methods. Accelerated generation of uric acid and impaired excretion in the kidney are promoted by several dietary factors, such as foods with higher content of sugars (fructose and xylitol), fat and purine bases, and by alcohol consumption, starvation and dehydration. In contrast, hyperglycemia and excess salt ingestion are conductive to accelerate urate excretion. Physicians should notice representative factors fluctuating serum uric acid levels as described above.
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PMID:[How do we set the standard value of serum uric acid levels?]. 1840 22

The inhibitor of catalase 3-amino-1,2,4-triazole (AMT) was used to study the physiological role of catalase in the yeast Saccharomyces cerevisiae under starvation. It was shown that AMT at the concentration of 10 mM did not affect the growth of the yeast. In vivo and in vitro the degree of catalase inhibition by AMT was concentration- and time-dependent. Peroxisomal catalase in bakers' yeast was more sensitive to AMT than the cytosolic one. In vivo inhibition of catalase by AMT in S. cerevisiae caused a simultaneous decrease in glucose-6-phosphate dehydrogenase activity and an increase in glutathione reductase activity. At the same time, the level of protein carbonyls, a marker of oxidative modification, was not affected. Possible mechanisms compensating the negative effects caused by AMT inhibition of catalase are discussed.
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PMID:Inhibition of catalase by aminotriazole in vivo results in reduction of glucose-6-phosphate dehydrogenase activity in Saccharomyces cerevisiae cells. 1845 71

Cryptococcus neoformans is a facultative intracellular pathogen. The most distinctive feature of C. neoformans is a polysaccharide capsule that enlarges depending on environmental stimuli. The mechanism by which C. neoformans avoids killing during phagocytosis is unknown. We hypothesized that capsule growth conferred resistance to microbicidal molecules produced by the host during infection, particularly during phagocytosis. We observed that capsule enlargement conferred resistance to reactive oxygen species produced by H(2)O(2) that was not associated with a higher catalase activity, suggesting a new function for the capsule as a scavenger of reactive oxidative intermediates. Soluble capsular polysaccharide protected C. neoformans and Saccharomyces cerevisiae from killing by H(2)O(2). Acapsular mutants had higher susceptibility to free radicals. Capsular polysaccharide acted as an antioxidant in the nitroblue tetrazolium (NBT) reduction coupled to beta-nicotinamide adenine dinucleotide (NADH)/phenazine methosulfate (PMS) assay. Capsule enlargement conferred resistance to antimicrobial peptides and the antifungal drug Amphotericin B. Interestingly, the capsule had no effect on susceptibility to azoles and increased susceptibility to fluconazole. Capsule enlargement reduced phagocytosis by environmental predators, although we also noticed that in this system, starvation of C. neoformans cells produced resistance to phagocytosis. Our results suggest that capsular enlargement is a mechanism that enhances C. neoformans survival when ingested by phagocytic cells.
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PMID:Capsule enlargement in Cryptococcus neoformans confers resistance to oxidative stress suggesting a mechanism for intracellular survival. 1855 13


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