Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04040 (Catalase)
 3,577 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cell-free extracts prepared from spherical and rod-shaped cells of Arthrobacter crystallopoietes were assayed for enzymes during various periods of starvation. The level of NADH oxidase dropped to 20 and 30%, respectively, in spherical and rod-shaped cells during the first 1 to 2 days of starvation and then remained constant for 9 days. Catalase activity decreased continuously and reached a low level in 9 days. Enzymes involved in glucose metabolism and the tricarboxylic acid cycle were stable for the duration of the experiment (about 1 week). Succinic dehydrogenase, fumarase and aconitase were stable during 21 days of starvation, which is the longest time enzymes have been shown to be stable in any bacterium under conditions of total starvation.
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PMID:Stability of enzymes in starving Arthrobacter crystallopoietes. 18 Feb 37

The effect of clofibrate treatment on hepatic ketogenic capacity was studied in rats. Ketogenesis from octanoate and oleate was increased 2- and 4,5-fold, respectively, in hepatocytes from fed, treated rats. In contrast to controls ketogenic rates did not increase upon starvation. While ketogenesis from oleate was higher in fed, treated animals than in fasted controls, endogenous ketogenesis was lower and increased upon starvation. Ketogenesis from octanoate and oleate was stimulated approx. 2-fold in homogenates from treated animals. Labeled pyruvate and succinate oxidation was unaltered. [1-14C]Oleate oxidation was severely inhibited by cyanide, both in homogenates from controls and treated animals. Clofibrate caused a 3-fold increase in hepatic carnitine levels. Catalase and glutamate dehydrogenase activities were also increased by the drug. Cytochrome c oxidase did not change. Despite their increased ketogenic capacity hepatocytes from treated rats esterified as much oleate as controls. The increased oxidation was matched by an increased oleate uptake. Plasma ketones were increased 2-fold in fasted, treated animals. Plasma free fatty acids were unaffected. It is concluded that the enhanced ketogenic capacity induced by clofibrate is the result of an increase in mitochondrial beta-oxidation, an increase in the activity of carnitine palmitoyltransferase and possibly of the observed increases in hepatic carnitine content and fatty acid uptake.
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PMID:Hepatic fatty acid oxidation and ketogenesis after clofibrate treatment. 65 51

The cardiac morphology of CD 1 mice undergoing two different schedules of acute (5 day) starvation and that of animals treated with a single dose (15 mg/kg i.p.) of doxorubicin, epirubicin or mitoxantrone were studied by light microscopy. Determinations of heart catalase were also carried out. Mice subjected to moderate starvation had a mean weight reduction of 18.7% and did not show heart morphological damage. A slight increase (38%) of heart catalase specific activity occurred in these animals. In animals subjected to severe starvation the weight loss was 32.2%. In this case considerable heart damage, in the form of myofibrillar loss, and a striking increase of catalase (158.5%) were seen. In the drug groups comparable weight reductions (about 15%) occurred 5 days after the treatment. Moderate heart lesions, represented by myolysis and especially by myocytic microvacuolation, were observed and appeared to be of similar degree in the 3 drug groups. Catalase specific activity increased by 119.9% in the doxorubicin animals, by 73% in the epirubicin mice and by 30.3% in the mitoxantrone ones. Light microscopy made it possible to distinguish between cardiac alterations induced by starvation and those specifically induced by antiblastics. Catalase may be helpful to indicate the existence of heart damage but it does not correlate well with the severity of the lesions by antiblastics. An additional cause of heart catalase elevation might be the free radical generation induced by the anthracyclines but not by mitoxantrone.
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PMID:Morphological changes and catalase activity in the hearts of CD 1 mice following acute starvation or single doses of doxorubicin, epirubicin or mitoxantrone. 316 42

In a study of the endocrine control of peroxisomes, the effects of acute glucagon treatment and fasting on hepatic peroxisomal beta-oxidation in rats have been investigated. The activity of the rate-limiting peroxisomal beta-oxidation enzyme, fatty acyl-CoA oxidase, was measured to determine whether activation of peroxisomal beta-oxidation could account for the increase in total hepatic fatty acid oxidation following acute glucagon exposure. Catalase, a peroxisomal enzyme not directly involved in beta-oxidation, was also measured as a control for total peroxisomal activity. No changes with acute glucagon treatment of intact animals were observed with either activity as measured in liver homogenates or partially purified peroxisomal fractions. These observations indicate the lack of acute control by glucagon of peroxisomal function at the level of total enzyme activity. Previous work on the effects of fasting on hepatic fatty acid beta-oxidation [H. Ishii, S. Horie, and T. Suga (1980) J. Biochem. 87, 1855-1858] suggested an enhanced role for the peroxisomal beta-oxidation pathway during starvation. It was found that the peroxisomal beta-oxidation system, as measured by fatty acyl-CoA oxidase activity, does increase with duration of fast when expressed on a per gram wet weight liver basis. However, when this activity is expressed as total liver capacity, a decline in activity with increasing duration of fast is observed. Furthermore, this decline in peroxisomal capacity parallels the decline in total liver capacity for citrate synthase, a mitochondrial matrix enzyme, and total liver protein. These data indicate that peroxisomal beta-oxidation activity is neither stimulated nor even preferentially spared from proteolysis during fasting.
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PMID:Glucagon and fasting do not activate peroxisomal fatty acid beta-oxidation in rat liver. 654 May 49

Catalase and superoxide dismutase (SOD) activities were determined in muscles from 12-month-old rats after severe starvation and after subsequent refeeding. Catalase increased in most muscles after starvation and decreased after refeeding, while SOD remained unchanged.
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PMID:Effect of starvation and refeeding on catalase and superoxide dismutase activities in skeletal and cardiac muscles from 12-month-old rats. 720 65

The effects of three-day fasting and one-day refeeding on some blood metabolites and parameters of lipid peroxidation were studied in eight non-pregnant merino ewes. Fasting produced an immediate decrease in blood glucose accompanied by an increase of free fatty acid, total lipid, total cholesterol and urea in the plasma. Starvation increased the concentration of thiobarbituric acid-reactive substances (malondialdehyde), with a slower but more sustained increase in the plasma than in the red blood cell haemolysate. Changes in glutathione peroxidase activity were the reverse of those in malondialdehyde concentration. Catalase activity was not measurable in plasma but was consistently increased in the haemolysate on fasting. Superoxide dismutase activity in the whole blood haemolysate significantly increased only on the first day of food deprivation. The vitamin E content of plasma showed no significant changes. The results indicate that energy deficiency, a well-known phenomenon in ruminants, affects not only the metabolic parameters of the blood but its lipid peroxidative status as well.
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PMID:Effect of fasting on blood lipid peroxidation parameters of sheep. 839 31

The marine oligotrophic ultramicrobacterium Sphingomonas alaskensis RB2256 has a physiology that is distinctly different from that of typical copiotrophic marine bacteria, such as Vibrio angustum S14. This includes a high level of inherent stress resistance and the absence of starvation-induced stress resistance to hydrogen peroxide. In addition to periods of starvation in the ocean, slow, nutrient-limited growth is likely to be encountered by oligotrophic bacteria for substantial periods of time. In this study we examined the effects of growth rate on the resistance of S. alaskensis RB2256 to hydrogen peroxide under carbon or nitrogen limitation conditions in nutrient-limited chemostats. Glucose-limited cultures of S. alaskensis RB2256 at a specific growth rate of 0.02 to 0.13 h(-1) exhibited 10,000-fold-greater viability following 60 min of exposure to 25 mM hydrogen peroxide than cells growing at a rate of 0.14 h(-1) or higher. Growth rate control of stress resistance was found to be specific to carbon and energy limitation in this organism. In contrast, V. angustum S14 did not exhibit growth rate-dependent stress resistance. The dramatic switch in stress resistance that was observed under carbon and energy limitation conditions has not been described previously in bacteria and thus may be a characteristic of the oligotrophic ultramicrobacterium. Catalase activity varied marginally and did not correlate with the growth rate, indicating that hydrogen peroxide breakdown was not the primary mechanism of resistance. More than 1,000 spots were resolved on silver-stained protein gels for cultures growing at rates of 0.026, 0.076, and 0.18 h(-1). Twelve protein spots had intensities that varied by more than twofold between growth rates and hence are likely to be important for growth rate-dependent stress resistance. These studies demonstrated the crucial role that nutrient limitation plays in the physiology of S. alaskensis RB2256, especially under oxidative stress conditions.
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PMID:Specific growth rate plays a critical role in hydrogen peroxide resistance of the marine oligotrophic ultramicrobacterium sphingomonas alaskensis strain RB2256. 1122 24

To date, there is scarce information on the metabolic and biochemical repercussions of Zn-deficiency in fish. In this work, the effect of dietary Zn-deficiency on the diet utilization and the metabolism of activated oxygen species in rainbow trout (Oncorhynchus mykiss) has been studied. Fish were randomly separated in different lots according to their Zn-starvation and diet intake. In crude extracts of liver, gut and muscle, total and isoenzymatic superoxide dismutase and catalase activities were analysed. Lipid peroxidation was also determined in the same tissues. Western blotting was performed using antibodies against manganese- and copperzinc-containing superoxide dismutase. Lots fed on the Zn-deficient diet and with low intake showed significantly lower weight gain and feed-conversion efficiency indexes than control trouts. However, these parameters returned to control values when trouts were recovered by feeding them a control diet ad libitum. In control trouts, three independent copperzinc superoxide dismutase isozymes were detected in liver, whereas only one isozyme was present in the other lots. However, by Western blotting analysis the presence of a manganese superoxide dismutase was found in liver from all lots except in control trouts. Catalase activity and lipid peroxidation values were mainly detected in liver and gut, respectively, and both parameters increased in all lots with respect to the control group. Our results thus suggest that in rainbow trout an oxidative stress appears to occur as a consequence of Zn-deficiency.
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PMID:Oxidative stress generated by dietary Zn-deficiency: studies in rainbow trout (Oncorhynchus mykiss). 1180 21

Some effects of cadmium exposure (100 microg/L for 4, 8, 12, and 24 h) on the estuarine polychaete Laeonereis acuta (Nereididae) were evaluated. This polychaete was able to accumulate cadmium in the body, with the metal stored mainly in the cytosolic fraction (>10 kDa). Activity of the antioxidant enzymes superoxide dismutase, glutathione S-transferase, and glutathione reductase (GR) as well as the total oxyradical scavenger capacity, the glutamate cysteine ligase catalytic subunit gene expression, and the metallothionein-like proteins content were not affected by cadmium at any exposure time tested. Catalase (CAT) activity, however, was significantly lower (p < 0.05) in worms treated with cadmium compared with that in controls after 8 h of exposure. At the same exposure time, lipid peroxide levels were increased (p < 0.05) in worms exposed to cadmium compared with those in control worms. Interestingly, CAT and GR activities decreased over time (p < 0.05) independent of cadmium treatment, which is a result that could be attributed to starvation. The effects caused by cadmium in the present study were observed only after 8 h of exposure, demonstrating that cadmium can generate oxidative stress.
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PMID:Short-term responses to cadmium exposure in the estuarine polychaete Laeonereis acuta (polychaeta, Nereididae): subcellular distribution and oxidative stress generation. 1670 67

The reductive repair of oxidized methionine residues performed by methionine sulfoxide reductase is important for the gastric pathogen Helicobacter pylori to maintain persistent stomach colonization. Methionine-containing proteins that are targeted for repair by Msr were identified from whole-cell extracts (after cells were exposed to O(2) stress) by using a coimmunoprecipitation approach. Proteins identified as Msr-interacting included catalase, GroEL, thioredoxin-1 (Trx1), and site-specific recombinase; with one exception (Trx1, the reductant for Msr) all these proteins have approximately twofold higher methionine (Met) content than other proteins. These Met-rich proteins were purified and were shown to individually form a cross-linked adduct with Msr. Catalase-specific activity in an msr strain was one-half that of the parent strain; this difference was only observed under oxidative stress conditions, and the activity was restored to nearly wild-type levels by adding Msr plus dithiothreitol to msr strain extracts. In agreement with the cross-linking study, pure Msr used Trx1 but not Trx2 as a reductant. Comparative structure modeling classified the H. pylori Msr in class II within the MsrB family, like the Neisseria enzymes. Pure H. pylori enzyme reduced only the R isomer of methyl p-tolyl-sulfoxide with an apparent K(m) of 4.1 mM for the substrate. Stress conditions (peroxide, peroxynitrite, and iron starvation) all caused approximately 3- to 3.5-fold transcriptional up-regulation of msr. Neither the O(2) level during growth nor the use of background regulatory mutants had a significant effect on msr transcription. Late log and stationary phase cultures had the highest Msr protein levels and specific activity.
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PMID:Methionine sulfoxide reductase in Helicobacter pylori: interaction with methionine-rich proteins and stress-induced expression. 1688 52


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