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)

Unlike the mature animal, immature mice transgenic for copper/zinc superoxide dismutase (SOD1) have greater brain injury after hypoxia-ischemia than their wild-type nontransgenic littermates. To assess the role of oxidative stress in the pathogenesis of this injury, we measured histopathological damage, lipid peroxidation products, enzymatic activities of catalase and glutathione peroxidase, and hydrogen peroxide (H2O2) concentration in these animals before and after hypoxic-ischemic injury. Lipid peroxidation products were significantly increased 2 hours after the insult in both transgenic and nontransgenic brains in hippocampus, the most damaged brain region. Catalase activity did not increase in response to SOD1 overexpression or injury in either group. However, glutathione peroxidase activity, unchanged in response to overexpression, decreased significantly 24 hours after injury in both groups. At 24 hours after injury, greater H2O2 accumulation was observed in transgenic brains. Because SOD1 dismutates superoxide to H2O2, overexpression of SOD1 in the presence of developmentally low activities of the catalytic enzymes glutathione peroxidase and catalase leads to an increased production of H2O2, and may explain the increased brain injury observed after hypoxia-ischemia in neonatal SOD1 mice.
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PMID:Copper/zinc superoxide dismutase transgenic brain accumulates hydrogen peroxide after perinatal hypoxia ischemia. 974 2

Bcl-2 is a gene family involved in the suppression of apoptosis in response to a wide range of cellular insults. Multiple papers have suggested a link between Bcl-2 and oxidative damage/antioxidant protection. We therefore examined parameters of antioxidant defense and oxidative damage in two different cell lines, NT-2/D1 (NT-2) and SK-N-MC, overexpressing Bcl-2 as compared with vector-only controls. Bcl-2 transfectants of both cell lines were more resistant to H(2)O(2) and showed increases in GSH level and Cu/Zn-superoxide dismutase (SOD1) activity, but not in Mn-superoxide dismutase, glutathione peroxidase, or glutathione reductase activities. Catalase activity was increased in SK-N-MC cells. Overexpression of Bcl-2 did not significantly decrease levels of oxidative DNA damage (measured as 8-hydroxyguanine) or lipid peroxidation, but it decreased levels of 3-nitrotyrosine in both cell lines and protein carbonyls in SK-N-MC cells only. It also increased proteasome activity in both cell lines. We conclude that Bcl-2 raises cellular antioxidant defense status, but this is not necessarily reflected in decreased levels of oxidative damage to DNA and lipids. The ability of Bcl-2 overexpression to decrease 3-nitrotyrosine levels suggests that it may decrease formation of peroxynitrite or other reactive nitrogen species; this was confirmed as decreased production of NO(2)(-)/NO(3)(-) in the transfected cells and a fall in the level of nNOS protein.
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PMID:Effect of overexpression of BCL-2 on cellular oxidative damage, nitric oxide production, antioxidant defenses, and the proteasome. 1174 29

In the present study, we generated transgenic mice that overexpress catalase or CuZn superoxide dismutase (CuZnSOD) in all tissues using large genomic DNA fragments. An 80 kb human genomic DNA, containing the 33 kb human CAT gene as well as the 41 kb of 5' and the 6 kb of 3' flanking regions, was obtained by screening a human P1 library and was used to produce transgenic mice Tg(CAT). Transgenic mice Tg(SOD1) were produced by a similar strategy using a 64 kb human genomic DNA containing the 10 kb human SOD1 gene and the 27 kb of both 5' and 3' flanking regions. Catalase mRNA levels were 2-6- fold higher and catalase activity levels were 2-4- fold higher in the various tissues of the hemizygous Tg(CAT) mice compared with wild type mice. The mRNA levels for CuZnSOD were 2-12- fold higher and the CuZnSOD activity levels were 2-5- fold higher in the hemizygous Tg(SOD1) mice compared with wild type mice. In summary, our study demonstrates that a strategy of using large genomic DNA containing either the entire human CAT or SOD1 gene with large flanking regions gives ubiquitous increased expression of CuZnSOD and catalase. In addition, the expression of catalase closely reflects the tissue specific pattern found in the endogenous gene. These transgenic mice will be useful in studying the role of oxidative stress/damage in aging and age-related pathologies.
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PMID:A strategy for the ubiquitous overexpression of human catalase and CuZn superoxide dismutase genes in transgenic mice. 1263 42

Honey bee (Apis mellifera) sperm remains viable in the spermatheca of mated female honey bees for several years. During this time, the sperm retains respiratory activity, placing it at risk of the damaging effects of reactive oxygen species common to many biological processes. Antioxidative enzymes might help reduce this damage. Here we use quantitative real-time RT-PCR to establish gene-expression profiles in male and female honey bee reproductive tissues for three antioxidative enzymes: catalase, glutathione-S-transferase (GST) and superoxide dismutase (SOD1, cytosolic). Catalase and GST showed ten- to twenty-fold transcript increases in the sperm storage organs of mated queens vs. unmated queens, whereas SOD1 levels are high in both mated and unmated queens. Male reproductive and somatic tissues showed relatively high levels of all three antioxidant-encoding transcripts. All three enzymes screened were higher in mature males vs. young males, although this effect did not appear to be confined to reproductive tissues and, hence, need not reflect a role in sperm longevity. Furthermore, antioxidative enzyme transcripts remained present, and apparently increased, in male tissues long after sperm had matured and seminal fluid was produced. We also found measurable levels of catalase transcripts in honey bee semen. The presence of catalase transcripts in both reproductive tissues and semen in bees suggests that this enzyme might play a key role in antioxidative protection.
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PMID:Sperm storage and antioxidative enzyme expression in the honey bee, Apis mellifera. 1505 61

In forensic medicine practice poisonings are rather frequent, and among them, those caused by fatal "substitution" of ethyl alcohol. One of the most frequently encountered "substitutes" for ethyl alcohol is methanol. The purpose of our research was to determine the concentration of malonic dialdehyde as the expression of lipid peroxidation and antioxidant enzyme activity after dosed chronic ethyl and methyl alcohol intoxication. The experiment was conducted on approx. 6 month-old male inbred Lewis rats each weighing approx. 250 g. Ethanol and methanol solution was given in the concentration 1.0 M. The control group of rats received water. Each experimental group numbered 30 rats, this number was divided into three sub-groups, which were put-down at 4, 8 and 12 weeks. The activity of superoxide dismutase (CuZu-SOD) was determined by the Misra-Fridovich method, catalase (CAT) by the Beers-Sizer method. The concentration of malonic dialdehyde (MDA) was determined using the method of Placer et al. by assessing the concentration of TBARS compounds. Results are expressed as a mean +/- SD. The paired Student's test for small groups were used. Superoxide dismutase SOD1 activity decreased compared with the control group throughout the duration of the experiment from 2212 U/gHb to 1676 U/gHb for ethanol and from 2212 U/gHb to 945 U/gHb for methanol. Catalase activity for methanol decreased from 9.1 U/gHb to 5.1 U/gHb, for ethanol to 7.4 U/gHb. In the 4th week of the experiment increase of malonyl dialdehyde concentration for methanol group was observed--from 0.14 umol/gHb to 0.34 umol/Hb; after 8th weeks it decreased to 0.2 umol/gHb and in the 12th week increased to 0.23 umol/gHb. For ethanol these changes was less visible and reached the level of 0.24 umol/l. The statistical processing of the results was performed on the basis of parametric tests (the t-Student test for small experiments) and computer software Statistica. The statistical significance was set for p<0.05.
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PMID:[Selected alcohols on the pro- and anti-oxidative processes in rat erythrocytes]. 1549 56

Markers of oxidative stress have been found in spinal cord, cortex, cerebrospinal fluid, and plasma of SALS patients. Mitochondrial and calcium metabolism dysfunction were also found in peripheral lymphocytes from SALS patients. In this study, we demonstrate that lymphocytes from SALS patients are more prone to undergo alteration of cell membrane integrity both in basal conditions and following oxidative stress induced by H2O2 treatment. The expression of the antioxidant proteins, Bcl-2, SOD1 and catalase in basal conditions, was significantly lower in lymphocytes from SALS patients than in lymphocytes from age and sex matched controls. Exposure to H2O2 induced a time-dependent decrease of Bcl-2 and SOD1 in control lymphocytes. Conversely, the levels of these proteins remained unchanged in SALS lymphocytes even after 18 h stress. Catalase expression was not significantly modified by oxidative stress. Our results demonstrate that two factors involved in the genesis and/or progression of the familial form of the disease with SOD1 mutation are altered also in the sporadic form of ALS and suggest that the oxidative stress protection pathway is deregulated in lymphocytes from ALS patients.
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PMID:Modified expression of Bcl-2 and SOD1 proteins in lymphocytes from sporadic ALS patients. 1649 3

Oxidative stress has long been associated with normal aging and age-related neurodegenerative disorders such as Alzheimer's disease (AD) and Parkinson's disease (PD). However, it is now evident that reactive oxygen species (ROS) such as superoxide (O(2-*)) and hydrogen peroxide (H(2)O(2)) also play pivotal roles in normal cell signaling. The focus of the present study was to examine the effects of the antioxidant enzymes CuZnSOD (SOD1) and catalase, which produce and remove H(2)O(2), respectively, on long-term potentiation (LTP) forms of synaptic plasticity during aging. Consistent wth previous studies, LTP, when induced in vitro in CA1 of the hippocampus with a high-frequency stimulation protocol, is significantly reduced in slices from older mice (22-26 months) relative to younger mice (2-4 months). Neither knockout of the endogenous catalase gene (Cat KO) nor acute enzymatic treatment with SOD1 altered LTP in slices from adult mice. Conversely, enzymatic applications of SOD1 inhibited LTP in slices from older mice. A much different set of results emerges with exogenous applications of catalase to hippocampal slices. Catalase significantly inhibited LTP in slices from adult mice but reversed age-related LTP deficits in slices from older mice. Measurements of H(2)O(2) showed that exogenous treatments with catalase lowered H(2)O(2) in synapse-enriched synaptoneurosome (SN) fractions prepared from adult mice. Notably, SNs from both Cat KO and old mice were deficient in removing extracellular challenges of H(2)O(2). Overall, the results suggest that dynamic alterations in extracellular H(2)O(2) metabolism affect synaptic plasticity in the hippocampus during aging.
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PMID:Age-dependent modulation of hippocampal long-term potentiation by antioxidant enzymes. 1694 35

Following experimental hind limb denervation in rats, this study demonstrates that oxidative stress occurs and advances an hypothesis about its origin. In fact: (i) ROS are formed; (ii) membrane lipids are oxidized; (iii) oxidized ion channels and pumps may lead to increased [Ca(2+)](i); all the above mentioned events increase with denervation time. In the denervated muscle, (iv) mRNA abundance of cytoprotective and anti-oxidant proteins (Hsp70, Hsp27, Sod1, Catalase, Gpx1, Gpx4, Gstm1), as well as (v) SOD1 enzymatic activity and HSP70i protein increase; (vi) an unbalance in mitochondrial OXPHOS enzymes occurs, presumably leading to excess mitochondrial ROS production; (vii) increased cPLA2alpha expression (mRNA) and activation (increased [Ca(2+)](i)) may lead to increased hydroperoxides release. Since anti-oxidant defences appear inadequate to counterbalance increased ROS production with increased denervation time, an anti-oxidant therapeutic strategy seems to be advisable in the many medical conditions where the nerve-muscle connection is impaired.
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PMID:Oxidative stress in the denervated muscle. 2029 22

Restraint stress induces physiological changes in the brain. In the present study, we observed the effects of repeated stress on ischemic damage associated with oxidative stress in gerbils. Animals were placed into restrainers for 5h (between 09:30 h and 14:30 h) for 21 consecutive days prior to 5 min of transient cerebral ischemia. Experimental groups were divided into 4 groups; 1) sham-operated control-group (sham-group), 2) ischemia-operated control-group (ischemia-group), 3) sham-operated stress-group (stressed-sham-group), and 4) ischemia-operated stress-group (stressed-ischemia-group). Serum corticosterone level in the ischemia-group was highest (330% vs the sham-group) at 12h post-ischemia, and serum corticosterone levels in the stressed-ischemia-group were significantly lower than the ischemia-group. Locomotor activity in the ischemia-group was significantly increased (300% vs the sham-group) at 1 day post-ischemia; however, locomotor activity in the stressed-ischemia-group was less increased compared to the ischemia-group. A few NeuN (neuron-specific soluble nuclear antigen)-positive ((+)) cells were found in the stratum pyramidale (SP) of the hippocampal CA1 region (CA1) 4 days post-ischemia in the ischemia-group; however, in the stressed-ischemia-group at 4 days post-ischemia, 83.8% of NeuN(+) neurons were found. In addition, we found a few Fluro-Jade B (a marker for neuronal degeneration)(+) and TUNEL(+) cells in the stressed-ischemia-group at 4 days post-ischemia. In gliosis, glial fibrillary acidic protein(+) astrocytes in the stressed-ischemia-groups was similar to the ischemia-groups; however, ionized calcium-binding adapter molecule 1(+) microglia in the stressed-ischemia-groups were much less activated than the ischemia-groups. Among antioxidants, Cu,Zn-superoxide dismutase (SOD1) immunoreactivity in the SP was higher in the stressed-ischemia-groups than the ischemia-groups. Catalase immunoreactivity in the SP of the stressed-ischemia-groups was similar to the ischemia-groups. However, Mn-superoxide dismutase and glutathione peroxidase immunoreactivity were lower than the ischemia-groups. In brief, our results indicate that repeated restraint stress significantly attenuates ischemic neuronal damage and locomotor activity following ischemia. In addition, SOD1 among antioxidants significantly increases in the stressed-ischemia-groups.
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PMID:Antioxidant enzymes are differently changed in experimental ischemic hippocampal CA1 region following repeated restraint stress. 2121 18

Allelic variation at the Cu-Zn superoxide dismutase (SOD1) locus has been shown to be associated with resistance of the snail, Biomphalaria glabrata, to infection by the trematode parasite, Schistosoma mansoni. SOD1 catalyses the production of hydrogen peroxide, a known cytotoxic component of the oxidative burst used in defence against pathogens. In our laboratory population of B. glabrata, the most resistant allele at SOD1 is over-expressed relative to the other two alleles. Because hydrogen peroxide also causes oxidative stress on host tissues, we hypothesised that over-expression of SOD1 might be compensated by epistatic interactions with other loci involved in oxidation-reduction (redox) pathways. Catalase, peroxiredoxins and glutathione peroxidases all degrade hydrogen peroxide. We tested whether alleles at each of these loci were in linkage disequilibrium with SOD1 in our population, as might be expected given strong epistatic selection. We found that SOD1, catalase (CAT) and a peroxiredoxin locus (PRX4) are in strong linkage disequilibrium in our population. We also found that these loci are tightly linked, within 1-2cM of each other, which explains the high linkage disequilibrium. This result raises the possibility that there is a linked cluster of redox genes, and perhaps other defence-relevant genes, in the B. glabrata genome. Whether epistatic interactions for fitness actually exist among these loci still needs to be tested. However the close physical linkage among SOD1, PRX4 and CAT, and subsequent high disequilibrium, makes such interactions a plausible hypothesis.
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PMID:Three genes involved in the oxidative burst are closely linked in the genome of the snail, Biomphalaria glabrata. 2320 63


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