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)

In an effort to understand the damaging actions of free radicals to neuronal electrophysiology, the superoxide generator, dihydroxyfumarate (DHF), was evaluated in slices of guinea pig hippocampus. Using field potential recording techniques, population spikes and population synaptic potentials were recorded in field CA1. Slices were exposed to 3 mM DHF either alone or in the presence of a protectant. DHF did not alter the ability of the afferent volley to generate a synaptic potential, but it did impair the ability of the synaptic potential to elicit a population spike. In addition, DHF induced lipid peroxidation as measured by the thiobarbituric acid assay. Superoxide dismutase (SOD) provided no protection. Instead, SOD treatment promoted DHF damage to synaptic potentials. Catalase alone mitigated the actions of DHF, but only in SOD plus catalase was the DHF-induced electrophysiological deficit and lipid peroxidation completely antagonized. The iron chelator, Desferal, did not protect but promoted synaptic damage. Desferal may be ineffective because of the nitroxide radical formed upon its reaction with DHF. The hydroxyl radical scavenger, dimethylsulfoxide, prevented lipid peroxidation and reduced the DHF-induced deficit but did not completely prevent the impairment of spike generation. These data suggest that DHF exerts its actions through generation of hydrogen peroxide which would further react with tissue iron to produce hydroxyl radicals.
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PMID:Electrophysiological consequences of exposure of hippocampal slices to dihydroxyfumarate, a generator of superoxide radicals. 131 16

Catalase gene expression was characterized in the scutellum of maize seedlings grown at normal (25 degrees C) and elevated temperatures (35 and 40 degrees C). Chronic elevated temperatures reduce scutellar catalase activity most noticeably in the inbred lines W64A and R6-67, which express all three CAT isozymes (CAT-1, CAT-2, and CAT-3). The observed decline in catalase activity is primarily attributed to a decrease in the amount of CAT-2 isozyme, due to diminished levels of the Cat2 transcript. As CAT-2 activity levels are regulated by the trans-acting gene locus Car1, it is possible that the Car1 gene product is inhibited at the elevated temperatures. In maize lines null for CAT-2 or both CAT-2 and CAT-3, the relative levels of Cat1 transcript, although steady throughout the 10 days post-imbibition scutellar profile, are slightly higher with increasing temperatures. This might indicate that, in thermally stressed seedlings, the accumulation and/or stability of Cat1 mRNA might compensate for the lack of Cat2 transcript in a tissue where Cat2 mRNA normally accumulates during the developmental period examined. These observations, along with the drastic reduction in seed germination and seedling height at chronically elevated growth temperatures, suggest that developmental arrest, rather than oxidative stress, might be the cause for the observed results relative to Cat gene expression under such conditions.
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PMID:Catalase gene expression in response to chronic high temperature stress in maize. 1090 10

Spatial memory is coordinated with different brain regions especially hippocampus (HIP) and medial prefrontal cortex (mPFC). Influence of noise stress on working and reference memory error in rats was evaluated by radial eight-arm maze experiment. Changes in the dendritic count were observed in the brain regions such as CA1, CA3 regions of HIP and layers II, III of mPFC. In order to understand the possible mechanism behind noise stress-induced changes, free radical status and acetylcholinesterase (AChE) activity in HIP and mPFC were evaluated. Plasma corticosterone level was also evaluated. Results obtained in this study showed that after noise-stress exposure, 100 dBA/4h per day for 30 days, working and reference memory error increased significantly (P < 0.05) when compared to control animals. Neuronal dendritic count in the HIP was reduced in the 2nd and 3rd order dendrites but not in the mPFC. Superoxide dismutase, lipid peroxidation, plasma corticosterone level and AChE activity were significantly increased in the 1 day, 15 days and 30 days stress groups animal significantly. Catalase and glutathione peroxidase activity were increased in the 1 day and 15 days noise-stress groups but decreased in the 30 days noise-stress group and GSH level was decreased in all the stress exposed animals. In conclusion, oxidative stress, increased AChE activity, reduced dendritic count in HIP, mPFC regions and elevated plasma corticosterone level which develops in long-term noise-stress exposed rats, might have caused the impairment of spatial memory.
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PMID:Effects of chronic noise stress on spatial memory of rats in relation to neuronal dendritic alteration and free radical-imbalance in hippocampus and medial prefrontal cortex. 1648 Nov 10

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

Excessive generation of free radicals and decreased levels of the antioxidant enzymes such as superoxide dismutase (SOD) and catalase have been observed after brain ischemic reperfusion injury. In the present study, we have investigated the neuroprotective potential of MnTMPyP (Mn(III)tetrakis(1-methyl-4-pyridyl)porphyrin pentachloride), a SOD/Catalase mimetic in bilateral carotid artery occlusion model of global cerebral ischemia in Mongolian gerbils. Five minutes of bilateral carotid artery occlusion produced global cerebral ischemia, which was evident from the neurological deficits, spontaneous motor activity and the decrease in the number of viable hippocampal CA1 neurons. Global ischemia was also associated with increased levels of malondialdehyde, decreased levels of SOD and catalase, and increased TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling) positive cells, indicating oxidative stress and DNA fragmentation. Administration of a single dose of MnTMPyP, 1 mg/kg i.p. (30 min before occlusion), produced no significant neuroprotection; however, 3 mg/kg i.p. (30 min before to occlusion) produced significant reduction in neurological score, spontaneous motor activity and CA1 pyramidal neuronal damage. MnTMPyP also attenuated the increased levels of malondialdehyde and improved the levels of SOD and catalase, and inhibited DNA fragmentation in the ischemic animals. Multiple administration of MnTMPyP, 3 mg/kg i.p. (three times: 30 min before, 1 h and 3 h after occlusion), produced better neuroprotection as compared to single dose administration. This study demonstrates that the neuroprotective effect of MnTMPyP in global ischemia is mediated through reduction in oxidative stress and DNA fragmentation.
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PMID:Neuroprotective effect of MnTMPyP, a superoxide dismutase/catalase mimetic in global cerebral ischemia is mediated through reduction of oxidative stress and DNA fragmentation. 1732 Aug 58

In peroxisomal biogenesis disorders, serious neurological abnormalities can be observed in the patients and the respective knockout mouse models. As a prerequisite for a better understanding of the relationship between the absence of peroxisomes and the observed neuropathology, knowledge of the regional and cell-type specific distribution of peroxisomal proteins in mouse brain is necessary. Therefore, we investigated the expression of distinct peroxins, peroxisomal membrane and matrix proteins (e.g. Pex5p, Pex14p, Pex13p, PMP70, catalase, peroxisomal thiolase, Acox1, "SKL"-PTS1 proteins) by indirect immunofluorescence 1) in primary cultures of the medial neocortex, hippocampus, and cerebellum of newborn mice and 2) in paraffin sections of mouse brain of different ages (newborn-adult). Quantitative analysis revealed a comparable abundance (number/microm(2)) of peroxisomes in cultured neurons and astrocytes of all three brain regions. In contrast, catalase immunoreactivity was higher in cultured astrocytes than in neurons. In mouse brain tissue, the abundance of peroxisomes decreased by half during postnatal development, also exhibiting prominent differences between distinct brain regions and cell types. Catalase protein levels in neuronal peroxisomes, however, decreased much more strongly in the neocortex, CA1-3 areas of the hippocampus, dentate gyrus, cerebellar nuclei, and cerebellar cortex but remained high in Bergmann glia and other astrocytes, epithelial cells of the choroid plexus, and ependyma. Similar age-dependent changes were found for thiolase and Acox1 protein levels. Developmental changes were confirmed by Western blot analysis using enriched peroxisomal and cytosolic fractions of the brain tissue as well as by measurement of catalase activity.
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PMID:Differential expression of peroxisomal matrix and membrane proteins during postnatal development of mouse brain. 1772 95

Bradykinin is considered an important mediator of the inflammatory response in both the peripheral and the central nervous system and it has attracted recent interest as a potential mediator of brain injury following stroke. Bradykinin is recognized to play an important role in ischemic brain. We investigated the effect of bradykinin postconditioning on ischemic damage after 8 min of ischemia (four-vessel occlusion) and 3 days of reperfusion. Bradykinin was administered after 2 days of reperfusion at a dose of 150 microg/kg (i.p.). Catalase (CAT) activity was significantly increased in all examined regions (cortex, hippocampus and striatum) 3 days after 8 min of ischemia, but postconditioning decreased this activity below the control values. The total activity of superoxide dismutase (SOD) 3 days after ischemia was at control level with or without postconditioning. However, the analysis of individual SODs separately revealed interesting differences; while the activity of CuZnSOD was significantly decreased 3 days after ischemia, the activity of MnSOD was significantly increased compared to control levels. In both cases, postconditioning returned SOD activity to control levels. These findings are interesting because MnSOD is a mitochondrial enzyme and its activity in the cytosol suggests that a possible mechanism of protection provided by postconditioning could include prevention of release of mitochondrial proteins to the cytoplasm, resulting in protection against the mitochondrial pathway of apoptosis. 8 min of ischemia alone caused the degeneration of 52.37% neurons in the hippocampal CA1 region 3 days later. Bradykinin used as postconditioning 2 days after the same interval of ischemia enabled the survival of more than 97% of CA1 neurons. This study demonstrated that bradykinin postconditioning induces protection against ischemic brain injury and promotes neuronal survival.
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PMID:Effects of bradykinin postconditioning on endogenous antioxidant enzyme activity after transient forebrain ischemia in rat. 1808 Jan 86

Cerebral hyaline astrocytic inclusions have been observed in a subset of patients with early onset epilepsy, brain structural anomalies, and developmental delay, which indicates that it may represent a unique clinicopathologic entity. To further characterize this condition we use proteomics to investigate differentially expressed proteins in epileptic brain tissue from three pediatric epileptic patients with cerebral hyaline astrocytic inclusions, ranging in age from 5-13 years, and compare to brain tissue from two normal controls. Catalase and carbonic anhydrase I both exhibited increased expression in epileptic brain tissue compared to controls. These findings were confirmed by Western blot analysis. Furthermore, both proteins were localized to astrocytes and in epileptic brain were located within the cerebral hyaline astrocytic inclusions, suggesting a potential role in the generation of this pathologic feature of early onset epilepsy with cerebral hyaline astrocytic inclusions.
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PMID:A proteomic analysis of pediatric seizure cases associated with astrocytic inclusions. 2222 May 88

Curcuma comosa Roxb. is widely used as a gynaecological traditional medicine in South-East Asia and recent behavioral studies have shown that C. comosa extract significantly improved the spatial memory in rats. The present study investigated the protective effects of Curcuma comosa hexane extract on the ethanol (EtOH)-induced oxidation in rat brains. Young female Wistar rats were given 20% of EtOH intraperitoneally to induce the oxidative stress. Subsequently, C. comosa hexane extract was intraperitoneally co-administered at the doses of 100 and 250 mg kg(-1) b.wt. to the EtOH-induced rats for 14 days. The neuron densities of CA1, CA3 and CA4 areas of the hippocampus were counted and the activities of hippocampal Catalase (CAT), Glutathione Peroxidase (GPx) and Superoxide Dismutase (SOD) were determined. EtOH significantly decreased the neuron densities in Cornu Ammonis (CA), including CA1 and CA3 areas; however, the decrease was prevented by C. comosa co-administration. EtOH administration also increased the CAT and GPx activities in the hippocampus which were reversed by C. comosa co-administration. Moreover, C. comosa administration increased the SOD activity in a dose-dependent manner in the EtOH treated groups. C. comosa prevented the neuron loss in the hippocampus caused by EtOH. The possible neural protective mechanism may involve with the changes in activities of the antioxidant enzymes in the hippocampus.
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PMID:Curcuma comosa prevents the neuron loss and affects the antioxidative enzymes in hippocampus of ethanol-treated rats. 2419 65

The catalase of maize scutella is coded for by two loci, Cat1 and Cat2, which are differentially expressed in this tissue during early seedling growth. Two variant lines have been previously identified in which the developmental program for the expression of the Cat2 structural gene in the scutellum has been altered. Line R6-67 exhibits higher than normal levels of CAT-2 catalase in this tissue after four days of postgerminative growth. This phenotype is controlled by a temporal regulatory gene designated Car1. Line A16 exhibits a CAT-2 null phenotype. Further analysis of Car1 verifies the initial indication that it is trans-acting and exhibits strict tissue (scutellum) specificity. A screen of other available inbred lines uncovered eight additional catalase high-activity lines. All eight lines exhibit significantly higher than normal levels of CAT-2 protein. Two of these lines have been shown to be regulated by Car1 as in R6-67. Another line (A338) uncovered during the screen exhibits a null phenotype for CAT-2 protein and resembles A16. Catalase activity levels are low in the scutellum and no CAT-2 CRM (cross-reacting material) is present in the tissues of this line. Also, unlike most maize lines, CAT-2 cannot be induced in the leaf tissue of A338 upon exposure to light. Finally, a single line (A337), demonstrating a novel catalase developmental program, was identified.
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PMID:Analysis of variants affecting the catalase developmental program in maize scutellum. 2425 26


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