Disease relevance of Cat

• MnSOD and catalase transgenes demonstrate that protection of islets from oxidative stress does not alter cytokine toxicity [1].
• The effect of catalase deficiency on progressive renal fibrosis has not been fully elucidated [2].
• In order to determine the molecular basis for Csb acatalasemia, we have isolated a cDNA clone for murine catalase and have used this probe to analyze Csa and Csb genomic DNA and catalase mRNA [3].
• EXPERIMENTAL DESIGN: Sod2 and catalase overexpressing HT-1080 fibrosarcoma cell lines were used to evaluate the H(2)O(2)-dependent regulation of matrix metalloproteinase (MMP)-1 promoter activity, mitogen-activated protein (MAP) kinase signaling, DNA-binding activity, and MMP mRNA levels [4].
• The effect of catalase deficiency on renal tubulointerstitial injury induced by unilateral ureteral obstruction (UUO) has been studied in homozygous acatalasemic mutant mice (C3H/AnLCs(b)Cs(b)) compared with wild-type mice (C3H/AnLCs(a)Cs(a)) [5].

Psychiatry related information on Cat

• Our results demonstrate that a reduction in several anti-oxidant defense mechanisms, including catalase and glutathione S-transferase mu, correlates with the emergence of the malignant phenotype [6].
• In mice subjected to 3-day periods of food deprivation an increase in plasma free fatty acids occurred together with a rise in the cardiac content of fatty acyl CoA-oxidase (+ 15.2%) and catalase (+ 136.2%) activities [7].
• Experiments where catalase was used to interrupt H2O2 exposure over a long time course revealed 15-30 minutes to be the critical period of exposure to 5 mM H2O2 necessary for a sustained increase in F actin as well as large increases in membrane blebbing and later cell death [8].
• We conclude that the alcohol drinking preference between the B6 and D2 inbred mouse strains is independent of the Ah receptor-but is genetically determined, in part, by the level of brain catalase activity which, in turn, regulates brain acetaldehyde concentrations [9].
• These results suggest that cyanamide could reduce locomotor activity through its inhibition of brain catalase, giving further support to the notion that brain catalase may be an important regulator of some ethanol-induced behavioural effects [10].

High impact information on Cat

• This augmented peroxisome population was accompanied by significant elevation of liver catalase activity [11].
• In addition, administration of scavengers of reactive oxygen metabolites, such as catalase and desferrioxamine, did not prevent the albuminuria in this model [12].
• Aminotriazole inhibition of lymphokine-activated cells' catalase or of toxoplasma catalase was effective in inducing these macrophages to display antitoxoplasma activity [13].
• Inhibition of IB and IM macrophage catalase by aminotriazole maintained toxoplasmastatic activity otherwise lost after 48 h of cultivation [13].
• The activities of the endogenous O2- and H2O2 scavenging enzymes, superoxide dismutase (SOD), glutathionine peroxidase (GP), and catalase, were measured in lysates of the intracellular parasite, Toxoplasma gondii, and in various macrophage populations [13].

Chemical compound and disease context of Cat

• Results showed a decrease in catalase activity of the PFC and ST after SE and death induced by cocaine and bupropion overdoses [14].
• In the toxicity group, increased concentrations of malondialdehyde (MDA) and lipid hydroperoxides (LOOH) and decreased glutathione peroxidase (GSH-Px) and catalase (CAT) activities were found compared to the control and olive oil groups (p < 0.05) [15].
• In Dalton lymphoma cells, the activities of glutathione S-transferase, glutathione peroxidase, and catalase decreased very distinctly (approximately 2-5, 2-5 and 5-11 times, respectively) at all time points, but glutathione reductase decreased significantly only at 72 h of cisplatin treatment [16].
• Catalase enrichment using recombinant adenovirus protects alphaTN4-1 cells from H(2)O(2) [17].
• Vitamin deficiency itself caused a 3- to 4- fold increase in cytosolic catalase activity and a smaller increase in the activity of microsomal cytochrome P-450 IVA (lauric acid omega- and omega-1 hydroxylase) in this same organ [18].

Biological context of Cat

• Thus an altered Sod1/(Gpx1 plus Cat) ratio may also affect gene expression by altering the binding and/or availability of transcription factors to DNA [19].
• We propose that it is the balance in the activity of the Sod to Gpx plus Cat ratio (Sod/(Gpx plus Cat)) that is an important determinant of cellular aging [19].
• Significant differences in copper zinc superoxide dismutase and catalase activities were not noted and the levels of total, reduced and oxidized glutathione were similar in transgene (+) and (-) animals [20].
• The level of catalase activity remained low in the remnant kidneys of acatalasemic mice until week 18 without compensatory up-regulation of glutathione peroxidase or superoxide dismutase (SOD) activity [2].
• In contrast, inactivation of catalase caused substantial cell death only in GPx1(-/-) cells but not in wild-type astrocytes [21].

Anatomical context of Cat

• Further studies showed that cortical injury from physical impact caused a significant decrease in NAD-linked electron transfer activities and energy coupling capacities in brain mitochondria of Cat knockout mice but not wild-type mice [22].
• The activities of the peroxisomal enzymes PCO and Cat were enhanced 5- to 25-fold and 1.5- to 3-fold respectively by treatment with the peroxisome proliferators [23].
• In contrast with iodoacetamide-treated red cells, catalase was not inactivated by 3-AT in glutathione peroxidase-deficient erythrocytes [24].
• Glutathione peroxidase gene expression was 15%, and catalase gene expression was not at all detectable in pancreatic islets [25].
• Catalase activity decreased dramatically at doses above 5 J (to 11.8% of initial activity in epidermis and 27.7% in dermis at 25 J) [26].

Associations of Cat with chemical compounds

• The mouse catalase (Cat or Cas1) gene was disrupted by replacing parts of intron 4 and exon 5 with a neomycin resistance cassette [22].
• Notably, SNs from both Cat KO and old mice were deficient in removing extracellular challenges of H(2)O(2) [27].
• An imbalance in the ratio of Sod to Gpx and Cat results in the accumulation of H2O2 which may participate in the Fenton reaction, resulting in the formation of noxious hydroxyl radicals [19].
• However, mice deficient in catalase were not more vulnerable to hyperoxia-induced lung injury; nor did their lenses show any increased susceptibility to oxidative stress generated by photochemical reaction, suggesting that the antioxidant function of catalase in these two models of oxidant injury is negligible [22].
• Coexpression of MnSOD and catalase provided synergistic protection against peroxynitrite and STZ [1].

Physical interactions of Cat

• Further evidence for the involvement of ROS in NF-kappaB activation is that 1 mM H2O2 enhanced NF-kappaB/DNA binding and that this activation was inhibited by catalase [28].

Regulatory relationships of Cat

• However, the mechanism by which catalase up-regulates COX-2 remains poorly understood [29].
• Treatment with exogenous TNF-alpha down-regulated catalase in H4IIE cells but not in Yv2-12 and Yv13-44 cells [30].
• Catalase activity in the cytosol was induced 5.2-fold and DT-diaphorase activity was increased 3.5- and 3.2-fold in the cytosol and mitochondria, respectively [31].
• The activity of antioxidant enzyme superoxide dismutase was enhanced significantly by TP treatment while catalase activity remained unaffected [32].
• Liver-specific catalase expression in transgenic mice inhibits NF-kappaB activation and DNA synthesis induced by the peroxisome proliferator ciprofibrate [33].

Other interactions of Cat

• However, MnSOD and/or catalase provided no protection against cytokine-induced injury [1].
• CuZnSOD and catalase activities peaked within 0.5 h following irradiation for nontoxic 0.5 microM hypericin and toxic 1.0 microM hypericin [34].
• GPx and catalase activities slowly went down, while GRed continued increasing as long as the levels of GSH were kept very low [35].
• Induction of COX-2 by catalase in smooth muscle cells, endothelial cells, and neuronal cells has been previously reported [29].
• Fibroblasts incubated with DFO or DMSO produced lower levels of MDA than controls, as did fibroblasts overexpressing MnSOD, catalase or PHGPx [36].

Analytical, diagnostic and therapeutic context of Cat

• We sought to generate a new line of catalase null mice by the gene targeting technique [22].
• Using a sensitive Northern blot hybridization technique, gene expression of superoxide dismutase (SOD), catalase, and glutathione peroxidase was studied in pancreatic islets and for comparison in various other mouse tissues (liver, kidney, brain, lung, skeletal muscle, heart muscle, adrenal gland, and pituitary gland) [25].
• Western blottings for catalase, GST, and SOD also showed enhanced increase in protein expression, supporting the increase in enzyme activities [37].
• However, overexpression of catalase in malignant cells did not result in increased resistance to oxidative stress as measured by cell viability and protein oxidation after treatment of the cells with hydrogen peroxide [38].
• After a single intraperitoneal injection of 170 mumol nickel(II)acetate/kg body wt., the activity of hepatic catalase (CAT) decreased by 25-56% in a strain- and time-dependent manner, the most susceptible being C57BL/6NCr greater than C3H/HeNCr-MTV- greater than B6C3F1 greater than or equal to BALB/cAnNCr mice [39].

References