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Gene Review

CAT  -  catalase

Canis lupus familiaris

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Disease relevance of CAT

  • In group II (n = 6), which received PBN and i.v. superoxide dismutase (SOD; 16,000 units/kg) plus catalase (12,000 units/kg), myocardial production of PBN adducts was undetectable during ischemia (delta = -100%, P less than 0.01 vs. group I) and markedly inhibited after reperfusion (delta = -86%, P less than 0.001) [1].
  • This study shows that (i) SOD and catalase are highly effective in blocking free radical reactions in vivo, (ii) the radicals generated in the "stunned" myocardium are derived from univalent reduction of O2, and (iii) inhibition of radical reactions improves functional recovery [1].
  • Failure of superoxide dismutase and catalase to alter size of infarction in conscious dogs after 3 hours of occlusion followed by reperfusion [2].
  • Evidence against the "early protection-delayed death" hypothesis of superoxide dismutase therapy in experimental myocardial infarction. Polyethylene glycol-superoxide dismutase plus catalase does not limit myocardial infarct size in dogs [3].
  • Seven additional animals undergoing 20 minutes of coronary occlusion also received the antioxidant enzymes superoxide dismutase and catalase, beginning 10 minutes before occlusion through the end of reperfusion [4].

Psychiatry related information on CAT

  • Tissue levels of reduced glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) were measured in the same samples to identify alterations in tissue free radical defense mechanisms due to ischemia-reperfusion [5].

High impact information on CAT

  • There was a loss of peroxisomal catalase activity in dogs with aerobic overgrowth, and an indication of mitochondrial disruption in dogs with anaerobic overgrowth, but little evidence for damage to other subcellular organelles [6].
  • However, there was no significant change in mucosal alpha-glucosidase and catalase activity or in in vitro mucosal uptake of 1 mM [14C]leucine when expressed per unit weight of intestinal mucosa [7].
  • Furthermore, the inhibitory effect of catalase on A23187-induced relaxations was abolished when coronary arteries were incubated in the presence of DAHP plus a liposoluble analogue of tetrahydrobiopterin, 6-methyltetrahydropterin (10(-4) mol/L) [8].
  • In DAHP-treated arteries, relaxations to A23187 and its stimulating effect on cGMP production were significantly reduced in the presence of catalase (1200 U/mL) [8].
  • Addition of superoxide dismutase plus catalase or an antagonist of endothelin-A receptors (BQ-123) reduced contractions in rings with endothelium but not in those without endothelium to suspensions of mononuclear cells from rejecting allotransplanted dogs [9].

Chemical compound and disease context of CAT


Biological context of CAT


Anatomical context of CAT

  • Pulse-labeling and immunoprecipitation examination indicated that the level of catalase synthesis in the acatalasemic dog reticulocytes was almost the same (approximately 80%) as that in the normal reticulocytes [15].
  • These results suggested that the proteolytic degradation mediated most likely by proteasome might be involved in disposing of the mutant catalase in acatalasemic erythroid cells [15].
  • Thus, SOD + catalase given at the time of reperfusion had no acute beneficial effect on either the extent of myocyte necrosis or postischemic contractile function in this canine model [18].
  • The results indicate that superoxide dismutase alone protects reperfused ischemic myocardium as well as does the combination of superoxide dismutase and catalase [19].
  • In four groups of dogs, superoxide dismutase plus catalase (groups I-III) or saline (controls) (group IV) was infused into the left atrium [20].

Associations of CAT with chemical compounds

  • On the other hand, the synthesized mutant catalase in reticulocytes was rapidly degraded (t(1/2): 1.8 h) compared with the normal catalase (t(1/2): 14.0 h) and this degradation was almost completely inhibited by lactacystin (LC) [15].
  • H2O2-induced PMN retention was completely inhibited by addition of catalase or the hydroxyl radical scavenger dimethylthiourea to the perfusate by incubation of the PMN with a monoclonal antibody (Mab) against CD18 (R15.7) or by perfusion of the H2O2-treated vessel with CL18/6, a Mab against canine ICAM-1 (intercellular adhesion molecule-1) [21].
  • Singlet oxygen scavengers ascorbic acid and histidine significantly protected SR Ca(2+)-ATPase against rose bengal-derived activated oxygen species, but superoxide dismutase and catalase did not attenuate the inhibition [22].
  • The results showed that irradiation of rose bengal formed a 1:2:2:1 quartet, characteristic of the DMPO-OH adduct, which was scavenged by ethanol but not by superoxide dismutase, catalase, or histidine [22].
  • SOD + catalase had no significant beneficial effect on infarct size measured by triphenyltetrazolium staining: area of necrosis averaged 38.5 +/- 6.1% vs. 46.3 +/- 6.2% of the area at risk in treated compared with control animals respectively (p = NS) [18].

Other interactions of CAT


Analytical, diagnostic and therapeutic context of CAT

  • No catalase protein and activity were detected by immunoblotting and spectrophotomeric assay in acatalasemic dog reticulocytes although almost the same level of mRNA expression as that in the normal reticulocytes was observed [15].
  • In group III (n = 8), the same dosages of SOD and catalase without PBN markedly enhanced contractile recovery (measured as systolic wall thickening) after reperfusion [P less than 0.01 at 3 hr vs. controls (group IV, n = 7)] [1].
  • Thus, in part 2 of the study, conscious unsedated dogs undergoing a 15-minute coronary occlusion were randomized to an intravenous infusion of either saline (19 coronary occlusions) or superoxide dismutase (SOD) plus catalase (CAT) (21 coronary occlusions) [26].
  • Canine myocardial reperfusion injury. Its reduction by the combined administration of superoxide dismutase and catalase [20].
  • Reductions in soluble and peroxisomal catalase activities which could compromise mucosal protection against free radicals in dogs with aerobic overgrowth, and a loss of particulate malate dehydrogenase activity indicative of mitochondrial disruption in dogs with anaerobic overgrowth, were also reversed after treatment [27].


  1. Direct evidence that oxygen-derived free radicals contribute to postischemic myocardial dysfunction in the intact dog. Bolli, R., Jeroudi, M.O., Patel, B.S., DuBose, C.M., Lai, E.K., Roberts, R., McCay, P.B. Proc. Natl. Acad. Sci. U.S.A. (1989) [Pubmed]
  2. Failure of superoxide dismutase and catalase to alter size of infarction in conscious dogs after 3 hours of occlusion followed by reperfusion. Gallagher, K.P., Buda, A.J., Pace, D., Gerren, R.A., Shlafer, M. Circulation (1986) [Pubmed]
  3. Evidence against the "early protection-delayed death" hypothesis of superoxide dismutase therapy in experimental myocardial infarction. Polyethylene glycol-superoxide dismutase plus catalase does not limit myocardial infarct size in dogs. Tanaka, M., Stoler, R.C., FitzHarris, G.P., Jennings, R.B., Reimer, K.A. Circ. Res. (1990) [Pubmed]
  4. Ascorbyl free radical as a real-time marker of free radical generation in briefly ischemic and reperfused hearts. An electron paramagnetic resonance study. Sharma, M.K., Buettner, G.R., Spencer, K.T., Kerber, R.E. Circ. Res. (1994) [Pubmed]
  5. Free radical defense mechanisms and neutrophil infiltration in postischemic skeletal muscle. Smith, J.K., Grisham, M.B., Granger, D.N., Korthuis, R.J. Am. J. Physiol. (1989) [Pubmed]
  6. Comparison of the biochemical changes in the jejunal mucosa of dogs with aerobic and anaerobic bacterial overgrowth. Batt, R.M., McLean, L. Gastroenterology (1987) [Pubmed]
  7. Cholecystokinin and secretin prevent the intestinal mucosal hypoplasia of total parenteral nutrition in the dog. Hughes, C.A., Bates, T., Dowling, R.H. Gastroenterology (1978) [Pubmed]
  8. Tetrahydrobiopterin and dysfunction of endothelial nitric oxide synthase in coronary arteries. Cosentino, F., Katusić, Z.S. Circulation (1995) [Pubmed]
  9. Mononuclear cells from dogs with acute lung allograft rejection cause contraction of pulmonary arteries. Cale, A.R., Ricagna, F., Wiklund, L., McGregor, C.G., Miller, V.M. Circulation (1994) [Pubmed]
  10. Thromboxane B2 in cardiac lymph. Effect of superoxide dismutase and catalase during myocardial ischemia and reperfusion. Michael, L.H., Zhang, Z., Hartley, C.J., Bolli, R., Taylor, A.A., Entman, M.L. Circ. Res. (1990) [Pubmed]
  11. Electrophysiological effects of anti-free radical interventions in canine Purkinje fibers. Rosenthal, J.E., Brown, R.L. J. Mol. Cell. Cardiol. (1988) [Pubmed]
  12. Cerulein-induced pancreatitis in the ex vivo isolated perfused canine pancreas. Clemens, J.A., Olson, J., Cameron, J.L. Surgery (1991) [Pubmed]
  13. Studies of myocardial protection in the immature heart. IV. Improved tolerance of immature myocardium to hypoxia and ischemia by intravenous metabolic support. Julia, P., Young, H.H., Buckberg, G.D., Kofsky, E.R., Bugyi, H.I. J. Thorac. Cardiovasc. Surg. (1991) [Pubmed]
  14. Pretreatment with catalase or dimethyl sulfoxide protects alloxan-induced acute lung edema in dogs. Kawada, T., Kambara, K., Arakawa, M., Segawa, T., Ando, F., Hirakawa, S., Emura, S., Shoumura, S., Isono, H. J. Appl. Physiol. (1992) [Pubmed]
  15. cDNA cloning of mutant catalase in acatalasemic beagle dog: single nucleotide substitution leading to thermal-instability and enhanced proteolysis of mutant enzyme. Nakamura, K., Watanabe, M., Takanaka, K., Sasaki, Y., Ikeda, T. Int. J. Biochem. Cell Biol. (2000) [Pubmed]
  16. The role of oxygen-derived free radicals in ischemia-induced increases in canine skeletal muscle vascular permeability. Korthuis, R.J., Granger, D.N., Townsley, M.I., Taylor, A.E. Circ. Res. (1985) [Pubmed]
  17. Free oxygen radicals contribute to platelet aggregation and cyclic flow variations in stenosed and endothelium-injured canine coronary arteries. Ikeda, H., Koga, Y., Oda, T., Kuwano, K., Nakayama, H., Ueno, T., Toshima, H., Michael, L.H., Entman, M.L. J. Am. Coll. Cardiol. (1994) [Pubmed]
  18. "Reperfusion injury" by oxygen-derived free radicals? Effect of superoxide dismutase plus catalase, given at the time of reperfusion, on myocardial infarct size, contractile function, coronary microvasculature, and regional myocardial blood flow. Przyklenk, K., Kloner, R.A. Circ. Res. (1989) [Pubmed]
  19. The independent effects of oxygen radical scavengers on canine infarct size. Reduction by superoxide dismutase but not catalase. Werns, S.W., Shea, M.J., Driscoll, E.M., Cohen, C., Abrams, G.D., Pitt, B., Lucchesi, B.R. Circ. Res. (1985) [Pubmed]
  20. Canine myocardial reperfusion injury. Its reduction by the combined administration of superoxide dismutase and catalase. Jolly, S.R., Kane, W.J., Bailie, M.B., Abrams, G.D., Lucchesi, B.R. Circ. Res. (1984) [Pubmed]
  21. Hydrogen peroxide pretreatment of perfused canine vessels induces ICAM-1 and CD18-dependent neutrophil adherence. Gasic, A.C., McGuire, G., Krater, S., Farhood, A.I., Goldstein, M.A., Smith, C.W., Entman, M.L., Taylor, A.A. Circulation (1991) [Pubmed]
  22. Singlet oxygen interaction with Ca(2+)-ATPase of cardiac sarcoplasmic reticulum. Kukreja, R.C., Kearns, A.A., Zweier, J.L., Kuppusamy, P., Hess, M.L. Circ. Res. (1991) [Pubmed]
  23. Greater susceptibility of failing cardiac myocytes to oxygen free radical-mediated injury. Tsutsui, H., Ide, T., Hayashidani, S., Suematsu, N., Utsumi, H., Nakamura, R., Egashira, K., Takeshita, A. Cardiovasc. Res. (2001) [Pubmed]
  24. Ontogeny of hepatic peroxisomal uricase activity in the mongrel puppy. Whitington, P.F., Stapleton, F.B. Pediatr. Res. (1983) [Pubmed]
  25. Cytochrome P-450 metabolites but not NO, PGI2, and H2O2 contribute to ACh-induced hyperpolarization of pressurized canine coronary microvessels. Tanaka, M., Kanatsuka, H., Ong, B.H., Tanikawa, T., Uruno, A., Komaru, T., Koshida, R., Shirato, K. Am. J. Physiol. Heart Circ. Physiol. (2003) [Pubmed]
  26. Postischemic myocardial "stunning". Identification of major differences between the open-chest and the conscious dog and evaluation of the oxygen radical hypothesis in the conscious dog. Triana, J.F., Li, X.Y., Jamaluddin, U., Thornby, J.I., Bolli, R. Circ. Res. (1991) [Pubmed]
  27. Response of the jejunal mucosa of dogs with aerobic and anaerobic bacterial overgrowth to antibiotic therapy. Batt, R.M., McLean, L., Riley, J.E. Gut (1988) [Pubmed]
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