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)

The effectiveness of 24-hour hypothermic machine perfusion with TP-V (a hyperosmolar colloid solution containing dextrose, sucrose and ATP-MgCl2) alone, or in combination with oxygen free radical scavengers, was evaluated in isolated-perfused canine heart-lungs. Heart-lungs were perfused at 4 degrees C in either TP-V (n = 6), TP-V/Allopurinol (500 mg/L) (n = 6), or TP-V/Allopurinol (500 mg/L) & Catalase (5000 U/L) (n = 5). Lung inflation was maintained with 100% nitrogen. Following preservation, the heart-lungs were perfused with an albumin-mannitol perfusate for 3 hours at 37 degrees C, for functional, hemodynamic, and laboratory determinations. Cold preservation with TP-V/Allopurinol, and TP-V/Allopurinol & Catalase resulted in physiologically normal LDH levels during the 3-hour normothermic isolated perfusion test period. Significantly lower enzyme activity for CPK was evident at 0 (p less than .005) and 3 hours (p less than .05) of perfusion, while no significant differences in lactate production were seen among the groups. In addition, pH, PCO2, PO2, and left ventricular, aortic, and coronary artery pressures all remained within normal physiologic range, with no significant differences seen among the three groups. 99m Technetium scans demonstrated adequate patency among the heart-lungs, with better flow seen in those perfused with TP-V/Allopurinol & Catalase. Histological specimens confirmed a decrease in myocardial and pulmonary damage when Allopurinol and/or Catalase was used. It appears that oxygen free radical scavengers provide some protection from canine heart-lungs which have been hypothermically preserved for 24 hours.
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PMID:Effect of 24-hour preservation with oxygen free radical scavengers on isolated-perfused canine heart-lungs. 302 18

Malignant hyperthermia (MH) is a severe familial disease in both the pig and the human, with 70% fatality when fully expressed in humans. MH produces rapid elevation of temperature in response to stresses, of which there are two general kinds: Societal or emotional stress, and chemical stressors. The most commonly encountered stressor is halothane, a general anesthetic in wide use. Besides large temperature increases, there occur some twenty symptoms. Much work in other laboratories has been concentrated on elevated CPK i the plasma. However, all the symptoms are consistent with a single disorder, namely oxidative damage, especially in membranes. A deficiency in the glutathione peroxidase (GPX) system is a prime factor, likely the molecular basis allowing abnormal oxidative damage in the MH pig. Catalase activities are normal in MH pigs, but they have only 20-50% normal GPX activities. The deficiency does not cause oxidative damage. It allows failure or protective mechanisms against it. The nonstressed MH animal exhibits less acute symptoms, e.g. enhanced red cell Heinz bodies, but such animals generally mature. Under stress, their inadequate protective mechanisms dependent on GPX are overwhelmed, resulting in gross symptoms and crisis. It is important to concentrate on the GPX system(s) and their adjacent pentose shunt metabolism. We propose that a deficiency in any of these two systems is the molecular basis of the disease. Many tissues are involve in MH, but the red cell obviously provides a convenient means for assay and for screening. This paper mainly pertains to porcine MH. However, preliminary work with humans indicates that human MH has a similar molecular basis.
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PMID:Malignant hyperthermia (MH): porcine erythrocyte damage from oxidation and glutathione peroxidase deficiency. 729 Nov 94