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)

Human blood platelets produce oxidant species when stimulated by collagen and thrombin. The oxidative burst of platelets has been studied by cytofluorimetry taking advantage of the fluorogenic dye DCFH2-DA, which is taken up and deacetylated by platelets and then oxidized to the fluorescent derivative DCF. The oxidation of DCFH2 is induced by stimulation with collagen but not with thrombin and inhibited by external catalase. Catalase also inhibited the aggregation induced by collagen, but not that induced by thrombin. Aspirin and indomethacin inhibited the formation of the fluorochrome only when platelets were stimulated by thrombin. Externally added H2O2 increased the cytoplasmic calcium content as probed by the fluorescence of Indo-1. The present data suggest that collagen induces the production of H2O2, which in turn may stimulate the aggregation of platelets through a calcium mobilization. Instead the stimulation by thrombin does not require the intermediacy of H2O2.
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PMID:Hydrogen peroxide is an intermediate in the platelet activation cascade triggered by collagen, but not by thrombin. 189 57

The aim of the paper was to compare the erythrocyte serum and hepatic chomogenate antioxidative factors in order to assess their involvement in the detoxification events. The catalase and superoxiddismutase levels, important factors of the cellular defence, were sensitivity modulated in an acute experiment on Wistar rats. Carbofuran was administered in a non-lethal dose (7 mg/b.w.) single or in the presence of certain antioxidative agents (Vitamin E, Caffeine, Aspirin) EDTA and Cysteine for their role in protecting membranes against oxidative damage. The erythrocyte parameters (SOD, Catalase) were well related to seric factors, especially ceruloplasmin level, with varied magnitudes. GGT a marker of hepatotoxicity and G1-DH, a mitochondrial marker, were in a good correlation with erythrocyte factors. The changes seem to modulate a transmembranary disturbance process, as in hepatocyte pictures.
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PMID:Interference of some enzymatic modulators in the hepatic aggression induced by xenobiotics. 754 89

A link between corticosteroid therapy and the development of cataract has been known for many years. However, the precise underlying molecular mechanism of pathology has not been characterised, although a role for direct deleterious interactions between corticosteroids and lenticular proteins has been investigated. Alpha-crystallin is a major lens protein that has exhibited chaperone properties in vitro. Catalase is a ubiquitous enzyme that is an important scavenger of hydrogen peroxide in vivo. The corticosteroid prednisolone-21-hemisuccinate was found to inactivate bovine liver catalase, in vitro in a progressive manner. Coincubation of alpha-crystallin with catalase in a 1:2 molar ratio (one alpha-crystallin to two catalase molecules) fully protected against this inactivation. The protection was specific. Aspirin-like analgesics, putative anti-cataract drugs offered no such protection.
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PMID:Alpha-crystallin acting as a molecular chaperone protects catalase against steroid-induced inactivation. 860 85

Some late complications of diabetes are associated with alterations in the structure and function of proteins due to glycation and free radicals generation. Aspirin inhibits protein glycation by acetylation of free amino groups. In the diabetic status, it was demonstrated that several enzymes of heme pathway were diminished. The aim of this work has been to investigate the in vivo effect of short and long term treatment with acetylsalicylic acid in streptozotocin induced diabetic mice. In both treatments, the acetylsalicylic acid prevented delta-aminolevulinic dehydratase and porphobilinogen deaminase inactivation in diabetic mice and blocked the accumulation of lipoperoxidative aldehydes. Catalase activity was significantly augmented in diabetic mice and the long term treatment with aspirin partially reverted it. We propose that oxidative stress might play an important role in streptozotocin induced diabetes. Our results suggest that aspirin can prevent some of the late complications of diabetes, lowering glucose concentration and probably inhibiting glycation by acetylation of protein amino groups.
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PMID:Preventive aspirin treatment of streptozotocin induced diabetes: blockage of oxidative status and revertion of heme enzymes inhibition. 1086 19