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 human promyelocytic leukemia cell line HL-60 undergoes induced myeloid differentiation, with acquisition of most polymorphonuclear leukocyte (PMN) functions, including generation of toxic oxygen species. We examined the concurrent changes in the cellular detoxifying defenses against superoxide and H2O2: superoxide dismutase, catalase, and the glutathione cycle. During induced differentiation, total superoxide dismutase activity declined to a level slightly more than 2-fold that of PMN, largely due to a decrease in Mn-superoxide dismutase; CuZn-superoxide dismutase showed virtually no change. Catalase activity declined only slightly (but significantly) to a level 1.3 that of PMN. GSH peroxidase activity fell and then rose back to its original level, remaining throughout differentiation more than 10-fold higher than activity in PMN. GSSG reductase activity declined to a level of 73% that of uninduced cells but twice that of PMN. GSH and GSSG contents both decreased, reaching equivalence to those of PMN. Concurrently, the ability of the cells to generate H2O2 increased 11-fold, a change similar to that previously reported for superoxide production. Thus, there is a paradoxical inverse relationship between the development of active oxygen generation and scavenging systems during myeloid differentiation in HL-60 cells.
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PMID:Changes in superoxide dismutase, catalase, and the glutathione cycle during induced myeloid differentiation. 346 51

The decay of nitroxide spin label electron paramagnetic resonance (EPR) absorption intensity was used to investigate the doxorubicin-mediated intracellular generation of free radicals. The effects of 50-500 micrograms/ml doxorubicin on human tumor cells (MCF-7, breast cancer cells, and HL-60, promyelocytic leukemia, cells) were studied by measuring 2,2,6,6-tetramethylpiperidine-1-oxyl (TEMPO) absorption intensity decay (TAID) at a TEMPO concentration of 10 microM. Doxorubicin accelerated the TAID in both cell lines with a detection limit of 50 micrograms/ml for MCF-7 cells and 500 micrograms/ml doxorubicin for HL-60 cells. Preincubation of cells with the iron chelating agent, deferoxamine (5 mM), partially prevented the effects of doxorubicin on the TAID. Catalase and copper, zinc-superoxide dismutase (Cu,Zn-SOD) had no influence on the effects of doxorubicin on the TAID in intact cells. However, Cu,Zn-SOD completely abolished the effects of doxorubicin on the TAID in a MCF-7 cell-free system. Our findings suggest that doxorubicin mediates the intracellular generation of O2.- and that iron is involved in this process.
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PMID:Doxorubicin-mediated free radical generation in intact human tumor cells enhances nitroxide electron paramagnetic resonance absorption intensity decay. 841 98

The present study was undertaken to examine the effect of L-ascorbic acid (LAA) on the growth of HL-60 promyelocytic leukemia cells, besides induction of apoptosis. LAA (> or = 10(-4) M) was found to markedly inhibit the proliferation of HL-60 in liquid culture and clonogenicity in semisolid culture. Moreover, LAA-treated HL-60 showed activity to produce chemiluminescence and expressed CD 66b cell surface antigens, indicating that LAA induces the differentiation of HL-60 mainly into granulocytes. The results are supported by morphological changes of LAA-treated HL-60 into segmented neutrophils. Therefore, the inhibitory effect of LAA on the growth of HL-60 cells seems to arise from the induction of differentiation. To assess the potential role of LAA, cells were exposed to oxygen radical scavengers in the absence or presence of LAA. Catalase abolished and superoxide dismutase promoted LAA-induced differentiation of HL-60. Thus, H2O2 produced as a result of LAA treatment seems to play a major role in induction of HL-60 differentiation.
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PMID:Induction of the differentiation of HL-60 promyelocytic leukemia cells by L-ascorbic acid. 1291 Dec 74

Baicalein is one component of the dried root of Scutellaria Baicalensis Georgi. (Huang Qin) which is widely used in the traditional Chinese herbal medicine. In this study, we report that baicalein was able to induce apoptosis in human promyelocytic leukemia cells (HL-60), as characterized by poly-(ADP-ribose) polymerase (PARP) cleavage and DNA fragmentation. The efficacious induction of apoptosis was observed at 100 microM for 6 h. Mechanistic analysis demonstrated that baicalein induced the cleavage of Bid protein, cytochrome c release from mitochondria into cytosol, and activation of caspase-3, -8 and -9. Moreover, baicalein caused elevation of intracellular hydrogen peroxide level. Catalase could effectively block baicalein-induced DNA fragmentation. These data indicate that baicalein may trigger an apoptotic death program through reactive oxygen species (ROS)-mediated mitochondrial dysfunction pathway. The findings enhance our understanding of anticancer function of baicalein in herbal medicine.
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PMID:Baicalein induces apoptosis through ROS-mediated mitochondrial dysfunction pathway in HL-60 cells. 1537 93