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)

Chondrocytes in dense suspension culture in agarose survive in serum-free DME because they secrete low molecular mass compounds supporting their own viability. This activity can be replaced by pyruvate, or sulfhydryl compounds, e.g., cysteine or dithioerythritol. Catalase, an enzyme decomposing H2O2, also protects the cells, whereas superoxide dismutase has no effect. Therefore, chondrocytes in culture are sensitive to toxic compounds derived from molecular oxygen, i.e., hydroxyl radicals or hydrogen peroxide spontaneously generated in DME containing ascorbate and ferrous ions. Poly-ADP-ribosylation is an important step in the cascade of events triggered by these compounds. To survive, chondrocytes do not require stimulation by growth factors. They remain resting cells in fully defined, serum-free culture also at low density. Proliferation and hypertrophy can be induced by serum, but not by low cell density alone.
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PMID:Resting chondrocytes in culture survive without growth factors, but are sensitive to toxic oxygen metabolites. 236 33

The tumor promoter phorbol-12-myristate-13-acetate (PMA) increases the poly ADP-ribosylation of acid extractable (0.2N H2SO4) nuclear proteins in mouse embryo fibroblasts C3H10T1/2. Catalase suppresses the reaction by approximately 50%. Polyacrylamide gel electrophoresis reveals that the core histones H2B, A24 and H3d serve as major poly ADP-ribose acceptors. Smaller amounts of poly ADP-ribose are associated with histones H2A/H3 and H1. Poly ADP-ribosylation of histones may change the nucleosomal structure and function and play a role in PMA induced modulation of gene expression in promotion.
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PMID:Poly ADP-ribosylation of histones in tumor promoter phorbol-12-myristate-13-acetate treated mouse embryo fibroblasts C3H10T1/2. 406 47

An important limitation in cell therapy for the regeneration of tissue is the initial lack of oxygen. After implantation of large 3D cell-seeded structures, cells die rather than contribute to tissue regenerating. Here we've tested oxygen-releasing materials to improve cell survival and growth after implantation. Calcium peroxide (CaO2) in a polymer matrix was used as source of oxygen. Two polymers were tested in order to slow down and extend the period of oxygen release, poly(D,L-lactic acid) and poly(lactic-co-glycolic acid). Compared to CaO2 particles, both releasing systems showed an initially higher and shorter oxygen release. Human mesenchymal stromal cells cultured on casted films of these oxygen-releasing composites required catalase to proliferate, indicating the production of cytotoxic hydrogen peroxide as intermediate. Poly(D,L-lactic acid) and poly(lactic-co-glycolic acid) are less suited for slowly oxygen-releasing materials. Catalase was able to reduce the cytotoxic effect of H2O2.
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PMID:Control of oxygen release from peroxides using polymers. 2615 78