Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.22.1 (DNase II)
 429 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

For studying the mechanism of hyperoxia toxic effect on metabolism in the rat brain localization of lysosomes enzymes - acid phosphatase, DNase II and acid peptid-hydrolases were investigated in the brain subcellular fractions under different phases of oxygen poisoning and in the in vitro experiments. Under hyperoxia redistribution of the lysosome enzymes is found between the fraction enriched with lysosomes and the soluble one. The character of redistribution evidences for disturbance of permeability in the brain lysosome membranes under hyperoxia. Urea possessing a protective effect under these conditions prevents from labilization of lysosome enzymes which is evoked by the effect of oxygen hyperoxia. When studying manifestation of the effect of lysosome hydrolases release on the substrate level there were found constancy of DNA content in the brain under hyperoxia and a decrease in polymeric property of the brain DNA an hour after the beginning of the terminal phase of oxygen poisoning.
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PMID:[Lysosome enzymes of brain in hyperoxia and under the effect of urea]. 120 6

In recent times, Cr(III)(picolinate)(3) [Cr(III)(pic)(3)] a nutritional supplement, is gaining attention because of its clastogenic and mutagenic properties. Earlier studies of ours indicated that Cr(III)(pic)(3) is cytotoxic to lymphocytes with ROS and mitochondrial events playing a role in bringing about apoptosis. Now, we report that, autoschizis is induced in lymphocytes in a concentration and time dependent manner which is confirmed through TEM and SEM. Lymphocytes treated with concentrations of 100microM of Cr(III)(pic)(3) exhibit features such as cytoplasmic bleb, self excision of cytoplasm, cytoplasmic leakage and membrane bound bodies formed from the excised pieces apart from apoptosis and necrosis. Though autoschizis has been described in tumor cell lines treated with menadione and ascorbate, occurrence of this cell death in normal T-lymphocytes is reported here. The cellular events that accompany autoschizis are found to be increase in intracellular Reactive Oxygen Species (ROS) and cytoplasmic lactate dehydrogenase, loss of mitochondrial membrane potential (MMP) and depletion of ATP. Further, autoschizis is effected through increases in DNase I and DNase II activity with a concomitant decrease in caspase-3 activity which leads to a random cleavage of the DNA as demonstrated by a smear like pattern after electrophoresis on agarose gel.
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PMID:Autoschizis of T-cells is induced by the nutritional supplement, Cr(III)picolinate. 1985 52

Tissue injury triggers a complex network of cellular and molecular responses. Although cell migration and proliferation are the most conspicuous, several other responses, such as apoptosis and increased protease activity, are necessary for a proper restitution of the tissue. In this work, we study the leukocyte elastase inhibitor (LEI) expression during wound healing of bovine corneal endothelial monolayers in culture. LEI is a multifunctional protein with anti-protease and anti-apoptotic activity. When properly cleaved, it is transformed into L-DNase II, a pro-apoptotic enzyme and translocated to the nucleus. We found that early after injury LEI increases its protein and mRNA expressions, without nuclear translocation and returns to basal levels immediately after wound closure. This increase is blocked by N-acetylcysteine, suggesting that production of reactive oxygen species immediately after wounding is involved in the LEI increase. Another finding of this work is that there is an acidification of the cells at the wound border which, in contrast to other cell types, does not determine nuclear translocation of the protein. Taken together, the results of this work suggest that the function of LEI during wound healing is related to its activity as a protease inhibitor and/or to its anti-apoptotic activity.
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PMID:Increase in the expression of leukocyte elastase inhibitor during wound healing in corneal endothelial cells. 2608 42