Biochemical and biophysical research communications
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Biochem. Biophys. Res. Commun. · Aug 1997
Apoptosis in human leukemic cells induced by lactoferricin, a bovine milk protein-derived peptide: involvement of reactive oxygen species.
We examined the activity of bovine lactoferricin (Lfcin-B), a peptide derived from a bovine milk protein lactoferrin (LF-B), to induce apoptosis in THP-1 human monocytic leukemic cells. Treatment with Lfcin-B at up to 50 micrograms/ml induced cell death in THP-1 cells in dose- and time-dependent manner, showing apparent morphological changes, hypodiploid forms of genomic DNA and apoptotic DNA fragmentation, whereas LF-B was inactive even at a high dose (500 micrograms/ml). The apoptosis-inducing effect of Lfcin-B increased with reduction of serum concentration, but was inhibited by addition of Zn2+, a inhibitor of Ca2+/Mg(2+)-dependent endonucleases in a dose-dependent manner. ⋯ In addition, THP-1 cells treated with Lfcin-B, but not LF-B, showed high levels of intracellular reactive oxygen species (ROS) from the early period (20 min) of Lfcin-B treatment. And the production of ROS by Lfcin-B was dependent upon the dose of Lfcin-B added. These results suggested that Lfcin-B, a LF-B-derived peptide, but not LF-B itself, is able to induce apoptosis in THP-1 human monocytic tumor cells, and that its apoptosis-inducing activity is related to the pathway mediated by production of the intracellular ROS and activation of Ca2+/Mg(2+)-dependent endonucleases.
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Biochem. Biophys. Res. Commun. · Mar 1997
Comparative StudyNa+/K+ ATPase in lower airway epithelium from cystic fibrosis and non-cystic-fibrosis lung.
The basolateral Na+/K+ ATPase plays a critical role in sodium reabsorption across airway epithelium. Nasal epithelium shows increased Na+/K+ ATPase activity in cystic fibrosis (CF) but Na+/K+ ATPase has not been characterized in human lung epithelium or compared in CF and normal lung. ⋯ Bronchial epithelial Na+/K+ ATPase activity was twofold higher in CF patients than in controls. The increased Na+/K+ ATPase activity may contribute to the increased sodium reabsorption seen in cystic fibrosis.
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Biochem. Biophys. Res. Commun. · Dec 1996
Biosynthesis of taxol: enzymatic acetylation of 10-deacetylbaccatin-III to baccatin-III in crude extracts from roots of Taxus baccata.
The biosynthesis of taxol is a multistep process. One intermediate reaction is the acetylation of 10-deacetylbaccatin-III (10-DAB) to baccatin-III, an assumed precursor of taxol. Here we describe the cell free acetylation of 10-DAB in crude extracts from roots of Taxus baccata saplings using 14C-or 3H-labeled acetyl-coenzyme A as the acetyl donor. ⋯ Furthermore, the acetylation product showed an identical UV spectrum as authentic baccatin-III. Crude extracts from cambium of stems yielded three- to fivefold lower activity. This is in agreement with our finding that the taxol titer in roots was considerably higher than that in cambium.
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Biochem. Biophys. Res. Commun. · Jul 1995
Cytochrome c oxidase catalysis of the reduction of nitric oxide to nitrous oxide.
Reduction of nitric oxide (NO) to nitrous oxide (N2O) is catalyzed by bovine heart cytochrome c oxidase (CcO) in anaerobic solutions at pH 7.2 and 20 degrees C. Cyanide inhibits and forms Fea3(3+)CN. The mononitrosyl (Fea3(2+)NO), but not the dinitrosyl (Fea3(2+)NO; CuB+NO), is a likely intermediate in N2O formation. ⋯ Conversion of NO to N2O is favored by low levels of both NO and O2, higher NO levels can inhibit both cytochrome c oxidase and NO reductase activities. Raising the O2 level will favor catalysis of NO oxidation to NO2 by CcO. The reactions of NO and the specific CcO activity that occur in tissue will be critically dependent on NO, O2, and CcO levels.
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Biochem. Biophys. Res. Commun. · Jul 1994
Dexamethasone inhibits the expression of an inducible nitric oxide synthase in infarcted rabbit myocardium.
Infarcted areas of rabbit myocardium show relatively higher inducible nitric oxide synthase activity, measured by the conversion of L-[14C]arginine to L-[14C]citrulline. The principal finding in this study is that dexamethasone (2 mg/kg) prevents the induction of inducible nitric oxide synthase in heart muscle when given before, or even 3 hr after coronary artery ligation. Additionally cyclic GMP levels remain unchanged following treatment with dexamethasone. It is possible that the enhanced production of nitric oxide by inducible nitric oxide synthase accounts, at least in part, for the depression of myocardial contractility seen in myocardial infarction and in other clinical conditions.