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At least 1,171 records · Page 65Linked to original sources
PubMed2001

Differential zinc and DNA binding by partial peptides of human protamine HP2.

The Zn(II) binding by partial peptides of human protamine HP2: HP2(1-15); HP2(1-25), HP2(26-40), HP2(37-47), and HP2(43-57) was studied by circular dichroism (CD). Precipitation of a 20-mer DNA by these partial peptides and the effects of Zn(II) thereon were investigated using polyacrylamide gel electrophoresis (GE). The results of this study suggest that reduced HP2 (thiol groups intact) can bind Zn(II) at various parts of the molecule. In the absence of DNA, the primary Zn(II) binding site in reduced HP2 is located in the 37-47 sequence (involving Cys-37, His-39, His-43, and Cys-47), while in the presence of DNA, the strongest Zn(II) binding is provided by sequences 12-22 (by His-12, Cys-13, His-19, and His-22) and 43-57 (His-43, Cys-47, Cys-53, and His-57). In its oxidized form, HP2 can bind zinc through His residues of the 7-22 sequence. Zn(II) markedly enhances DNA binding by all partial peptides. These findings suggest that Zn(II) ions may be a regulatory factor for sperm chromatin condensation processes.

Binding Sites↗
PubMed2003

[Prevention of bacteremia from central venous catheters in hemodialysis: value of application of a mixture of rifampicin and protamine at the insertion site].

During the last 8.5 years, authors observed only 3 bacteremias out of 249 catheters in place in different sites corresponding to a total of 10,063 days with central venous catheterization in hemodialysis (0.30/1000 catheter days). This good result seems to be correlated mainly with the preventive application, on catheter insertion-site, of a rifampin and protamine sulphate mixture. This protocol appears worthy to be known because, at the present time, whatever the new preventive strategies, infection rates reported in the literature are generally more consequent and it is necessary to consider all the possibilities of decreasing them.

Administration, Topical↗
PubMed2002

[Expression of rat protamine gene in MEL cells].

OBJECTIVE: To investigate the expression of rat protamine (RP) gene in MEL cells and the effect on cell growth. METHODS: Eukaryotic expression plasmid pCR-3.1-RP was constructed and transfected into MEL cells. The changes of cell growth rate, mitotic index and colony-forming rate in semi-solid medium were investigated. RESULTS: Transfected MEL cells showed lower growth rate, mitotic index and colony-forming rate. Volumes of cells were reduced and reduction of RNA transcription was observed. CONCLUSION: These results suggest that expression of RP in MEL cell may inhibit the cell growth and proliferation.

Animals↗
PubMedDate not supplied

[Comparison of amino acid sequences of sturgeon triprotamines using protamines from Acipenser stellatus gonads as an example].

The amino acid sequence of the triprotamine stelline C from mature sperm nuclei of Acipenser stellatus has been established by automated sequence analysis of the protein and from data provided by thermolysine peptides. The complete amino acid sequence of stelline C is: R-R-R-R-R-H-A-S-T-K-L-K-R-R-R-R-R-R-R-H-G-K-K-S-H-K. The comparison of the primary structure of stelline C with that of other triprotamines from Acipenser stellatus shows that they are similar except for the absence of N-terminal alanine in the stelline A molecule. The main structure difference between stelline C and other fish protamines is that the stelline C molecule begins with five arginine residues.

Amino Acid Sequence↗
PubMed1992

Influence of platelet activating factor antagonists on the protamine sulphate stimulated release of histamine from peritoneal mast cells of rats in vitro.

The phospholipase (PL)A2 inhibitor p-bromophenacyl bromide (p-BPB), the antagonists of the platelet activating factor (PAF) 3-(4-(2-chlorophenyl)-9-methyl-6H-thieno(3,2-f)-(1,2,4)triazolo(4, 3-a)(1,4)diazepine-2-yl)-1-(4-morpholinyl)-1-propanone (a thieno-triazolo-diazepine, WEB 2086) and terpene-ginkgolide B and the antihistamine with PAF antagonistic qualities 4,9-dihydro-4-(1-methyl-4-piperidinylidene)-10H-benzo[2,5]cyclo hep ta[1,2-b]thiophen-10-one (ketotifen) inhibit in the order p-BPB greater than terpene-ginkgolide B greater than ketotifen greater than WEB 2086 with decreasing activity the protamine sulphate activated histamine release from peritoneal rat mast cells (pRMC) in vitro. All compounds also inhibit the PAF induced aggregation of human platelets. The order of inhibition of the histamine release by these compounds does not agree with the order of their inhibitory activity on PAF induced aggregation of human platelets, indicating that the inhibition of the mast cell degranulation caused by PAF antagonists does not occur via PAF receptors. A generally membrane stabilizing quality of terpene-ginkgolide B and WEB 2086 may be ruled out as the cause of degranulation inhibition because none of the compounds suppresses the cytotoxic, triton X-100 induced release of histamine from pRMC. The mechanism of mast cell degranulation inhibition by PAF antagonists is unclear. An inhibition of PLA2 and/or inhibition of the Ca(2+)-activation are suggested.

Acetophenones↗
PubMed1992

The altered glomerular filtration slits seen in puromycin aminonucleoside nephrosis and protamine sulfate-treated rats contain the tight junction protein ZO-1.

Nephrosis induced in rats by puromycin aminonucleoside treatment (PAN) results in the apical displacement of the glomerular filtration slit membrane by newly formed, intercellular occluding-type junctions. Similar changes can also be induced by acute kidney perfusion with protamine sulfate (PS). We have investigated the molecular nature of these altered junctions using an antibody to ZO-1, a protein found exclusively in tight junctions. Immunoblotting demonstrates ZO-1, a 225-kd band, in glomerular extracts of normal, PAN-, and PS-treated rats. By immunofluorescence, ZO-1 was localized at the base of podocytes outlining the capillary loops of glomeruli from all three experimental groups. At the electron microscope level, using immunoperoxidase or immunogold labeling, ZO-1 was concentrated along the cytoplasmic surfaces of the slit diaphragms of normal rats. In PAN or PS rats, it was concentrated along both the newly formed occluding-type junctions and the remaining slit diaphragms. When podocalyxin (the major membrane sialoprotein of the podocyte) was similarly localized, it was found exclusively apical to the displaced slit membrane. Based on morphology and the presence of ZO-1, the altered junctions seen in PAN and PS rats appear to represent bona fide tight junctions. Their rapid (15-minute) induction in PS-treated rats suggests that on neutralization of the cell surface charge by polycation perfusion, discontinuous tight junctions form from a preexisting pool of junctional proteins. These findings raise the possibility that glomerular hydraulic conductivity may be regulated in part by regulating the relative patency and width of the filtration slits through focal tight junction assembly.

Animals↗
PubMed1992

Demonstration of a testis-specific trans-acting factor Tet-1 in vitro that binds to the promoter of the mouse protamine 1 gene.

We have established testis-specific in vitro transcription of the mouse protamine 1 (MP1) gene using rat testis nuclear extracts. Addition of testis nuclear extracts to brain extracts enhanced transcription from the MP1 upstream sequence-carrying adenovirus major late promoter. Moreover, the MP1 upstream region from positions -92 to -41 alone exhibited transcriptional activation in a tissue-specific manner. DNase I footprinting demonstrated the presence of a DNA-binding factor around position -60 (Tet-1) in testis nuclear extracts, but not in other tissues. Gel shift analysis also revealed the presence of testis-specific Tet-1. Since mutational analysis in transcriptional and binding assays demonstrates that the Tet-1 site is responsible for transcriptional activation, we suggest that Tet-1 is a novel tissue-specific trans-acting factor. The Tet-1-recognizing sequence was delineated to the 11-mer TGACTTCATAA at position -64. Although the first 8-mer in the Tet-1 11-mer shares homology with the cyclic AMP-responsive element, Tet-1 is demonstrated to be distinct from known cAMP-responsive element-binding factors.

Adenoviridae↗
PubMed2004

[Preparation of lipid-protamine-DNA complexes and evaluation of their transfection efficiencies in vitro].

AIM: To develop a novel non-viral gene delivery systems lipid-polycation-DNA complexes (LPD) and investigate their transfection efficiencies in vitro. METHODS: LPD were prepared as follows by first mixing the plasmid DNA and protamine together, then the resulted polyplexes were incubated for 10 min at room temperature, followed by addition of preformed cationic liposomes. The morphology of LPD was observed by transmission electron microscopy. The diameter and surface charge of LPD were measured by photon correlation spectroscopy (PCS). The nuclease protection ability of LPD was evaluated by agarose gel electrophoresis. Estimation of transfection efficiency was performed by galactosidase assay in Chang, HepG2 and SMMC-7721 cells. RESULTS: The average diameter and the zeta potential of LPD were 143.5 nm and 32.6 mV, respectively. LPD could protect the plasmid DNA from nuclease degradation after 2 hours incubation at 37 degrees C while the naked DNA degraded rapidly. The average transfection efficiencies were (69 +/- 6)%, (43 +/- 7)% and (96.2 +/- 1.8)% in Chang cells, HepG2 cells and SMMC-7721 cells respectively. CONCLUSION: LPD could be prepared easily with small particle sizes and high transfection activities. LPD may be good non-viral vectors for applications in gene delivery.

Carcinoma, Hepatocellular↗
PubMed2005

[Pulmonary hemorrhage after abciximab. Risk factors and the role of protamine].

Large clinical trials have demonstrated the clinical effectiveness of therapy with inhibitors of the platelet surface-membrane glycoprotein IIb-IIIa receptor in a broad range of patients with ischemic heart disease. Abciximab, a platelet glycoprotein IIb-IIIa receptor blocker, is associated with improved long-term prognosis in patients who require angioplasty and stent placement. Severe bleeding from abciximab use is an uncommon event. We describe a patient with severe pulmonary hemorrhage after treatment with abciximab, and discuss predisposing factors and protamine infusion in this potentially fatal complication.

Abciximab↗
PubMed2005

[Determination of expression of protamine-2 mRNA in different positions of the testis of patients with nonobstructive azoospermia].

OBJECTIVE: To investigate the relationship between the expression of protamine-2 (P-2) mRNA and the results of sperm extraction in the corresponding testis tissues of patients with nonobstructive azoospermia. METHODS: Based on pathological diagnosis, 38 cases of azoospermia at the mean age of 32.4 (ranging 24 - 42) years were divided into a nonobstructive (NOA) group and an obstructive (OA) group. Two specimens were taken from different positions of one testis, each divided into three portions for general pathological test, sperm separation and mRNA extraction, respectively. The expression of P-2 mRNA was determined by RT-PCR and image analysis assay. RESULTS: Among the 38 cases, 27 were diagnosed as nonobstructive and 11 as obstructive azoospermia. No regularity was found as to the positions where sperm could or could not be successfully isolated. The expression of P-2 mRNA was 1.40 +/- 0.21 in the tissues where sperm was isolated and 0.51 +/- 0.23 (P < 0.05) in those where no sperm was isolated. CONCLUSION: The expression of P-2 mRNA in the testicular tissues from the patient with nonobstructive azoospermia could reveal the results of sperm extraction in the corresponding tissues.

Adult↗
PubMed1990

Protamine and mast-cell-mediated angiogenesis in the rat.

Different doses of protamine sulphate (PS) given s.c. (at 12-h intervals) were tested for signs of non-specific toxicity measured as effect on body weight and small-gut proliferation as well as on mast-cell secretion and mast-cell-mediated mitogenesis in the mesenteric windows following i.p. injection of Compound 48/80, a potent mast cell secretagogue, in normal rats. In a non-toxic dose range, the effect of PS on mast-cell-mediated angiogenesis, effected by 48/80, was quantified as the number of vessels per mm of mesenteric window in histological sections at x 400. No intelligible dose-effect relationship was discernible between the dose of PS given and the effect on angiogenesis. Only in a tight interval, at 40 mg PS/kg but not at 20 or 60 mg PS/kg, was the angiogenesis statistically significantly suppressed. Hence, it was concluded that PS can be angiostatic but does not exert a more general angiostatic effect in the autogenous systems used.

Animals↗
PubMed1991

[Purification and characterization of precursors of mouse protamine mP2].

Mouse protamine 2 (62 residues) is synthesized as a precursor pmP2 (106 residues) which is subsequently processed during the end of spermiogenesis. Three proteins with molecular and electrophoretic properties similar to those of pmP2 were isolated from testis purified nuclei. The comparison of their amino acid composition and of their N-terminal sequence with those of pmP2 shows that the three isolated proteins are products of pmP2 precursor processing. The three intermediate proteins pmP2/5, pmP2/11 and pmP2/20 which contain 102, 96 and 87 residues respectively, are generated from pmP2 precursors after N-terminal excision of 4, 10 and 19 residues, respectively.

Amino Acid Sequence↗
PubMed1991

Inhibition of leukocyte rolling in venules by protamine and sulfated polysaccharides.

Intravital video microscopy was used to investigate leukocyte margination in 80 mesenteric venules (19 to 54 microns) of 50 anesthetized rabbits. After intravenous (IV) bolus injection, sulfated polysaccharides reduced in a reversible and dose-dependent way the number of leukocytes rolling slowly along the venular wall. The presence of sulfate groups is essential because other negatively charged or neutral polysaccharides had no effect. It was not caused by an increase in RBC velocity or chelation of divalent cations. Inhibition by sulfated dextrans (n = 7) was independent of molecular weight (mol wt 13,000 to 500,000) but was influenced by the average number of sulfate groups per monosaccharide. With substitution 0.13, the 90%-inhibition dose was 104 mg/kg, with 0.7 it was 56 mg/kg, and between substitution 1 and 2 it ranged from 20 to 23 mg/kg. At 100 mg/kg, plasma concentration was 0.6 to 0.7 mg/mL. Xylan sulfate (mol wt 6,000, substitution 1.8) gave 90% inhibition at 11 mg/kg, and heparin gave 90% inhibition at 97 mg/kg. Duration of inhibition (0.5 to 2 hours) depended on mol wt and appeared to be related to plasma clearance. Because protamine also inhibited rolling (12 mg/kg; less than 10 minutes), we propose that repetitive formation and breakup of ionic bonds between sulfate groups and positively charged amino acids is involved in leukocyte rolling. During inhibition of rolling, systemic lymphocyte/monocyte levels appeared to increase. Granulocyte counts did not change, indicating that rolling is not the main mechanism responsible for the marginal granulocyte pool.

Animals↗
PubMed1986

[Control of the therapeutic heparin dosage in platelet rich citrate plasma after protamine neutralization].

A laboranalytical method for estimating the anticoagulative effect of therapeutic heparin doses based on coagulation physiology is presented. Corresponding to our expectation this method is overcome by the direct measuring heparin with chromogenic substrates. On the other hand there are some advantages against the often practically used prolongation of PTT. By neutralisation of the heparin influence with protamine sulphate it is possible to discriminate between the heparin effect and additional disturbances in consequence of deficit in a coagulation factor. An absence of the heparin effect should always lead to the use of an antithrombin III assay.

Blood Platelets↗
PubMed1985

Neutralisation of heparan sulphate and low molecular weight heparin by protamine.

The neutralisation by protamine sulphate (PS) of heparan sulphate (HS), a low molecular weight heparin (LMWH), and a reference preparation of unfractionated heparin (UH), was studied by activated partial thromboplastin time (APTT) and anti-Xa clotting assays. UH was most easily neutralised in the APTT assay by PS (on a weight for weight basis), followed by LMWH and HS. The neutralisation of APTT activity by PS closely followed the loss of activity in the anti-Xa clotting assay, when plasma was used as the source of At III. When the anti-Xa clotting assay was carried out using purified At III in place of plasma, HS and LMWH were neutralised by much lower amounts of PS and resembled UH neutralisation more closely. Resistance of HS anti-Xa activity to PS neutralisation decreased with increasing plasma dilution. The presence of bovine albumin with purified At III concentrate increased the resistance of HS to PS neutralisation. It is concluded that PS binding to UH, HS and LMWH is probably related more to their degree of sulphation than molecular weight and that non-specific interactions between PS and plasma proteins inhibit the binding of PS to HS and LMWH.

Factor X↗
PubMedDate not supplied

[Effect of vicasol and protamine sulfate on the indices of the blood kallikrein-kinin system and of aortic carbohydrate metabolism in nicotine poisoning].

The experiments on rats showed that 6-day nicotine intoxication was followed by an increase of the initial esterase activity (IEA) of the blood, a decrease of oxygen uptake by the aorta tissue. Vicasol produced an activation of kininogenesis in control rats and a reduction of IEA in animals under nicotine intoxication; irrespective of the background, the drug stimulated the aorta tissue respiration. Acute administration of protamine sulfate increased IEA and against the background of nicotine intoxication it increased oxygen uptake by the vessel tissue.

Animals↗