Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P30536 (PBS)
 9,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The photogeneration of nitric oxide (NO) using laser flash photolysis was investigated for S-nitroso-glutathione (GSNO) and S-nitroso-N-acetylcysteine (NacySNO) at pH 6.4 (PBS/HCl) and 7.4 (PBS). Irradiation of S-nitrosothiol with light (lambda = 355 nm followed by absorption spectroscopy) resulted in the homolytic decomposition of NacySNO and GSNO to generate radicals (GS and NacyS ) and NO. The release of NO from donor compounds measured with an ISO-Nometer apparatus was larger at pH 7.4 than pH 6.4. NacySNO was also incorporated into dipalmitoyl-phosphatidylcholine liposomes in the presence and absence of zinc phthalocyanine (ZnPC), a well-known photosensitizer useful for photodynamic therapy. Liposomes are usually used as carriers for hydrophobic compounds such as ZnPC. Inclusion of ZnPC resulted in a decrease in NO liberation in liposomal medium. However, there was a synergistic action of both photosensitizers and S-nitrosothiols resulting in the formation of other reactive species such as peroxynitrite, which is a potent oxidizing agent. These data show that NO release depends on pH and the medium, as well as on the laser energy applied to the system. Changes in the absorption spectrum were monitored as a function of light exposure.
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PMID:Nitric oxide release from the S-nitrosothiol zinc phthalocyanine complex by flash photolysis. 1271 77

Previously, we have shown that the lymphatic absorption of retinol is significantly decreased in rats fed a low zinc diet. This study was conducted to determine whether the absorption of beta-carotene also is altered in zinc-deficient male rats. The absorption of beta-carotene was estimated by determining the amount of retinol appearing in the mesenteric lymph during intraduodenal infusion of beta-carotene. One group of rats was fed the AIN-93G diet but low in zinc (LZ; 3 mg/kg) and the other was fed the same diet adequate in zinc (AZ; 30 mg/kg). The LZ and AZ rats were trained to meal feed equal amounts of the diets twice daily. At 6 weeks, each rat with lymph cannula was infused via an intraduodenal catheter at 3 ml/h for 8 h with a lipid emulsion containing 65.0 nM beta-carotene, 565.1 microM triolein, 27.8 kBq 14C-triolein (14C-OA), 72 mg albumin, and 396 microM Na-taurocholate in 24 ml PBS (pH 6.7). The lymphatic output of retinol over the 8-h period was significantly lower in LZ rats than in AZ rats. The absorption of 14C-OA also was significantly lower in LZ rats. No significant differences were observed between groups in intestinal beta-carotene 15,15'-dioxygenase, retinal reductase, and retinal oxidase activities. The findings demonstrate that low zinc intake or marginal zinc deficiency significantly lowers the absorption of beta-carotene as estimated by lymphatic retinol output. The results also indicate that the decrease in retinol output in LZ rats is not linked to defects in beta-carotene cleavage and subsequent conversion of retinal to retinol in the intestinal mucosa. This study suggests that zinc status is an important factor determining the intestinal absorption of beta-carotene and hence the nutritional status of vitamin A.
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PMID:Low zinc intake decreases the lymphatic output of retinol in rats infused intraduodenally with beta-carotene. 1274 42

Pseudallescheria boydii is an opportunistic filamentous fungus that causes serious infections in humans. Virulence attributes expressed by P. boydii are unknown. Conversely, peptidases are incriminated as virulence factors in several pathogenic fungi. Here we investigated the extracellular peptidase profile in P. boydii. After growth on Sabouraud for 7 days, mycelia of P. boydii were incubated for 20 h in PBS-glucose. The cell-free PBS-glucose supernatant was submitted to SDS-PAGE and 12 secretory polypeptides were observed. Two of these polypeptides (28 and 35 kD) presented proteolytic activity when BSA was used as a copolymerized substrate. The extracellular peptidases were most active in acidic pH (5.5) and fully inhibited by 1,10-phenanthroline, a zinc-metallopeptidase inhibitor. Other metallo-, cysteine, serine and aspartic proteolytic inhibitors did not significantly alter these activities. To confirm that these enzymes belong to the metallo-type peptidases, the apoenzymes were obtained by dialysis against chelating agents, and supplementation with different cations, especially Cu(2+) and Zn(2+), restored their activities. Except for gelatin, both metallopeptidases hydrolyzed various co-polymerized substrates, including human serum albumin, casein, hemoglobin and IgG. Additionally, the metallopeptidases were able to cleave different soluble proteinaceous substrates such as extracellular matrix components and sialylated proteins. All these hydrolyses were inhibited by 1,10-phenanthroline. Interestingly, Scedosporium apiospermum (the anamorph of P. boydii) produced a distinct extracellular peptidase profile. Collectively, our results demonstrated for the first time the expression of acidic extracellular metallopeptidases in P. boydii capable of degrading several proteinaceous compounds that could help the fungus to escape from natural human barriers and defenses.
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PMID:Pseudallescheria boydii releases metallopeptidases capable of cleaving several proteinaceous compounds. 1648 86

Myelin transcription factor 1 (Myt1) is a zinc-finger DNA binding protein that influences developing oligodendrocyte progenitor (OP) cell proliferation, differentiation, and myelin gene transcription in vitro. The potential of Myt1 to play a role in OP responses leading to remyelination was examined using murine hepatitis virus strain A59 (MHV) to induce spinal cord demyelination and potential relevance to human pathology was evaluated in multiple sclerosis (MS) lesions. In MHV-infected mice, the density of Myt1 expressing cells markedly increased in lesioned areas of spinal cord white matter. Myt1 expressing cells proliferated most extensively during active demyelination and subsequently accumulated to maximal levels during early remyelination. Cells with nuclear Myt1 immunoreactivity were mainly OP cells, identified by co-localization with platelet-derived growth factor alpha receptor, with additional phenotypes being either oligodendrocytes or neural stem cells, identified by CC1 antigen and Musashi1, respectively. The density of OP cells expressing Myt1 was significantly increased in white matter of MHV-infected mice during demyelination and early remyelination then as remyelination advanced the values returned to levels comparable to PBS-injected control mice. In MHV lesions, Myt1 was not expressed in astrocytes, lymphocytes, or macrophage/microglial cells. MS lesions demonstrated increased Myt1 expression in both the periplaque white matter adjacent to lesions and within early remyelinating lesions. These results suggesta potential role for Myt1 in the regeneration of oligodendrocyte lineage cells in response to demyelination.
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PMID:Myelin transcription factor 1 (Myt1) expression in demyelinated lesions of rodent and human CNS. 1733 Aug 75

Zinc is present in high concentration in many structures of the limbic circuitry, however the role of zinc as a neuromodulator in such synapses is still uncertain. In this work, we verified the effects of zinc chelation in an animal model of epileptogenesis induced by amygdala rapid kindling. The basolateral amygdala was electrically stimulated ten times per day for 2 days. A single stimulus was applied on the third day. Stimulated animals received injections of PBS or the zinc chelator diethildythiocarbamate acid (DEDTC) before each stimulus series. Animals were monitored with video-EEG and were perfused 3h after the last stimulus for subsequent neo-Timm and Fluoro-Jade B analysis. Zinc chelation decreased the duration of both behavioral seizures and electrical after-discharges, and also decreased the EEG spikes frequency, without changing the progression of behavioral seizure severity. These results indicate that the zinc ion may have a facilitatory role during kindling progression.
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PMID:Chelatable zinc modulates excitability and seizure duration in the amygdala rapid kindling model. 1837 19

Electrochemical oxidation of serotonin (SN) onto zinc oxide (ZnO)-coated glassy carbon electrode (GCE) results in the generation of redox mediators (RMs) that are strongly adsorbed on electrode surface. The electrochemical properties of zinc oxide-electrogenerated redox mediator (ZnO/RM) (inorganic/organic) hybrid film-coated electrode has been studied using cyclic voltammetry (CV). The scanning electron microscope (SEM), atomic force microscope (AFM), and electrochemical techniques proved the immobilization of ZnO/RM core/shell microparticles on the electrode surface. The GCE modified with ZnO/RM hybrid film showed two reversible redox peaks in acidic solution, and the redox peaks were found to be pH dependent with slopes of -62 and -60 mV/pH, which are very close to the Nernst behavior. The GCE/ZnO/RM-modified electrode exhibited excellent electrocatalytic activity toward the oxidations of ascorbic acid (AA), dopamine (DA), and uric acid (UA) in 0.1M phosphate buffer solution (PBS, pH 7.0). Indeed, ZnO/RM-coated GCE separated the anodic oxidation waves of DA, AA, and UA with well-defined peak separations in their mixture solution. Consequently, the GCE/ZnO/RMs were used for simultaneous detection of DA, AA, and UA in their mixture solution. Using CV, calibration curves for DA, AA, and UA were obtained over the range of 6.0 x 10(-6) to 9.6 x 10(-4)M, 1.5 x 10(-5) to 2.4 x 10(-4)M, and 5.0 x 10(-5) to 8 x 10(-4)M with correlation coefficients of 0.992, 0.991, and 0.989, respectively. Moreover, ZnO/RM-modified GCE had good stability and antifouling properties.
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PMID:Zinc oxide/redox mediator composite films-based sensor for electrochemical detection of important biomolecules. 1857 67

Vibrio anguillarum is one of the causative agents of vibriosis, a systemic disease of fish characterized by acute hemorrhagic septicemia. The extracellular zinc metalloprotease (EmpA) is a putative virulence factor involved in pathogenicity of V. anguillarum. Here we described the results of immunization against V. anguillarum with the plasmid expressing the mutated EmpA (m-EmpA7), which had no protelytic activity or cytotoxicity. In vitro protein expression of m-empA7 gene was determined by fluorescent microscopy and Western-blot after transfection of Chinese hamster ovary (CHO) and human embryonic kidney (HEK293T) cell lines. All three groups of fish immunized with a single intramuscular (i.m.) injection of different doses of the m-EmpA7 DNA vaccine showed significant serum antibody levels after vaccination, compared with the fish injected with the control eukaryotic expression vector pEGFP-N1 and PBS. In addition, fish receiving the DNA vaccine developed a protective response to a live V. anguillarum challenge 4 weeks post-inoculation, as demonstrated by increased survival of vaccinated fish over the control and by decreased histological alterations in vaccinated fish. Furthermore, humoral immune responses and protective effects were significantly increased at higher vaccine doses using a single intramuscularly injection route.
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PMID:Protection of Japanese flounder (Paralichthys olivaceus) against Vibrio anguillarum with a DNA vaccine containing the mutated zinc-metalloprotease gene. 1935 19

Heme oxygenase-1 (HO-1) has been shown to exert immunosuppressive, anti-inflammatory, anti-apoptotic and anti-proliferative effects. Its unique positive effects indicate that this enzyme might be a potential therapeutic target for psoriasis. To determine the effect of pharmacologic up-regulation of HO-1 on psoriasis, we generated a guinea pig model of psoriasiform skin lesions using propranolol induction. In this in vivo model, the 3-week propranolol challenge generated the psoriasiform pathological changes on the ears of guinea pigs. And then, guinea pigs were intraperitoneally injected with 5 mg/kg cobalt protoporphyrin (CoPP), a potent HO-1 inducer, 20 mg/kg zinc protoporphyrin, an inhibitor of HO-1, or PBS as controls, once a week from 9 weeks of age to 14 weeks old. CoPP induced notably HO-1 expression at both mRNA and protein levels. Moreover, CoPP treatment led to a significant reduction of the psoriasiform histopathological changes and remarkable amelioration of the psoriasiform skin lesions, compared with PBS treatment, with a concomitant reduction in proliferating cell nuclear antigen expression. Additionally, CoPP treatment resulted in a decreased TNF-alpha and significantly increased IL-10 release. Our results suggest that HO-1 induction therapy ameliorates the psoriasiform skin lesions by suppressing keratinocyte hyperproliferation and attenuating production of inflammatory responses.
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PMID:Therapeutic effects of heme oxygenase-1 on psoriasiform skin lesions in guinea pigs. 1941 14

Zinc has been shown to disturb the innate host defense response by interfering in the activation of neutrophils and subsequent oxidative burst, although the exact role of this metal, either as an activator or inhibitor, remains a matter of controversy among research groups. These apparent discrepancies may be due to experimental settings, through modification of zinc availability to neutrophils, or to inaccurate detections of reactive species. Thus, the main objective of the present study was to provide clarification on the role of zinc on the activation of human neutrophils and the subsequent oxidative burst. For that purpose, different detection methods and incubation media were used. The obtained results showed that phosphate buffers (PBS and HBSS) complex with zinc and interfere with the results obtained with this metal. By using Tris-G, it was clearly demonstrated that zinc, at low concentrations (5-12.5 microM), activates NADPH oxidase, mainly via protein kinase C, leading to the formation of superoxide radical (O(2*-). Higher concentrations of zinc results on a rapid dismutation of O2*- to oxygen and hydrogen peroxide, which in turn is used by myeloperoxidase to generate hypochlorous acid (HOCl).
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PMID:Zinc activates neutrophils' oxidative burst. 1976 Jan 8

Although several studies reported that cytotoxic effects of various nanoparticles are partially due to induction of oxidative stress, it is unclear how oxidative state of the cell per se could influence its sensitivity to cytotoxic nanoparticles. This is of clinical significance because certain pathological conditions such as inflammation is associated with elevated oxidative stress and this may alter sensitivity of cells and tissues to cytotoxic nanoparticles. Hence, this study investigated how initial exposure of BEAS-2B human bronchial epithelial cells to oxidative stress influences subsequent response to cytotoxic challenge with zinc oxide (ZnO) nanoparticles (approximately 10nm). Oxidative stress was induced by exposing BEAS-2B cells to 5 and 10 microM of H(2)O(2) for 45 min in PBS (with Ca(2+)). Subsequently, the H(2)O(2) solutions were washed off and the cells were exposed to varying concentrations (5-25 microg/ml) of ZnO nanoparticles in culture media for 24h, followed by cell viability assessment with the WST-8 assay. The results demonstrated that initial transient exposure of cells to oxidative stress accentuated cytotoxicity of ZnO nanoparticles. In the negative control unexposed to H(2)O(2), >99% of cells remained viable up to a ZnO nanoparticle concentration of 10 microg/ml, but displayed a steep decrease in viability above 10 microg/ml ZnO. By contrast, cells that were initially exposed to 5 and 10 microM of H(2)O(2), displayed a sharp drop in viability even at concentrations below 10 microg/ml ZnO. At 10 microg/ml ZnO, cells initially exposed to 10 microM H(2)O(2) displayed a viability of 40.6+/-2.0%, which is significantly lower than the corresponding values of 72.8+/-2.0% and 99.9+/-1.1% obtained for initial exposure to 5 microM H(2)O(2) and the negative control, respectively. Hence, initial exposure of BEAS-2B cells to oxidative stress sensitized their subsequent response to cytotoxic challenge with ZnO nanoparticles.
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PMID:Toxicity of zinc oxide (ZnO) nanoparticles on human bronchial epithelial cells (BEAS-2B) is accentuated by oxidative stress. 2041 30


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