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Zinc Protoporphyrin IX (zinc + protoporphyrin_ix)
Selected AbstractsFormation of zinc protoporphyrin IX in Parma-like ham without nitrate or nitriteANIMAL SCIENCE JOURNAL, Issue 2 2009Jun-ichi WAKAMATSU ABSTRACT Zinc protoporphyrin IX (ZPP) is a characteristic red pigment in meat products that are manufactured without the addition of a curing agent such as nitrate or nitrite. To examine the effects of impurities such as mineral components in sea salt on the formation of ZPP, we manufactured Parmatype dry-cured hams that were salted with refined salt or sea salt and examined the involvement of oxidation-reduction potential (ORP) in the formation of ZPP. The content of ZPP was increased drastically after 40 weeks. Microscopic observation showed strong fluorescence caused by ZPP muscle fiber after 40 weeks. Conversely, heme content varied considerably during processing. ORP increased during processing. However, there was no obvious difference between ham salted with refined salt and that salted with sea salt. Therefore, it was concluded that impurities in sea salt were not involved in the formation of ZPP. [source] Inhibition of heme oxygenase-1 by zinc protoporphyrin IX reduces tumor growth of LL/2 lung cancer in C57BL miceINTERNATIONAL JOURNAL OF CANCER, Issue 3 2007Kaeko Hirai Abstract Heme oxygenase (HO)-1 is a key player reducing cytotoxicity and enhancing protumoral effects of nitric oxide (NO). We examined zinc protoporphyrin (ZnPP) IX, an HO-1 inhibitor, to affect tumor growth of LL/2 mouse lung cancer cells. ZnPPIX reduced HO-1 expression and HO activity in LL/2 cells, whereas cobalt PPIX (CoPPIX), an HO-1 activator, increased both. LL/2 cells treated with sodium nitropurusside, an NO donor, showed growth inhibition dose-dependently, which was enhanced by ZnPPIX cotreatment, but was reduced by CoPPIX. In mice tumors, ZnPPIX decreased HO-1 expression. LL/2-tumors were found in 88% (7/8) vehicle-treated mice, whereas tumors were found in 38% (3/8) and 25% (2/8) mice treated with 5 and 20 ,g/mouse ZnPPIX, respectively (p = 0.0302). Tumor growth was inhibited dose-dependently by ZnPPIX. Vascular endothealial growth factor concentration in tumors was reduced by ZnPPIX (p = 0.0341). Microvessel density (MVD) in ZnPPIX-treated tumors was lower than that in vehicle-treated tumors (p = 0.0362). Apoptotic cell count in ZnPPIX-treated tumors was higher than that in vehicle-treated tumors (p = 0.0003). In contrast, CoPPIX treatment increased HO-1 expression, enhanced tumorigenicity and MVD and reduced apoptosis. From these findings, inhibition of HO-1 by ZnPPIX provides relevant antitumoral effects. © 2006 Wiley-Liss, Inc. [source] Porphyrin-based, light-activated antimicrobial materialsJOURNAL OF POLYMER SCIENCE (IN TWO SECTIONS), Issue 15 2003Jadranka Bozja Abstract New light-activated antimicrobial materials with a potentially wide range of possible uses in civilian settings were synthesized by the grafting of protoporphyrin IX and zinc protoporphyrin IX to nylon fibers. These fibers were shown to be active against Staphylococcus aureus at light exposures of 10,000 lux and greater and against Escherichia coli at 60,000 lux. They were ineffective against both strains in the absence of light. At 40,000 lux, these fibers showed increased antimicrobial activity against S. aureus with increasing exposure time. © 2003 Wiley Periodicals, Inc. J Polym Sci Part A: Polym Chem 41: 2297,2303, 2003 [source] Grafting of light-activated antimicrobial materials to nylon filmsJOURNAL OF POLYMER SCIENCE (IN TWO SECTIONS), Issue 1 2003Jennifer Sherrill Abstract Protoporphyrin IX and zinc protoporphyrin IX were grafted to the surface of nylon-6,6 films via an ethylene diamine bridge and a poly(acrylic acid) (PAA) scaffold. X-ray photoelectron spectroscopy showed that approximately 57% of the nylon surface was covered by PAA and approximately 6% of the carboxylic acid groups in PAA were grafted to the ethylene diamine derivative of protoporphyrin IX or its zinc salt. © 2002 Wiley Periodicals, Inc. J Polym Sci Part A: Polym Chem 41: 41,47, 2003 [source] Role of Vascular Heme Oxygenase in Reduced Myogenic Reactivity Following Chronic HypoxiaMICROCIRCULATION, Issue 2 2006JAY S. NAIK ABSTRACT Objective: Exposure to chronic hypoxia (CH) results in a persistent endothelium-dependent vascular smooth muscle hyperpolarization that diminishes vasoconstrictor reactivity. Experiments were performed to test the hypothesis that products of both cytochrome P450 epoxygenase (CYP) and heme oxygenase (HO) are required for the persistent diminished myogenic reactivity following CH. Methods: The authors examined myogenic responses of mesenteric arteries isolated from control and CH (48 h; PB = 380 mmHg) rats in the presence of a HO inhibitor (zinc protoporphyrin IX; ZnPPIX) or combined HO and CYP epoxygenase inhibition (sulfaphenazole). Arteries were isolated and cannulated and the vascular smooth muscle was loaded with the Ca2 + indicator Fura-2. Results: Control vessels maintained their internal diameter in response to step increases in intraluminal pressure, whereas arteries from CH animals passively distended. ZnPPIX augmented myogenic reactivity and [Ca2 +] in arteries from CH animals. Combined administration of sulfaphenazole and ZnPPIX did not have an additional effect compared to ZnPPIX alone. Myogenic reactivity in control vessels was not altered by ZnPPIX or ZnPPIX + sulfaphenazole. Conclusions: HO appears to play a role in regulating myogenic reactivity following CH. Furthermore, these data suggest that products of HO and CYP are both required for the observed attenuation in vasoreactivity following CH. [source] On the Role of Iron and one of its Chelating Agents in the Production of Protoporphyrin IX Generated by 5-Aminolevulinic Acid and its Hexyl Ester Derivative Tested on an Epidermal Equivalent of Human SkinPHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 4 2006Pascal Uehlinger ABSTRACT Photodynamic therapy (PDT) with 5-aminolevulinic acid (ALA) or its derivatives as precursors of protoporphyrin IX (PPIX) is routinely used in dermatology for the treatment of various pathologies. However, this methodology suffers to some extent from a limited efficacy. Therefore, the main goal of this study was to investigate the modulation and pharma-cokinetics of PPIX buildup after a 5 h incubation with ALA (1.5 mM) and one of its derivatives, the hexyl ester of ALA (h-ALA) (1.5 mM), on the human epidermal equivalent EpidexÔ. PPIX production was modulated with (L+) ascorbic acid iron (II) salt (LAI) or the iron (II)-specific chelating agent deferoxamine (DFO). PPIX fluorescence from the EpidexÔ layers was measured up to 150 h after the precursor administration using a microspectrofluorometer (,ex: 400 ± 20 nm; ,det: 635 nm). The maximum PPIX fluorescence intensity induced by h-ALA was about 1.7x larger than that induced by ALA. The addition of DFO resulted in a more than 50% increase in PPIX fluorescence for both precursors. The decay half life measured for PPIX fluorescence is 30 and 42.5 h, respectively, for ALA and h-ALA. These half lives are doubled when the samples contain DFO. In the samples with the highest fluorescence intensity, a modified fluorescence spectrum was observed after 10 h, with the emergence of a peak at 590 nm, which is attributed to zinc protoporphyrin IX (Zn PPIX). [source] Formation of zinc protoporphyrin IX in Parma-like ham without nitrate or nitriteANIMAL SCIENCE JOURNAL, Issue 2 2009Jun-ichi WAKAMATSU ABSTRACT Zinc protoporphyrin IX (ZPP) is a characteristic red pigment in meat products that are manufactured without the addition of a curing agent such as nitrate or nitrite. To examine the effects of impurities such as mineral components in sea salt on the formation of ZPP, we manufactured Parmatype dry-cured hams that were salted with refined salt or sea salt and examined the involvement of oxidation-reduction potential (ORP) in the formation of ZPP. The content of ZPP was increased drastically after 40 weeks. Microscopic observation showed strong fluorescence caused by ZPP muscle fiber after 40 weeks. Conversely, heme content varied considerably during processing. ORP increased during processing. However, there was no obvious difference between ham salted with refined salt and that salted with sea salt. Therefore, it was concluded that impurities in sea salt were not involved in the formation of ZPP. [source] Cilostazol enhances apoptosis of synovial cells from rheumatoid arthritis patients with inhibition of cytokine formation via Nrf2-linked heme oxygenase 1 inductionARTHRITIS & RHEUMATISM, Issue 3 2010So Youn Park Objective To assess the effects of cilostazol in inhibiting proliferation and enhancing apoptosis in synovial cells from patients with rheumatoid arthritis (RA). Methods Synovial cell proliferation was measured by MTT assay. The expression of NF-,B, I,B,, Bcl-2, Bax, heme oxygenase 1 (HO-1), and Nrf2 was determined by Western blotting. Results Cilostazol suppressed synovial cell proliferation by arresting the G2/M phases of the cell cycle, and this was reversed by KT5720, an inhibitor of protein kinase A. Cilostazol increased the number of TUNEL-positive cells, with increased cytochrome c release and apoptosis-inducing factor translocation as well as increased caspase 3 activation. Cilostazol (10 ,M) and cobalt protoporphyrin IX (CoPP) increased HO-1 messenger RNA and protein expression. These effects were suppressed by zinc protoporphyrin IX (ZnPP), an HO-1 inhibitor. Cilostazol and CoPP significantly increased I,B, in the cytosol and decreased NF-,B p65 expression in the nucleus. Increased expression of tumor necrosis factor , (TNF,), interleukin-1, (IL-1,), and IL-6 induced by lipopolysaccharide was attenuated by cilostazol and CoPP, and this was reversed by ZnPP. In mice with collagen-induced arthritis treated with cilostazol (10 and 30 mg/kg/day), paw thickness was decreased with increased apoptotic cells in the joints. In synovial cells transfected with small interfering RNA (siRNA) targeting HO-1, cilostazol did not suppress expression of TNF,, IL-1,, and IL-6, in contrast to findings with negative control cells. Cilostazol- and CoPP-induced HO-1 expression was diminished in cells transfected with Nrf2 siRNA. Conclusion Cilostazol suppressed proliferation of synovial cells from RA patients by enhancing apoptosis, and also inhibited cytokine production via mediation of cAMP-dependent protein kinase activation,coupled Nrf2-linked HO-1 expression. [source] Brazilin and the extract from Caesalpinia sappan L. protect oxidative injury through the expression of heme oxygenase-1BIOFACTORS, Issue 3 2007Byung-Min Choi Abstract In this study, we examined the protective effects of Caesalpinia sappan L. and its major component, brazilin, against tert-butylhydroperoxide (t-BHP)-induced cell death in House Ear Institute-Organ of Corti 1 (HEI-OC1) cells. We found that the extract of C. sappan L. and brazilin induced antioxidant response element (ARE)-luciferase activity and heme oxygenase-1 (HO-1) expression in a concentration-dependent manner. The inductive effect of brazilin was more potent than the extract of C. sappan L. and the expression of HO-1 reached a peak at 12 h after brazilin treatment. The extract and brazilin protected the cells against t-BHP-induced cell death. Their protective effects were abrogated by zinc protoporphyrin IX (ZnPP IX), a HO inhibitor. These results demonstrate that the extract of C. sappan L. and brazilin induce the expression of HO-1 and the enzyme diminishes t-BHP-induced cell death in HEI-OC1 cells. [source] | |||||||||||||