Dentifrícios branqueadores contendo Blue covarine: revisão de literatura / Bleaching dentifrices containing "Blue covarine" literature review

Introdução: O efeito branqueador dos dentifrícios contendo Blue covarine é fundamentado no seu mecanismo de ação, caracterizado pela sua deposição na superfície dentária, alterando a percepção da cor. Objetivo: Revisar a literatura e buscar evidência científica sobre o efeito branqueador do Blue Covarine em tecidos mineralizados e materiais restauradores estéticos. Materiais e métodos: Para a revisão da literatura foram feitas buscas nas bases de dados PubMed, LILACS, BBO, SciELO e MEDLINE para identificar estudos clínicos e laboratoriais que avaliassem a ação branqueadora do agente óptico Blue covarine. Como estratégia de busca foram utilizados os descritores "Blue covarine", "Blue covarine e pasta de dentes", "Blue covarine and toothpaste", "Blue covarine e dentifrícios", "Blue covarine and dentifrices", "Blue covarine e dentifrícios branqueadores", "Blue covarine and whitening dentifrices", "Blue covarine e dentifrícios clareadores", "Blue covarine and bleaching dentifrices", "Blue covarine e pasta de dentes branqueadoras", "Blue covarine and whitening toothpaste", "Blue covarine e pasta de dentes clareadoras", "Blue covarine and bleaching toothpaste". Resultados: Dois pesquisadores selecionaram e analisaram criticamente 31 artigos, sendo 2 revisões da literatura, 4 estudos clínicos e 25 estudos laboratoriais. Divergências quanto ao desenho de estudo, métodos, amostra, critérios clínicos e parâmetros laboratoriais foram observados, além de conflitos de interesse. Conclusão: O Blue Covarine presente nos dentifrícios branqueadores parece ser efetivo na promoção do branqueamento dentário apenas quando associado aos agentes abrasivos presentes nas formulações, evidenciando que ensaios clínicos e laboratoriais, com metodologias semelhantes, são necessários para se obter evidência científica conclusiva sobre o efeito deste agente branqueador.(AU)

Introduction: The whitening effect of dentifrices containing Blue Covarine is based on its mechanism of action, characterized by its deposition on the tooth surface, altering the perception of color. Objective: To review the literature and seek scientific evidence on the whitening effect of Blue Covarine on mineralized tissues and aesthetic restorative materials. Materials and methods: For the literature review, searches were carried out in the PubMed, LILACS, BBO, SciELO and MEDLINE databases, in order to identify clinical and laboratory studies that evaluated the whitening action of the optical agent Blue Covarine. As a search strategy, the descriptors "Blue Covarine", "Blue Covarine and toothpaste", "Blue Covarine and dentifrices", "Blue Covarine and whitening dentifrices", "Blue Covarine and bleaching dentifrices", "Blue Covarine and whitening toothpaste", "Blue Covarine and bleaching toothpaste". Results: Two researchers selected and critically analyzed 31 articles, including 2 literature reviews, 4 clinical studies and 25 laboratory studies. Differences in study design, methods, sample, clinical criteria and laboratory parameters were observed, in addition to conflicts of interest. Conclusion: Blue Covarine present in whitening dentifrices seems to be effective in promoting dental whitening only when associated with abrasive agents present in the formulations, showing that clinical and laboratory tests, with similar methodologies, are necessary to obtain conclusive scientific evidence on the effect of this bleaching agent.(AU)

Whitening toothpaste containing activated charcoal, blue covarine, hydrogen peroxide or microbeads: which one is the most effective?

Abstract The efficacy of whitening toothpastes is questionable and controversial. Clinicians, patients and researchers have expressed concern with whitening toothpastes due to the risk of wearing the dental structure and the potential for disappointment if the advertised cosmetic results are not achieved. Objective: This study compared the whitening performance of toothpastes with different whitening technologies after initial and continued use. Material and Methods: Ninety bovine incisors were stained using a concentrated solution of black tea. They were randomly distributed into 6 groups, according to the toothpaste whitening technology: activated charcoal (B&W), blue covarine (WAD), hydrogen peroxide (LWA), microbeads (Oral B 3D White Perfection - 3DW) and optimized abrasives (XW4D). They were compared to a traditional toothpaste without a whitening agent (TA - control). Specimens underwent a brushing machine with controlled pressure, time and temperature. A calibrated examiner measured the color using a VITA-Classical scale before the first brushing cycle (T0), after the first brushing cycle (TI), and after a brushing cycle that simulates continuous use (TCU). Whitening performance was evaluated by the difference of shades (ΔSGU) between T0-TI and T0-TCU timepoints, using the Kruskal-Wallis and Dunn's non-parametric test. The Wilcoxon test was used to evaluate the cumulative effect (α=0.05). Results: Statistically significant differences were observed between toothpastes in both TI and TCU (p<0.05). The time of use also had a significant effect (p<0.05). Conclusion: Only WAD and 3DW showed whitening performance after the first use (TI). The greatest whitening performance after continuous use was obtained by WAD, followed by LWA and 3DW. The use of conventional toothpaste (TA) promotes no tooth whitening. Clinical relevance: Microbead abrasives (3DW) and blue covarine (WAD) were the active technology tested that presented the best global tooth whitening performance.

Does a toothpaste containing blue covarine have any effect on bleached teeth? An in vitro, randomized and blinded study

Abstract The objective of this study was to analyze the effect of bleaching toothpastes, both conventional and those containing the new whitening agent Blue Covarine, on teeth previously bleached by conventional techniques (in-office and at-home). Squared bovine enamel/dentin blocks (6.0 x 6.0 x 2.0 mm) were randomly distributed in 6 groups (n = 15), according to the technique used to bleach them (in-office: HP35%; at-home: PC10%) and the type of bleaching toothpaste (none: control; Blue Covarine containing: BC; and without Blue Covarine: NBC). Experimental groups denominated HP35%, HP35%BC and HP35%NBC received in-office tooth bleaching before toothbrushing, and groups PC10%, PC10%BC and PC10%NBC were subjected to at-home tooth bleaching prior to toothbrushing. After bleaching treatment, groups HP35%BC, PC10%BC, HP35%NBC and PC10%NBC underwent daily tooth brushing in a brushing machine for 3 minutes (150 strokes/min, with a load of 375 g). Tooth color alteration was measured by reflectance spectroscopy (Vita EasyShade, Vident, Brea, CA, USA) at: T0 (baseline) - after in-office or at-home bleaching treatment; T1 - immediately after tooth brushing; T2 - 7 days and T3 - 14 days after tooth brushing. Data was analyzed by repeated measures mixed ANOVA and the Bonferroni post hoc test, with a significance level of 5%. Statistically significant differences were found between different experimental groups, evaluation times and for the interaction between them (p < 0.001). Tooth brushing using either bleaching toothpaste (conventional or with Blue Covarine) showed no color alteration on teeth previously bleached by in-office and at-home tooth bleaching. The use of bleaching toothpastes on previously bleached teeth did not produce a color alteration.

Can a bleaching toothpaste containing Blue Covarine demonstrate the same bleaching as conventional techniques? An in vitro, randomized and blinded study

ABSTRACT Objective The purpose of this in vitro study was to compare the efficacy of a bleaching toothpaste containing Blue Covarine vs. conventional tooth bleaching techniques using peroxides (both in-office and at-home). Material and Methods Samples were randomly distributed into five experimental groups (n=15): C - Control; BC – Bleaching toothpaste containing Blue Covarine; WBC – Bleaching toothpaste without Blue Covarine; HP35 - In-office bleaching using 35% hydrogen peroxide; and CP10 – At-home bleaching with 10% carbamide peroxide. The dental bleaching efficacy was determined by the color difference (ΔE), luminosity (ΔL), green-red axis (Δa), and blue-yellow axis (Δb). The CIELab coordinates were recorded with reflectance spectroscopy at different times: T0 - baseline, T1 – immediately after bleaching, T2 - 7 days, T3 - 14 days, and T4 - 21 days after the end of treatments. Data were analyzed by a repeated measures mixed ANOVA and post hoc Bonferroni test, with a significance level of 5%. Results No significant differences were found between the treatment groups C, BC, and WBC. The groups HP35 and CP10 showed significantly higher whitening efficacy than groups C, BC, and WBC. Conclusions There were no significant differences in the whitening efficacy between a Blue Covarine containing toothpaste, a standard whitening toothpaste, and a control. Neither of the whitening toothpastes tested were as effective as in-office or at-home bleaching treatments.

Effect of quercetin on the production of nitric oxide in murine macrophages stimulated with lipopolysaccharide from Prevotella intermedia

PURPOSE: Nitric oxide (NO) is a short-lived bioactive molecule that is known to play an important role in the pathogenesis of periodontal disease. In the current study, we investigated the effect of the flavonoid quercetin on the production of NO in murine macrophages activated with lipopolysaccharide (LPS) from Prevotella intermedia, a pathogen related to inflammatory periodontal disease, and tried to elucidate the underlying mechanisms of action. METHODS: LPS was isolated from P. intermedia ATCC 25611 cells by the standard hot phenol-water method. The concentration of NO in cell culture supernatants was determined by measuring the accumulation of nitrite. Inducible NO synthase (iNOS) and heme oxygenase-1 (HO-1) protein expression, phosphorylation of c-Jun N-terminal kinase (JNK) and p38, inhibitory kappaB (IkappaB)-alpha degradation, and signal transducer and activator of transcription 1 (STAT1) phosphorylation were analyzed via immunoblotting. RESULTS: Quercetin significantly attenuated iNOS-derived NO production in RAW246.7 cells activated by P. intermedia LPS. In addition, quercetin induced HO-1 protein expression in cells activated with P. intermedia LPS. Tin protoporphyrin IX (SnPP), a competitive inhibitor of HO-1, abolished the inhibitory effect of quercetin on LPS-induced NO production. Quercetin did not affect the phosphorylation of JNK and p38 induced by P. intermedia LPS. The degradation of IkappaB-alpha induced by P. intermedia LPS was inhibited when the cells were treated with quercetin. Quercetin also inhibited LPS-induced STAT1 signaling. CONCLUSIONS: Quercetin significantly inhibits iNOS-derived NO production in murine macrophages activated by P. intermedia LPS via anti-inflammatory HO-1 induction and inhibition of the nuclear factor-kappaB and STAT1 signaling pathways. Our study suggests that quercetin may contribute to the modulation of host-destructive responses mediated by NO and appears to have potential as a novel therapeutic agent for treating inflammatory periodontal disease.

Preparation of a zinc porphyrinated nanofibrous membrane and its ammonia sensing property / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To prepare a zinc porphyrinated polyimide nanofibrous membrane for rapid detection of trace amount of ammonia.</p><p><b>METHODS</b>Zinc porphyrin chromophore was copolymerized into polyimide backbones and the according nanofibrous membrane was prepared by electrospinning technique. Ammonia detection was achieved by recording the color and spectral changes of the membrane before and after exposing to the target gas. The sensitivity, selectivity and detection limit of prepared membrane were further studied.</p><p><b>RESULTS</b>The obtained nanofibrous membrane preserved typical photophysical properties of zinc porphyrin chromophores. When exposed to ammonia, a dual chromo and spectrum responses of the nanofibrous membrane were observed. The binding affinity constant and the detection limit of zinc porphyrinated polyimide nanofibrous membrane calculated from surface plasmon resonance (SPR) analysis and UV-vis were 3.33 X10³ L/mol and 3.13 mg/m³, respectively.</p><p><b>CONCLUSION</b>The membrane prepared in this study exhibits good sensitivity, selectivity and reproducibility towards ammonia detection.</p>

Possible in vivo mechanisms involved in photodynamic therapy using tetrapyrrolic macrocycles

Photodynamic therapy (PDT) mediated by oxidative stress causes direct tumor cell damage as well as microvascular injury. To improve this treatment new photosensitizers are being synthesized and tested. We evaluated the effects of PDT with 5,10,15,20-tetrakis(4-methoxyphenyl)-porphyrin (TMPP) and its zinc complex (ZnTMPP) on tumor levels of malondialdehyde (MDA), reduced glutathione (GSH) and cytokines, and on the activity of caspase-3 and metalloproteases (MMP-2 and -9) and attempted to correlate them with the histological alterations of tumors in 3-month-old male Wistar rats, 180 ± 20 g, bearing Walker 256 carcinosarcoma. Rats were randomly divided into five groups: group 1, ZnTMPP+irradiation (IR) 10 mg/kg body weight; group 2, TMPP+IR 10 mg/kg body weight; group 3, 5-aminolevulinic acid (5-ALA+IR) 250 mg/kg body weight; group 4, control, no treatment; group 5, only IR. The tumors were irradiated for 15 min with red light (100 J/cm², 10 kHz, 685 nm) 24 h after drug administration. Tumor tissue levels of MDA (1.1 ± 0.7 in ZnTMPP vs 0.1 ± 0.04 nmol/mg protein in control) and TNF-α (43.5 ± 31.2 in ZnTMPP vs 17.3 ± 1.2 pg/mg protein in control) were significantly higher in treated tumors than in controls. Higher caspase-3 activity (1.9 ± 0.9 in TMPP vs 1.1 ± 0.6 OD/mg protein in control) as well as the activation of MMP-2 (P < 0.05) were also observed in tumors. These parameters were correlated (Spearman correlation, P < 0.05) with the histological alterations. These results suggest that PDT activates the innate immune system and that the effects of PDT with TMPP and ZnTMPP are mediated by reactive oxygen species, which induce cell membrane damage and apoptosis.

Aprotinin Inhibits Vascular Smooth Muscle Cell Inflammation and Proliferation via Induction of HO-1

Aprotinin is used clinically in cardiopulmonary bypass surgery to reduce transfusion requirements and the inflammatory response. The mechanism of action for the anti-inflammatory effects of aprotinin is still unclear. We examined our hypothesis whether inhibitory effects of aprotinin on cytokine-induced inducible nitric oxide synthase (iNOS) expression (IL-1beta plus TNF-alpha), reactive oxygen species (ROS) generation, and vascular smooth muscle cell (VSMC) proliferation were due to HO-1 induction in rat VSMCs. Aprotinin induced HO-1 protein expression in a dose-dependent manner, which was potentiated during inflammatory condition. Aprotinin reduced cytokine mixture (CM)-induced iNOS expression in a dose dependent manner. Furthermore, aprotinin reduced CM-induced ROS generation, cell proliferation, and phosphorylation of JNK but not of P38 and ERK1/2 kinases. Aprotinin effects were reversed by pre-treatment with the HO-1 inhibitor, tin protoporphyrin IX (SnPPIX). HO-1 is therefore closely involved in inflammatory-stimulated VSMC proliferation through the regulation of ROS generation and JNK phosphorylation. Our results suggest a new molecular basis for aprotinin anti-inflammatory properties.

Heme Oxygenase-1 Induced by Aprotinin Inhibits Vascular Smooth Muscle Cell Proliferation Through Cell Cycle Arrest in Hypertensive Rats

Spontaneous hypertensive rats (SHR) are an established model of genetic hypertension. Vascular smooth muscle cells (VSMC) from SHR proliferate faster than those of control rats (Wistar-Kyoto rats; WKY). We tested the hypothesis that induction of heme oxygenase (HO)-1 induced by aprotinin inhibits VSMC proliferation through cell cycle arrest in hypertensive rats. Aprotinin treatment inhibited VSMC proliferation in SHR more than in normotensive rats. These inhibitory effects were associated with cell cycle arrest in the G1 phase. Tin protoporphyrin IX (SnPPIX) reversed the anti-proliferative effect of aprotinin in VSMC from SHR. The level of cyclin D was higher in VSMC of SHR than those of WKY. Aprotinin treatment downregulated the cell cycle regulator, cyclin D, but upregulated the cyclin-dependent kinase inhibitor, p21, in VSMC of SHR. Aprotinin induced HO-1 in VSMC of SHR, but not in those of control rats. Furthermore, aprotinin-induced HO-1 inhibited VSMC proliferation of SHR. Consistently, VSMC proliferation in SHR was significantly inhibited by transfection with the HO-1 gene. These results indicate that induction of HO-1 by aprotinin inhibits VSMC proliferation through cell cycle arrest in hypertensive rats.

Catalytic metalloporphyrin protects against paraquat neurotoxicity in vivo / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To examine the neuroprotective effects of a novel manganese porphyrin, manganese (III) meso-tetrakis (N,N'-diethylimidazolium-2-yl) porphyrin (MnTDM), in the mouse model of Parkinson's disease (PD) induced by paraquat (PQ).</p><p><b>METHODS</b>Male C57BL/6 mice were subcutaneously injected with either saline or PQ at 2-day intervals for a total of 10 doses, MnTDM was subcutaneously injected with the PQ 2 h before treatment. Performance on the pole and swim test were measured 7 days after the last injection and animals were sacrificed one day later. Levels of dopamine (DA) and its metabolites in the striatum were measured by high-performance liquid chromatography with an electrochemical detector (HPLC-ECD). Thiobarbituric acid (TBA) method was used to assay the lipid peroxidation product, malondialdehyde (MDA), and the number of tyrosine hydroxylase (TH) positive neurons was estimated using immunohistochemistry.</p><p><b>RESULTS</b>Pretreatment with MnTDM significantly attenuated PQ-impaired behavioral performance, depleted dopamine content in striata, increased MDA, and dopaminergic neuron loss in the substantia nigra.</p><p><b>CONCLUSIONS</b>Oxidative stress plays an important role in PQ-induced neurotoxicity which can be potentially prevented by manganese porphyrin. These findings also propose a possible therapeutical strategy for neurodegenerative disorders associated with oxidative stress such as PD.</p>

Microbial demetallization of crude oil using Aspergilus sp.: vanadium oxide octaethyl porphyrin [VOOEP] as a model of metallic petroporphyrins

An isolate from polluted soil identified as Aspergillus sp. MS-100 was able to consume vanadium oxide octaethyl porphyrin as a model for protoporphyrins in crude oil. The isolate degrades about 55% of vanadium oxide octaethyl porphyrin [VOOEP] under optimum conditions during 7 days. The release of more than 0.96 mgL-1 of free vanadium into the aqueous phase was confirmed using atomic absorption. By using the Taguchi experimental design method, the optimum values of pH, temperature and initial concentration of VOOEP were determined as 5.5, 30C, and 20 mg/l, respectively. The reduction of VOOEP in the culture medium was accelerated by Ag+ and inhibited by Zn2+ and EDTA. The Sn2+ and Pb2+ ions showed a stimulatory effect at 0.1 mM and an inhibitory effect at 1 mM

Effects of Heme Oxygenase-1 Inducer and Inhibitor on Experimental Autoimmune Uveoretinitis

PURPOSE: Experimental autoimmune uveoretinitis (EAU) is an animal model of posterior uveitis and heme oxygenase-1 (HO-1) is a well-known anti-oxidant factor. However, there is no report a protective role of HO-1 on EAU in vivo. To verify that HO-1 is induced in EAU by interphotoreceptor retinoid-binding protein (IRBP), that an HO-1 inducers ameliorates the associated inflammation, and that an HO-1 inhibitor exacerbates this inflammation. METHODS: Forty four Lewis rats were given either 40 mol/kg hemin or 40 mol/kg SnPP (tin protoporphyrin IX) by intraperitoneal injection and twenty two uveitis control rats were injected with 0.5 mL of saline once daily 5-20 days after IRBP immunization inducing EAU. Three normal control rats were used for Western blotting and ELISA assay of HO-1. The clinical uveitis signs of inflammation were scored in the three groups from 0 to 4 on alternate three days. To confirm the clinical results, histological and immunohistochemical stain of HO-1 were performed on the day of peak inflammation and Western blotting and ELISA assay of HO-1 were performed on 6th, 12th and 18th day after IRBP immunization. RESULTS: Hemin, an inducer of HO-1, ameliorated the clinical signs of EAU. In contrast, SnPP-treated rats show that the severity of the clinical sign were exacerbated at the peak period of the disease. These results are roughly compatible with histological, immunoblotting, and immunohistochemical evaluations and an ELISA assay of HO-1. CONCLUSIONS: We suggest that HO-1 plays an important protective role in EAU.

Roles of heme oxygenase-1 in curcumin-induced growth inhibition in rat smooth muscle cells

In vascular smooth muscle cells (VSMCs), induction of the heme oxygenase-1 (HO-1) confers vascular protection against cellular proliferation mainly via its up-regulation of the cyclin-dependent kinase inhibitor p21(WAF1/CIP1) that is involved in negative regulation of cellular proliferation. In the present study, we investigated whether the phytochemical curcumin and its metabolite tetrahydrocurcumin could induce HO-1 expression and growth inhibition in rat VSMCs and, if so, whether their antiproliferative effect could be mediated via HO-1 expression. At non-toxic concentrations, curcumin possessing two Michael-reaction acceptors induced HO-1 expression by activating antioxidant response element (ARE) through translocation of the nuclear transcription factor E2-related factor-2 (Nrf2) into the nucleus and also inhibited VSMC growth triggered by 5% FBS in a dose-dependent manner. In contrast, tetrahydrocurcumin lacking Michael-reaction acceptor showed no effect on HO-1 expression, ARE activation and VSMC growth inhibition. The antiproliferative effect of curcumin in VSMCs was accompanied by the increased expression of p21(WAF1/CIP1). Inhibition of VSMC growth and expression of p21(WAF1/CIP1) by curcumin were partially, but not completely, abolished when the cells were co- incubated with the HO inhibitor tin protoporphyrin. In human aortic smooth muscle cells (HASMCs), curcumin also inhibited growth triggered by TNF-alpha and increased p21(WAF1/CIP1) expression via HO-1-dependent manner. Our findings suggest that curcumin has an ability to induce HO-1 expression, presumably through Nrf2-dependent ARE activation, in rat VSMCs and HASMCs, and provide evidence that the antiproliferative effect of curcumin is considerably linked to its ability to induce HO-1 expression.

Radiotherapy versus radiotherapy enhanced by vinorelbine in locally advanced non-small cell lung cancer

Experimental studies have shown that vinorelbine is a powerful radiosensitizer in vitro.In this study, 173 patients with inoperable non-small cell lung cancer, Stage III, were entered into arandomized trial comparing radiotherapy only [RT][45 Gy/15 fractions/3 weeks][arm A] versus RT and a dailylow dose of vinorelbine [4 mg/m2][arm B].An overall response rate of 58.9% was observed in arm A and%0.6%in arm B, respectively. Nodifferences in the pattern of relapse were noted between the two treatment groups. Median time to progression was10.6 months for arm A and 14.2 months for arm B. Median survivals were 10.3 months and 9.97 months,respectively. Toxicity was acceptable and no treatment-related death occurred in either treatment schedule. In thisstudy no significant advantage of the combined treatment over radiation therapy only was found.The encouraging, results achieved in some trials together with the intractability of the disease suggestthat further effects efforts should be made to optimize clinical trial protocols, perhaps by reviewing theradiobiological and pharmacological basis of the combined treatment.Non-small cell lung cancer, vinorelhine, Radiotherapy, Radiosensitizer

Effect of photodynamic therapy with metalloporphyrin compound on human prostate cancer PC-3 cells in vitro / 中华男科学杂志

<p><b>OBJECTIVE</b>To investigate the effect of the photodynamic therapy (PDT) with the new water-soluble metalloporphyrin compound on human prostate cancer PC-3 cells in vitro and the anticancer mechanism of PDT.</p><p><b>METHODS</b>The new water-soluble manganese, 5,10,15, 20-tetra (N-methyl4-pyridyl) porphinato (2-) tetraiodide salt, was synthesized. The PC-3 cells were treated with the compound of serial concentrations(0, 0.1, 1, 1.0 micromol/L) followed by irradiation of different dosages of visible light. The techniques of MTT and Annexin-V/propidium iodide double-labeled flow cytometry (FCM) were applied to measuring the inhibitory effect of the compound on the growth activity and apoptosis of the cells.</p><p><b>RESULTS</b>When the metalloporphyrin compound concentration was within 10 micromol/L and the irradiation time was within 30 min, the water-soluble metalloporphyrin compound had a significant inhibitory effect on the proliferation of PC-3 cells and induced PC-3 cell apoptosis, and the effects depended greatly on metalloporphyrin concentration and illumination dosages. Higher concentrations and dosages induced the death of the majority of PC-3 cells.</p><p><b>CONCLUSION</b>The PDT of the water-soluble metalloporphyrin compound followed by light irradiation has a distinctive killing effect on PC-3 cells in vitro, and the rates of proliferation inhibition and cell apoptosis are correlated with metalloporphyrin concentration and the dosages of light irradiation. The results suggest that the mechanism of metalloporphyrin PDT may be involved with the induction of apoptosis in human prostate cancer cells.</p>

Sequence-dependent cleavage of HBV DNA by combining with triple helix-forming oligodeoxyribonucleotides modified with manganese porphyrin in vitro / 中华实验和临床病毒学杂志

<p><b>OBJECTIVE</b>To observe the ability of triple helix-forming oligonucleotides (TFO) modified with manganese porphyrin to combine with and cleave HBV DNA fractions.</p><p><b>METHODS</b>The ends of TFO were modified with manganese porphyrin and acridine; At 37 degrees C and pH 7.4 condition in vitro, TFO modified with manganese porphyrin and acridine were bound with 32P labeled HBV DNA fragments, the affinity and specificity binding to target sequence were tested by electrophoretic mobility shift and DNase 1 footprinting assays, the ability to cleave HBV DNA fractions was observed with cleavage experiments.</p><p><b>RESULTS</b>TFO modified with manganese porphyrin and acridine could bind to target sequence in a sequence-dependent manner with Kd values of 3.5 x 10(-7) mol/L and a relative affinity of 0.008. In the presence of KHSO5, TFO modified with manganese porphyrin and acridine could cleave target sequence in the region forming triple DNA.</p><p><b>CONCLUSION</b>In the presence of KHSO5, TFO modified with manganese porphyrin and acridine could cleave target HBV-DNA in sequence-dependent manner.</p>

Synthesis and anti-active oxygen properties of water-soluble metal porphyrins / 药学学报

<p><b>AIM</b>To synthesize four water-soluble metal porphyrins [5, 10, 15, 20-tetra[4-(4'-pyridine-1) butyloxy phenyl] metalloporphyrins bromide, metal = Zn (I), Cu (II), Mn (III) and Co (IV)] as analogous enzyme having two anti-active oxygen functions.</p><p><b>METHODS</b>The first function, scavenging O2-, has been proved by using riboflavine-methionine photoreduction methods. The second function, scavenging H2O2, has been demonstrated by using the oxidating Vit C. The third function, scavenging HO*, has been demonstrated by using Fenton reaction. The complexes were measured by the mice liver homogenate technique of mice.</p><p><b>RESULTS</b>Four model compounds could scavenge O2- in the concentration range of 1.0 x 10(-5) - 1.0 x 10(-6) mol x L(-1), decompose H2O2 in the concentration of 1.5 x 10(-6) - 1.0 x 10(-6) mol x L(-1), scavenge HO* in the concentration of 2.0 x 10(-8) - 1.0 x 10(-8) mol x L(-1). All showed that they had obvious action of decreasing the lipid peroxidation in the concentration of 1.0 x 10(-7) mol x L(-1).</p><p><b>CONCLUSION</b>All above-mentioned complexes were considered to be qualified analogous enzymes of anti-active oxygen.</p>

Role of reactive oxygen species in extracellular signal-regulated protein kinase phosphorylation and 6-hydroxydopamine cytotoxicity.

A number of reports indicate the potential for redox signalling via extracellular signal-regulated protein kinases (ERK) during neuronal injury. We have previously found that sustained ERK activation contributes to toxicity elicited by 6-hydroxydopamine (6-OHDA) in the B65 neuronal cell line. To determine whether reactive oxygen species (ROS) play a role in mediating ERK activation and 6-OHDA toxicity, we examined the effects of catalase, superoxide dismutase (SOD1), and metalloporphyrin antioxidants ('SOD mimetics') on 6-OHDA-treated cells. We found that catalase and metalloporphyrin antioxidants not only conferred protection against 6-OHDA but also inhibited development of sustained ERK phosphorylation in both differentiated and undifferentiated B65 cells. However, exogenously added SOD1 and heat-inactivated catalase had no effect on either toxicity or sustained ERK phosphorylation. This correlation between antioxidant protection and inhibition of 6-OHDA-induced sustained ERK phosphorylation suggests that redox regulation of ERK signalling cascades may contribute to neuronal toxicity.

Combination and cleavage of HBV DNA fragments by triple helix-forming oligonucleotides modified with manganese porphyrin in vitro / 中华医学杂志(英文版)

<p><b>OBJECTIVE</b>To observe the ability of triple helix-forming oligonucleotides (TFOs) modified with manganese porphyrin to combine with and cleave HBV DNA fractions.</p><p><b>METHODS</b>TFO were modified with manganese porphyrin and acridines, and then reacted with the (32)P labeled HBV DNA fragments at 37 degrees C in vitro (pH 7.4). Electrophoretic mobility shift assays and DNase I footprinting tests were used to show the affinity and specificity of TFO to bind to target sequences. The ability of TFO to cleave HBV DNA fragments was tested by cleavage experiments.</p><p><b>RESULTS</b>TFO modified with manganese porphyrin and acridine could bind to the target sequence in a sequence-dependent manner, with a Kd value of 3.5 x 10(-7) mol/L and a relative affinity of 0.008. In the presence of potassium monopersulfate (KHSO(5)), TFO modified with manganese porphyrin and acridine could cleave the target sequence where the triplex DNA was formed.</p><p><b>CONCLUSION</b>In the presence of KHSO(5), TFO modified with manganese porphyrin and acridine could bind and cleave the target HBV-DNA in a sequence-dependent manner.</p>

The Significance of Perfusion Defect at Myocardial Perfusion MR Imaging in a Cat Model of Acute Reperfused Myocardial Infarction

OBJECTIVE: To determine whether the size of a perfusion defect seen at myocardial perfusion MR imaging represents the extent of irreversibly damaged myocardium in acute reperfused myocardial infarction. MATERIALS AND METHODS: In nine cats, reperfused myocardial infarction was induced by occlusion of the left anterior descending coronary artery for 90 minutes and subsequent reperfusion for 90 minutes. At single-slice myocardial perfusion MR imaging at the midventricular level using a turbo-FLASH sequence, 60 short-axis images were sequentially obtained with every heart beat after bolus injection of gadomer-17. The size of the perfusion defect was measured and compared with both the corresponding unstained area seen at triphenyl tetrazolium chloride (TTC) staining and the hyperenhanced area seen at gadophrin-2-enhanced MR imaging performed in the same cat six hours after myocardial perfusion MR imaging. RESULTS: The sizes of perfusion defects seen at gadomer-17-enhanced perfusion MR imaging, unstained areas at TTC staining, and hyperenhanced areas at gadophrin-2-enhanced MR imaging were 20.4+/-4.3%, 29.0+/-9.7%, and 30.7+/-10.6% of the left ventricular myocardium, respectively. The perfusion defects seen at myocardial perfusion MR imaging were significantly smaller than the unstained areas at TTC staining and hyperenhanced areas at gadophrin-2-enhanced MR imaging (p < .01). The sizes of both the perfusion defect at myocardial perfusion MR imaging and the hyperenhanced area at gadophrin-2- enhanced MR imaging correlated well with the sizes of unstained areas at TTC staining (r = .64, p = .062 and r = .70, p = .035, respectively). CONCLUSION: In this cat model, the perfusion defect revealed by myocardial perfusion MR imaging underestimated the true size of acute reperfused myocardial infarction. The defect may represent a more severely damaged area of infarction and probably has prognostic significance.