Nucleases from Prevotella intermedia can degrade neutrophil extracellular traps.

Periodontitis is an inflammatory disease caused by periodontal bacteria in subgingival plaque. These bacteria are able to colonize the periodontal region by evading the host immune response. Neutrophils, the host's first line of defense against infection, use various strategies to kill invading pathogens, including neutrophil extracellular traps (NETs). These are extracellular net-like fibers comprising DNA and antimicrobial components such as histones, LL-37, defensins, myeloperoxidase, and neutrophil elastase from neutrophils that disarm and kill bacteria extracellularly. Bacterial nuclease degrades the NETs to escape NET killing. It has now been shown that extracellular nucleases enable bacteria to evade this host antimicrobial mechanism, leading to increased pathogenicity. Here, we compared the DNA degradation activity of major Gram-negative periodontopathogenic bacteria, Porphyromonas gingivalis, Prevotella intermedia, Fusobacterium nucleatum, and Aggregatibacter actinomycetemcomitans. We found that Pr. intermedia showed the highest DNA degradation activity. A genome search of Pr. intermedia revealed the presence of two genes, nucA and nucD, putatively encoding secreted nucleases, although their enzymatic and biological activities are unknown. We cloned nucA- and nucD-encoding nucleases from Pr. intermedia ATCC 25611 and characterized their gene products. Recombinant NucA and NucD digested DNA and RNA, which required both Mg2+ and Ca2+ for optimal activity. In addition, NucA and NucD were able to degrade the DNA matrix comprising NETs.

Pressure-induced nano-crystallization of silicate garnets from glass.

Transparent ceramics are important for scientific and industrial applications because of the superior optical and mechanical properties. It has been suggested that optical transparency and mechanical strength are substantially enhanced if transparent ceramics with nano-crystals are available. However, synthesis of the highly transparent nano-crystalline ceramics has been difficult using conventional sintering techniques at relatively low pressures. Here we show direct conversion from bulk glass starting material in mutianvil high-pressure apparatus leads to pore-free nano-polycrystalline silicate garnet at pressures above ∼10 GPa in a limited temperature range around 1,400 °C. The synthesized nano-polycrystalline garnet is optically as transparent as the single crystal for almost the entire visible light range and harder than the single crystal by ∼30%. The ultrahigh-pressure conversion technique should provide novel functional ceramics having various crystal structures, including those of high-pressure phases, as well as ideal specimens for some mineral physics applications.

Involvement of lipoprotein PpiA of Streptococcus gordonii in evasion of phagocytosis by macrophages.

Streptococcus gordonii is a commensal gram-positive bacterium that resides in the human oral cavity, and is one of the most common causes of infective endocarditis (IE). Bacterial surface molecules play an important role in establishing IE, and several S. gordonii proteins have been implicated in binding to host cells during the establishment of IE. In this study, we identified a putative lipoprotein, peptidyl-prolyl cis/trans isomerase (PpiA), and clarified its role in evasion of phagocytosis by macrophages. Attenuation of the gene encoding prolipoprotein diacylglyceryl transferase (Lgt) altered the localization of PpiA from the cell surface to the culture supernatant, indicating that PpiA is lipid-anchored in the cell membrane by Lgt. Both human and murine macrophages showed higher phagocytic activity towards ppiA and lgt mutants than the wild-type, indicating that the presence of PpiA suppresses phagocytosis of S. gordonii. Human macrophages treated with dextran sulfate had significantly impaired phagocytosis of S. gordonii, suggesting that class A scavenger receptors in human macrophages are involved in the phagocytosis of S. gordonii. These results provide evidence that S. gordonii lipoprotein PpiA plays an important role in inhibiting phagocytic engulfment and in evasion of the host immune response.

Toll-like receptor 2-mediated modulation of growth and functions of regulatory T cells by oral streptococci.

This study was designed to determine whether oral streptococci modulate the growth and functions of regulatory T cells. Heat-killed cells of wild-type strains of Streptococcus gordonii and Streptococcus mutans induced the Toll-like receptor 2 (TLR2) -mediated nuclear factor-κB (NF-κB) activation, but their lipoprotein-deficient strains did not. Stimulation with these streptococci resulted in a significant increase in the frequency of CD4(+) CD25(+) Foxp3(+) regulatory T cells in splenocytes derived from both TLR2(+/+) and TLR2(-/-) mice, but the level of increase in TLR2(+/+) splenocytes was stronger than that in TLR2(-/-) splenocytes. Both strains of S. gordonii enhanced the proliferation of CD4(+) CD25(+) Foxp3(+) regulatory T cells isolated from TLR2(+/+) mice at the same level as those from TLR2(-/-) mice in an interleukin-2-independent manner. However, wild-type and lipoprotein-deficient strains of both streptococci did not enhance the suppressive activity of the isolated regulatory T cells in vitro, but rather inhibited it. TLR ligands also inhibited the suppressive activity of the regulatory T cells. Inhibition of the suppressive activity was recovered by the addition of anti-IL-6 antibody. Pretreatment of antigen-presenting cells with the NF-κB inhibitor BAY11-7082 enhanced the suppressive activity of the regulatory T cells. These results suggested that interleukin-6 produced by antigen-presenting cells inhibits the suppressive activity of the regulatory T cells. Wild-type strain, but not lipoprotein-deficient strain, of S. gordonii reduced the frequency of CD4(+)  CD25(+)  Foxp3(+) regulatory T cells in the acute infection model, whereas both strains of S. gordonii increased it in the chronic infection model mice. Hence, this study suggests that oral streptococci are capable of modulating the growth and functions of regulatory T cells in vitro and in vivo.

Micro-organism and cell viability on antimicrobially modified titanium.

When titanium is anodized by discharge in NaCl solution, both antimicrobial activity and osteoconductivity are conferred. The viability of adherent micro-organisms and cells on antimicrobial titanium remains uncertain. We hypothesized that a thin peroxidation barrier would efficiently destroy adherent bacteria, whereas adherent osteoblastic cells would be viable, since these cells adhere to the surface indirectly though serum proteins. The efficacy of antimicrobial titanium appears to be based on peroxidation, since peroxidation products were detected in parallel with the destruction of bacterial cell-surface structures. The peroxidation effect of antimicrobial titanium was confined to the surface within narrow limits. The viability of osteoblastic cells on the surface was strongly dependent on the presence of serum protein, whereas that of adherent Streptococcus mutans was not affected by the presence of serum proteins. Therefore, differences in the adherent systems used by bacteria and osteoblastic cells are important determinants of their viability on antimicrobial titanium.

Role of prolipoprotein diacylglyceryl transferase (Lgt) and lipoprotein-specific signal peptidase II (LspA) in localization and physiological function of lipoprotein MsmE in Streptococcus mutans.

INTRODUCTION: To clarify the role that prolipoprotein diacylglyceryl transferase (Lgt) and lipoprotein-specific signal peptidase II (LspA) play in the physiological function of MsmE, we constructed lgt-deficient and lspA-deficient mutants of Streptococcus mutans 109c and examined the potential role of Lgt and LspA in membrane anchoring and growth in a melibiose medium of S. mutans. METHODS: The lgt-, lspA-, and msmE-deficient mutants of S. mutans 109c were constructed by double-crossover recombination of their respective genes. Localization of MsmE was demonstrated by Western blot analysis with an MsmE antiserum. The growth of S. mutans cells was examined in a Trypton medium containing melibiose or glucose. RESULTS: In the S. mutans lgt mutant, localization of the surface lipoprotein MsmE changed with the culture supernatant. The growth of the S. mutans lgt and lspA mutants was remarkably reduced in the melibiose medium; however, growth was recovered in the strains complemented with the lgt or the lspA gene. Therefore, lipid-modification by Lgt and subsequent signal peptide cleavage by LspA were crucial for membrane anchoring and the physiological function of MsmE in S. mutans. CONCLUSION: These results demonstrate that MsmE is required for melibiose metabolism in S. mutans and that modification by Lgt and LspA are important processes for the physiological function of MsmE.

Pulmonary exposure to diesel exhaust particle components enhances circulatory chemokines during lung inflammation.

This study examines the effects of DEP components on circulatory CC and CXC chemokines, potent activators and chemoattractants for macrophage and leukocyte subpopulations, in a murine model of lung inflammation. ICR mice were divided into six experimental groups which received intratracheal inoculation of vehicle, LPS alone (2.5 mg/kg), organic chemicals in DEP (DEP-OC: 4 mg/kg) extracted with dichloromethane, residual carbonaceous nuclei after the extraction (washed DEP: 4 mg/kg), DEP-OC + LPS, or washed DEP + LPS. Intratracheal instillation of each DEP component alone did not significantly change the circulatory level of macrophage inflammatory protein (MIP)-1alpha, MIP-2, and macrophage chemoattractant protein-1 (MCP-1) 24 h after the exposure as compared with vehicle instilled alone. In the LPS group, MCP-1, but not MIP-1alpha or MIP-2, was significantly greater than in the vehicle group. The combined administration of LPS and washed DEP caused a further three to five-fold increase in MIP-1alpha, MIP-2, and MCP-1 proteins in the serum as compared with LPS administered alone. No significant difference between the LPS + DEP-OC group and the LPS group was observed. These results indicate that pulmonary exposure to washed DEP enhances circulatory level of chemokines during lung inflammation. The enhancement may be important in the aggravations of systemic inflammatory responses and ischemic cardiovascular conditions associated with air pollution.

The DNA mismatch repair gene hMSH2 is a potent coactivator of oestrogen receptor alpha.

The DNA mismatch repair gene is a key regulator in the elimination of base-base mismatches and insertion/deletion loops (IDLs). Human MutS homologue 2 (hMSH2), originally identified as a human homologue of the bacterial MutS, is a tumour suppressor gene frequently mutated in hereditary non-polyposis colorectal cancer. Hereditary non-polyposis colorectal cancer is characterised by the early onset of colorectal cancer and the development of extracolonic cancers such as endometrial, ovarian, and urological cancers. Oestrogen receptor (ER) alpha and beta are members of a nuclear receptor (NR) superfamily. Ligand-dependent transcription of ER is regulated by the p160 steroid receptor coactivator family, the thyroid hormone receptor-associated proteins/the vitamin D receptor-interacting proteins (TRAP/DRIP) mediator complex, and the TATA box-binding protein (TBP)-free TBP associated factor complex (TFTC) type histone acetyltransferase complex. Here, we report the interaction between ER alpha/beta and hMSH2. Immunoprecipitation and glutathione-S-transferase pull-down assay revealed that ER alpha and hMSH2 interacted in a ligand-dependent manner, whereas ER beta and hMSH2 interacted in a ligand-independent manner. Oestrogen receptor alpha/beta bound to hMSH2 through the hMSH3/hMSH6 interaction domain of hMSH2. In a transient expression assay, hMSH2 potentiated the transactivation function of liganded ER alpha, but not that of ER beta. These results suggest that hMSH2 may play an important role as a putative coactivator in ER alpha dependent gene expression.

Activation of distinct signal transduction pathways in hypertrophied hearts by pressure and volume overload.

OBJECTIVE: Two types of hemodynamic overload, pressure and volume overload, result in morphologically distinct types of cardiac remodeling. We explored the possibility that distinct hemodynamic overload may differentially activate the signal transduction pathway. METHODS: Pressure and volume overload were induced by thoracic aortic banding and carotid-jugular shunt formation in rabbits, respectively. Phosphorylation activities of mitogen-activated protein (MAP) kinase families, Akt, and signal transducer and activator of transcription (STAT) 3 in the left ventricular myocardium were determined by Western blotting using phospho-specific antibodies and were compared between hypertrophied hearts by pressure and volume overload. RESULTS: Pressure and volume overload produced concentric and eccentric cardiac hypertrophy in rabbits, respectively. In pressure-overloaded hearts, extracellular signal-regulated kinase (ERK) 1/2, p38 MAP kinase, and STAT3 were transiently activated prior to hypertrophic changes. In contrast, activation of ERK1/2, but not p38 MAP kinase and STAT3, was observed only at 12 weeks after shunt surgery. Pressure overload evoked short and biphasic activation of Akt at 15 min and 1 day after aortic banding. In contrast, volume overload induced sustained activation of Akt from 1 day to 1 week. Concordant phosphorylation of downstream targets of Akt, glycogen synthase kinase-3beta (GSK-3beta) and p70 ribosomal S6 kinase (p70(S6K)), in response to Akt activation was observed at 15 min after pressure overload. However in volume-overloaded hearts, phosphorylation of GSK-3beta and p70(S6K) was observed at 6 weeks and at 6 and 12 weeks, respectively, and was not coincident with Akt activation. These findings suggest that phosphorylation of GSK-3beta and p70(S6K) is regulated by an alternative pathway other than Akt in volume-overloaded hearts. CONCLUSION: Pressure and volume overload-induced cardiac hypertrophy is associated with distinct patterns of activation of signal transduction pathways. These data may suggest that stimulus-specific heterogeneity in the signaling pathway plays a role in determining the type of cardiac hypertrophy.

Fatty acid metabolism assessed by 125I-iodophenyl 9-methylpentadecanoic acid (9MPA) and expression of fatty acid utilization enzymes in volume-overloaded hearts.

BACKGROUND: The peroxisome proliferator-activated receptor (PPAR) alpha is a member of the nuclear receptor superfamily and regulates gene expression of fatty acid utilization enzymes. In cardiac hypertrophy and heart failure by pressure-overload, myocardial energy utilization reverts to the fetal pattern, and metabolic substrate switches from fatty acid to glucose. However, myocardial metabolism in volume-overloaded hearts has not been rigorously studied. The aim of the present study was to examine fatty acid metabolism and protein expressions of PPARalpha and fatty acid oxidation enzymes in volume-overloaded rabbit hearts. METHODS: Volume-overload was induced by carotid-jugular shunt formation. Sham-operated rabbits were used as control. Chronic volume-overload increased left ventricular weight and ventricular cavity size, and relative wall thickness was decreased, indicating eccentric cardiac hypertrophy. (125)I-iodophenyl 9-methylpentadecanoic acid (9MPA) was intravenously administered, and animals were sacrificed at 5 min after injection. The 9MPA was rapidly metabolized to iodophenyl-3-methylnonanoic acid (3MNA) by beta-oxidation. Lipid extraction from the myocardium was performed by the Folch method, and radioactivity distribution of metabolites was assayed by thin-layer chromatography. The protein was extracted from the left ventricular myocardium, and levels of PPARalpha and fatty acid oxidation enzymes were examined by Western blotting. RESULTS: Myocardial distribution of 9MPA tended to be more heterogeneous in shunt than in sham rabbits (P = 0.06). In volume-overloaded hearts by shunt, the conversion from 9MPA to 3MNA by beta-oxidation was faster than the sham-control hearts (P < 0.05). However, protein levels of PPARalpha and fatty acid utilization enzymes were unchanged in shunt rabbits compared with sham rabbits. CONCLUSIONS: These data suggest that myocardial fatty acid metabolism is enhanced in eccentric cardiac hypertrophy by volume-overload without changes in protein expressions of PPARalpha and fatty acid utilization enzymes. Our data may provide a novel insight into the subcellular mechanisms for the pathological process of cardiac remodelling in response to mechanical stimuli.

Protein kinase C and extracellular signal regulated kinase are involved in cardiac hypertrophy of rats with progressive renal injury.

Increased cardiovascular mortality is an unresolved problem in patients with chronic renal failure. Cardiac hypertrophy is observed in the majority of patients with chronic renal failure undergoing haemodialysis. However, the mechanisms, including signal transduction pathways, responsible for cardiac hypertrophy in renal failure remain unknown. We examined the subcellular localization of protein kinase C (PKC) isoforms and phosphorylation activities of 3 mitogen-activated protein (MAP) kinase families in hypertrophied hearts of progressive renal injury rat model by subtotal nephrectomy (SNx). We also examined the effects of a novel angiotensin II type-1 receptor antagonist, CS-866, on the PKC translocation, MAP kinase activity and cardiac hypertrophy in SNx rats. The left ventricle/body weight ratios were significantly larger in SNx rats than in sham rats at 1, 2, and 4 weeks after surgery. The translocation of PKCalpha and epsilon isoforms to membranous fraction was observed in SNx rat hearts at 1, 2, and 4 weeks after surgery. Activation of extracellular signal regulated kinase (ERK) 1/2, but not p38 MAP kinase and c-Jun N-terminal kinase (JNK), was observed at 1 and 2 weeks after surgery. Angiotensin II receptor blockade with CS-866 (1 mg kg-1 day-1) prevented cardiac hypertrophy, PKC translocation and ERK1/2 activation in SNx rats without significant changes in blood pressure. These data suggest that PKC and ERK1/2 are activated by an angiotensin II receptor-mediated pathway and might play an important role in the progression of cardiac hypertrophy in renal failure.

Angiotensin-converting enzyme inhibition improves cardiac fatty acid metabolism in patients with congestive heart failure.

This study aimed to examine whether angiotensin-converting enzyme (ACE) inhibition improved cardiac fatty acid metabolism in patients with congestive heart failure (CHF). Myocardial 123I-beta-methyl-iodophenylpentadecanoic acid (123I-BMIPP) imaging was performed in 25 patients with CHF and in 10 control subjects. Myocardial 123I-BMIPP images were obtained 30 min and 4 h after tracer injection. The heart-to-mediastinum (H/M) ratio of 123I-BMIPP uptake and the washout rate of 123I-BMIPP from the myocardium were calculated. Patients were given enalapril for 6 months, and 123I-BMIPP imaging was repeated. H/M ratios on early and delayed images were lower in CHF patients than in normal controls (P<0.01). The washout rate of 123I-BMIPP from the myocardium was faster in CHF patients than in controls (P<0.01). As the severity of the New York Heart Association (NYHA) functional class increased, the H/M ratio decreased and the washout rate increased. The washout rate of 123I-BMIPP was inversely correlated with left ventricular fractional shortening (R=-0.62, P<0.01). ACE inhibition with enalapril increased the H/M ratio on delayed images (P<0.05) and reduced the washout rate of 123I-BMIPP (P<0.05) in CHF patients. These data suggest that: (1) angiotensin II-mediated intracellular signalling activation may be a possible mechanism for the decreased myocardial uptake and enhanced washout of 123I-BMIPP in heart failure patients; and (2) the improvement in fatty acid metabolism by ACE inhibition may represent a new mechanism for the beneficial effect of this therapy in heart failure.

The genetic relatedness of Porphyromonas gingivalis clinical and laboratory strains assessed by analysis of insertion sequence (IS) element distribution.

OBJECTIVES: Porphyromonas gingivalis is frequently found in periodontitis lesions. This organism contains a large number of insertion sequence (IS) elements. We sought to determine the distribution of seven IS elements from strain W83 among nine P. gingivalis laboratory strains and nine clinical isolates and to use these findings to determine strain relationships. METHODS: Southern blots of BamHI digested genomic DNA digests were probed with insertion sequence elements ISPg1-7. RESULTS: The restriction fragment length polymorphism (RFLP) patterns revealed that five of the nine laboratory strains, including strain W83, were nearly identical for all seven IS elements. Two of nine clinical isolates were similar to the five laboratory strains. Two of the four remaining laboratory strains had similar or identical RFLP patterns. The remaining two laboratory strains had limited similarity to clinical strains. Four of the clinical isolates had identical RFLP patterns for all seven IS elements. The three remaining clinical isolates were unique in their RFLP patterns. Several strains lacked from one to four of the IS elements. Similar strain relationships were suggested regardless of the IS element examined. CONCLUSIONS: Transposition and recombination between IS elements are not sufficiently pervasive to obscure strain relationships, though this does not preclude the possibility that such events play an important role in allowing P. gingivalis to adapt to new environments. Given the level of genetic diversity observed, it may be especially important to examine genetically diverse strains when drawing conclusions based on the W83 P. gingivalis genomic database.

Pulsed Doppler tissue imaging for the assessment of myocardial viability: comparison with 99mTc sestamibi perfusion imaging.

The aim of the present study was to examine whether Doppler tissue imaging demonstrated comparable diagnostic performance for the detection of viable myocardium compared to myocardial perfusion imaging with Tc hexakis-2-methoxyisobutylisonitrile (MIBI). We studied 30 patients with old myocardial infarction who underwent percutaneous transluminal coronary angioplasty (PTCA). Myocardial single photon emission computed tomography (SPECT) with Tc-MIBI and two-dimensional echocardiography were carried out within 7 days before PTCA. We measured regional Tc-MIBI uptake for each myocardial segment from SPECT and peak systolic velocity and a ratio of regional pre-ejection period to regional ejection time (PEP/ET) from pulsed Doppler tissue imaging. Biplane left ventriculography was performed before interventional procedures and repeated 3 months after PTCA. Myocardial viability was determined when wall motion was improved at least one grade after PTCA. The peak systolic velocity was positively correlated with regional Tc-MIBI uptake (R =0.59, P<0.01). The PEP/ET demonstrated inverse correlation with Tc-MIBI uptake ( R=-0.59, P<0.01). Peak systolic velocity of viable segments was higher than that of non-viable segments ( P<0.05). The PEP/ET was lower in viable segments than in non-viable segments ( P<0.05). Peak systolic velocity and PEP/ET demonstrated high diagnostic accuracy for detecting viable myocardium compared with Tc-MIBI perfusion imaging (80% and 79% vs 90%). These data indicate that measurements of regional peak systolic velocity and PEP/ET by Doppler tissue imaging are useful for evaluating myocardial viability quantitatively and provide helpful information for a clinical judgment in an interventional strategy.

[Ganglioneuroma detected in a patient over age 60].

We report a case of ganglioneuroma in a 67-year-old woman who presented with an abnormal shadow at a medical examination. She was admitted and chest radiography disclosed a mass in the upper right mediastinum. We suspected a mediastinal tumor after chest CT, chest MRI and bronchofiberscopic examination, and so surgical treatment was performed. The histopathological diagnosis was ganglioneuroma. Ganglioneuroma is thought of as a children's disease and adult onset is rare. We reasoned that ganglioneuroma should be included among the mediastinal tumors in patients over 60.

[Results of questionnaire on open disclosure to patients with malignant lung tumors comparison of responses before and after chemotherapy].

To investigate patient attitudes towards open disclosure of malignant disease, we conducted a questionnaire survey of 17 patients with malignant lung tumors, to whom the nature of their disease was revealed. The questionnaire used a 100 mm analog scale. Ten of the patients were treated by chemotherapy and their questionnaire results before and after treatment were compared. It was found that they were mostly satisfied about being truthfully informed and that, indeed, they were anxious to know their true diagnoses. They were also keen to have their true prognosis revealed, but not as much as the diagnosis. They also wished to be informed about treatment and its effects. These attitudes showed no marked changes resulting from the administration of chemotherapy, and we therefore concluded that chemotherapy itself had no influence on patients' feelings about disclosure. The questionnaire was well accepted and was useful in judging attitudes to open disclosure.

Generation of methoxide from methane and oxygen under mild conditions over an Sm2O3 catalyst investigated by in situ IR spectroscopy.

The generation of methoxide over an Sm2O3 catalyst was clearly observed under a CH4-O2 atmosphere at 323 K by in situ Fourier transform IR spectroscopy.

Elevated nitric oxide synthase activity concurrent with antigen-induced airway hyperresponsiveness in rats.

To characterize the airway nitric oxide synthase (NOS) activities concurrent with airway hyperresponsiveness (AHR), a common feature of allergic asthma, the NOS activities of airway tissue homogenates from the antigen-induced AHR rats were determined by the ability of tissue homogenates to convert L-arginine to L-citrulline (Cit). A significantly higher level of total NOS activities was found in homogenates from the AHR rats (19.9 +/- 1.3 pmol Cit/min/mg protein) compared to those from sensitized control and normal control groups (9.8 +/- 1.2 and 8.8 +/- 1.2 pmol Cit/min/mg protein, respectively; P < .01). The nitrite concentration in bronchoalveolar lavage fluids, which indicates the in vivo generation of NO in airways, from the AHR rats (7.40 +/- 0.71 microM) was significantly greater than that from nonsensitized normal animals (1.45 +/- 1.12 microM, P < .01). Although the protein levels of endothelial (eNOS) and neuronal type NOS (nNOS) determined by immunoblotting were within normal levels, the amount of inducible NOS (iNOS) protein was markedly and significantly elevated in airway tissue homogenates from the AHR rats. Immunohistochemical staining of airway tissues with specific antibody against iNOS demonstrated a distinct localization of iNOS on epithelial cells and infiltrated inflammatory cells in the bronchi of the hyperresponsive rats, but only negligible staining of epithelia was observed in the nonsensitized normal group. No difference in constitutive NOS (eNOS and nNOS) localization was observed between groups. The present findings indicate that the NOS activities in airway tissues are elevated in antigen-induced AHR rats, which is mainly derived from the induction of iNOS in the airways. Downregulation of constitutive eNOS and nNOS is not found in this animal model of AHR.

Effect of the natural antioxidant 2"-O-glycosylisovitexin on superoxide and hydroxyl radical generation.

The inhibitory effect of 2"-O-glycosyl isovitexin (2"-O-GIV) isolated from green barley leaves on superoxide and hydroxyl radical generation was investigated using electron spin resonance spectroscopy. 2"-O-GIV exhibited dose-related inhibitory activity both towards superoxide generation and hydroxyl radical generation. 2"-O-GIV inhibited superoxide formation by 97% at a level of 25 mM and inhibited hydroxyl radical formation by 91% at a level of 500 microM. The results suggest that the inhibitory activity of 2"-O-GIV is due to trapping radicals.