Activated oxygen metabolites

2003 ◽  
Vol 21 (12) ◽  
pp. 2235-2238 ◽  
Author(s):  
Rhian M Touyz
Keyword(s):  
Activated Oxygen ◽  
Activated Oxygen Metabolites ◽  
Oxygen Metabolites

scholarly journals Effects of Non-Surgical Periodontal Treatment on Reactive Oxygen Metabolites and Glycemic Control in Diabetic Patients with Chronic Periodontitis

Antioxidants ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1056
Author(s):  
Simone Marconcini ◽  
Enrica Giammarinaro ◽  
Saverio Cosola ◽  
Giacomo Oldoini ◽  
Annamaria Genovesi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Glycemic Control ◽  
Systemic Inflammation ◽  
Glycated Hemoglobin ◽  
Reactive Oxygen ◽  
Periodontal Treatment ◽  
Diabetic Patients ◽  
Reactive Oxygen Metabolites ◽  
Periodontal Infection ◽  
Oxygen Metabolites

Background: Periodontal infection may contribute to poor glycemic control and systemic inflammation in diabetic patients. The aim of the present study is to evaluate the efficacy of non-surgical periodontal treatment in diabetic patients by measuring oxidative stress outcomes. Methods: Sixty diabetic patients with periodontitis were enrolled, treated with scaling and full-mouth disinfection, and randomly prescribed chlorhexidine mouthwash, antioxidant mouthwash, or ozone therapy. Reactive oxygen metabolites (ROMs), periodontal parameters, and glycated hemoglobin were measured at baseline and then at 1, 3, and 6 months after. Results: At baseline, all patients presented with pathologic levels of plasmatic ROM (388 ± 21.36 U CARR), higher than the normal population. Probing depth, plaque index, and bleeding on probing values showed significant clinical improvements after treatment, accompanied by significant reductions of plasma ROM levels (p < 0.05). At the 6-month evaluation, the mean ROM relapsed to 332 ± 31.76 U CARR. Glycated hemoglobin decreased significantly (∆ = −0.52 units) after treatment. Both the test groups showed longer-lasting improvements of periodontal parameters. Conclusion: In diabetic patients, periodontal treatment was effective at reducing plasma ROM, which is an indicator of systemic oxidative stress and inflammation. The treatment of periodontal infection might facilitate glycemic control and decrease systemic inflammation.

Investigation of activated oxygen molecules on the surface of Y2O3nanocrystals by Raman scattering

2013 ◽  
Vol 114 (9) ◽  
pp. 093512 ◽  
Author(s):  
J. Q. Xu ◽  
S. J. Xiong ◽  
X. L. Wu ◽  
T. H. Li ◽  
J. C. Shen ◽  
...  
Keyword(s):  
Raman Scattering ◽  
Activated Oxygen

Interactions betweenTrypanosoma bruceiandBabesiaspp. andPlasmodiumspp. in mice

Parasitology ◽  
1985 ◽  
Vol 90 (2) ◽  
pp. 241-254 ◽  
Author(s):  
Stephanie M. Millott ◽  
F. E. G. Cox
Keyword(s):  
Trypanosoma Brucei ◽  
Babesia Microti ◽  
Cell Populations ◽  
Time Interval ◽  
Oxygen Species ◽  
Plasmodium Chabaudi ◽  
Subsequent Infection ◽  
Activated Oxygen ◽  
Large Numbers ◽  
Intracellular Parasites

Swiss mice with chronicTrypanosoma bruceiinfections become refractory to subsequent infection withBabesia microtiandB. rodhaini. Infection withB. microti7 days afterT. bruceiresulted in an obvious inhibition of the babesia parasitaemias and this inhibition became more profound as the time interval between the infections increased, until at 17–20 days the parasitaemias were totally abolished. Even after intravenous injection of large numbers of parasites parasitaemias were inhibited. Similar inhibition was obtained in BALB/c mice but not in C57BL/6 mice. Mice with establishedT. bruceiinfections also showed reduced susceptibility toB. rodhaini. In mice similarly infected withT. bruceiand the malaria parasitesPlasmodium chabaudi chabaudiandP. c. adamithe pre-patent periods were noticeably prolonged but the subsequent parasitaemias were unaffected. Infections withP. yoeliiwere unaffected.Trypanosoma bruceiinfections were not affected by the intracellular parasites. Among the mechanisms investigated to explain these findings were changes in red blood cell populations, cross-reacting antigens, the release of toxic factors and the generation of activated oxygen species. None of these could account for the inhibition observed.

Generation of reactive oxygen metabolites by phagocytosing endothelial cells

1988 ◽  
Vol 72 (1) ◽  
pp. 19-27 ◽  
Author(s):  
Peter Görög ◽  
Jeremy D. Pearson ◽  
Vijay V. Kakkar
Keyword(s):  
Endothelial Cells ◽  
Reactive Oxygen ◽  
Reactive Oxygen Metabolites ◽  
Oxygen Metabolites

Pulsed DC electric fields couple to natural NAD(P)H oscillations in HT-1080 fibrosarcoma cells

2001 ◽  
Vol 114 (8) ◽  
pp. 1515-1520 ◽  
Author(s):  
A.J. Rosenspire ◽  
A.L. Kindzelskii ◽  
H.R. Petty
Keyword(s):  
Electric Field ◽  
Electric Fields ◽  
Cell Function ◽  
Low Frequency ◽  
Reactive Oxygen Metabolites ◽  
Pulsed Dc ◽  
Fibrosarcoma Cells ◽  
Chemotactic Factors ◽  
Oxygen Metabolites ◽  
Dc Electric Fields

Previously, we have demonstrated that NAD(P)H levels in neutrophils and macrophages are oscillatory. We have also found that weak ultra low frequency AC or pulsed DC electric fields can resonate with, and increase the amplitude of, NAD(P)H oscillations in these cells. For these cells, increased NAD(P)H amplitudes directly signal changes in behavior in the absence of cytokines or chemotactic factors. Here, we have studied the effect of pulsed DC electric fields on HT-1080 fibrosarcoma cells. As in neutrophils and macrophages, NAD(P)H levels oscillate. We find that weak (~10(-)(5) V/m), but properly phased DC (pulsed) electric fields, resonate with NAD(P)H oscillations in polarized and migratory, but not spherical, HT-1080 cells. In this instance, electric field resonance signals an increase in HT-1080 pericellular proteolytic activity. Electric field resonance also triggers an immediate increase in the production of reactive oxygen metabolites. Under resonance conditions, we find evidence of DNA damage in HT-1080 cells in as little as 5 minutes. Thus the ability of external electric fields to effect cell function and physiology by acting on NAD(P)H oscillations is not restricted to cells of the hematopoietic lineage, but may be a universal property of many, if not all polarized and migratory eukaryotic cells.

Gentamicin enhanced production of hydrogen peroxide by renal cortical mitochondria

1987 ◽  
Vol 253 (4) ◽  
pp. C495-C499 ◽  
Author(s):  
P. D. Walker ◽  
S. V. Shah
Keyword(s):  
Hydrogen Peroxide ◽  
Mitochondrial Respiration ◽  
Critical Role ◽  
Reactive Oxygen ◽  
Reactive Oxygen Metabolites ◽  
Enhanced Production ◽  
Production Of Hydrogen ◽  
Hydrogen Peroxide Generation ◽  
Dose Dependent ◽  
Oxygen Metabolites

Agents that affect mitochondrial respiration have been shown to enhance the generation of reactive oxygen metabolites. On the basis of the well-demonstrated ability of gentamicin to alter mitochondrial respiration (stimulation of state 4 and inhibition of state 3), it was postulated that gentamicin may enhance the generation of reactive oxygen metabolites by renal cortical mitochondria. The aim of this study was to examine the effect of gentamicin on the production of hydrogen peroxide (measured as the decrease in scopoletin fluorescence) in rat renal cortical mitochondria. The hydrogen peroxide generation by mitochondria was enhanced from 0.17 +/- 0.02 nmol . mg-1 . min-1 (n = 14) in the absence of gentamicin to 6.21 +/- 0.67 nmol . mg-1 . min-1 (n = 14) in the presence of 4 mM gentamicin. This response was dose dependent with a significant increase observed at even the lowest concentration of gentamicin tested, 0.01 mM. Production of hydrogen peroxide was not increased when gentamicin was added to incubation media in which mitochondria or substrate was omitted or heat-inactivated mitochondria were used. The gentamicin-induced change in fluorescence was completely inhibited by catalase (but not by heat-inactivated catalase), indicating that the decrease in fluorescence was due to hydrogen peroxide. Thus this study demonstrates that gentamicin enhances the production of hydrogen peroxide by mitochondria. Because of their well-documented cytotoxicity, reactive oxygen metabolites may play a critical role in gentamicin nephrotoxicity.

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