Antioxidant vitamin supplements do not reduce reactive oxygen species activity inHelicobacter pylorigastritis in the short term

Reactive oxygen species have been implicated inHelicobacter pylori-mediated gastric carcinogenesis, whereas diets high in antioxidant vitamins C and E are protective. We have examined the effect of vitamin C and E supplements in combination withH. pylorieradication on reactive oxygen species activity inH. pylorigastritis.H. pylori-positive patients were randomized into four groups: triple therapy alone (Bismuth chelate, tetracycline, and metronidazole for 2 weeks), vitamins alone (200 mg vitamin C and 50 mg vitamin E, both twice per day for 4 weeks), both treatments or neither. Plasma and mucosal ascorbic acid, malondialdehyde and reactive oxygen species were determined before and after treatment. Compared with normal controls (n61),H. pylori-positive patients (n117) had higher mucosal reactive oxygen species and malondialdehyde levels and lower plasma ascorbic acid. Plasma ascorbic acid doubled in both groups of patients receiving vitamins and mucosal levels also increased. Malondialdehyde and reactive oxygen species fell in patients in whomH. pyloriwas eradicated but vitamin supplements were not effective either alone or in combination withH. pylorieradication. Supplements of vitamins C and E do not significantly reduce mucosal reactive oxygen species damage inH. pylorigastritis.

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Reactive oxygen species activity and lipid peroxidation inHelicobacter pylori associated gastritis: relation to gastric mucosal ascorbic acid concentrations and effect of H pylori eradication

Gut ◽

10.1136/gut.42.6.768 ◽

1998 ◽

Vol 42 (6) ◽

pp. 768-771 ◽

Cited By ~ 86

Author(s):

I M Drake ◽

N P Mapstone ◽

C J Schorah ◽

K L M White ◽

D M Chalmers ◽

...

Keyword(s):

Gastric Cancer ◽

Reactive Oxygen Species ◽

Ascorbic Acid ◽

Gastric Mucosa ◽

Reactive Oxygen ◽

Gastric Epithelium ◽

Oxygen Species ◽

Enhanced Chemiluminescence ◽

Species Activity ◽

H Pylori

Background—Helicobacter pylori is an independent risk factor for gastric cancer, and this association may be due to the bacterium causing reactive oxygen species mediated damage to DNA in the gastric epithelium. High dietary ascorbic acid intake may protect against gastric cancer by scavenging reactive oxygen species.Aims—To assess reactive oxygen species activity and damage in gastric mucosa in relation to gastric pathology and mucosal ascorbic acid level, and to determine the effect of H pylori eradication on these parameters.Patients—Gastric biopsy specimens were obtained for analysis from 161 patients undergoing endoscopy for dyspepsia.Methods—Reactive oxygen species activity and damage was assessed by luminol enhanced chemiluminescence and malondialdehyde equivalent estimation respectively. Ascorbic acid concentrations were measured using HPLC.Results—Chemiluminescence and malondialdehyde levels in gastric mucosa were higher in patients with H pylori gastritis than in those with normal histology. Successful eradication of the bacterium led to decreases in both parameters four weeks after treatment was completed. Gastric mucosal ascorbic acid and total vitamin C concentrations were not related to mucosal histology, but correlated weakly with reactive oxygen species activity (chemiluminescence and malodialdehyde levels).Conclusions—Data suggest that reactive oxygen species play a pathological role in H pylori gastritis, but mucosal ascorbic acid is not depleted in this condition.

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The effect of H. pylori eradication and antioxidant vitamin supplementation on gastric mucosal reactive oxygen species damage and gastric juice ascorbic acid

Gastroenterology ◽

10.1016/s0016-5085(98)80478-2 ◽

1998 ◽

Vol 114 ◽

pp. A117

Author(s):

S Everett ◽

I Drake ◽

K White ◽

D Chalmers ◽

C Schorah ◽

...

Keyword(s):

Reactive Oxygen Species ◽

Ascorbic Acid ◽

Gastric Juice ◽

Reactive Oxygen ◽

Vitamin Supplementation ◽

Antioxidant Vitamin ◽

Oxygen Species ◽

H Pylori

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PP-032 Reactive oxygen species activity and lipid peroxidation in Helicobacter pylori associated premalignant lesions and effect of H. pylori eradication

International Journal of Infectious Diseases ◽

10.1016/s1201-9712(09)60183-1 ◽

2008 ◽

Vol 12 ◽

pp. S65

Author(s):

G. Manoj ◽

S.K. Tiwari ◽

G. Sivaram ◽

R. Saikant ◽

Z. Abid ◽

...

Keyword(s):

Reactive Oxygen Species ◽

Lipid Peroxidation ◽

Helicobacter Pylori ◽

Reactive Oxygen ◽

Premalignant Lesions ◽

Oxygen Species ◽

Species Activity ◽

H Pylori

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CBIO-07. CELL DEATH INDUCED BY AN OSCILLATING MAGNETIC FIELD IN PATIENT DERIVED GLIOBLASTOMA CELLS IS MEDIATED BY REACTIVE OXYGEN SPECIES

Neuro-Oncology ◽

10.1093/neuonc/noaa215.067 ◽

2020 ◽

Vol 22 (Supplement_2) ◽

pp. ii17-ii17

Author(s):

Shashank Hambarde ◽

Martyn Sharpe ◽

David Baskin ◽

Santosh Helekar

Keyword(s):

Reactive Oxygen Species ◽

Cell Death ◽

Cell Viability ◽

Cortical Neurons ◽

Reactive Oxygen ◽

Great Promise ◽

Antioxidant Vitamin ◽

Ros Generation ◽

Oxygen Species ◽

Novel Therapy

Abstract Noninvasive cancer therapy with minimal side effects would be ideal for improving patient outcome in the clinic. We have developed a novel therapy using strong rotating magnets mounted on a helmet. They generate oscillating magnetic fields (OMF) that penetrate through the skull and cover the entire brain. We have demonstrated that OMF can effectively kill patient derived glioblastoma (GBM) cells in cell culture without having cytotoxic effects on cortical neurons and normal human astrocytes (NHA). Exposure of GBM cells to OMF reduced the cell viability by 33% in comparison to sham-treated cells (p< 0.001), while not affecting NHA cell viability. Time lapse video-microscopy for 16 h after OMF exposure showed a marked elevation of mitochondrial reactive oxygen species (ROS), and rapid apoptosis of GBM cells due to activation of caspase 3. Addition of a potent antioxidant vitamin E analog Trolox effectively blocked OMF-induced GBM cell death. Furthermore, OMF significantly potentiated the cytotoxic effect of the pro-oxidant Benzylamine. The results of our studies demonstrate that OMF-induced cell death is mediated by ROS generation. These results demonstrate a potent oncolytic effect on GBM cells that is novel and unrelated to any previously described therapy, including a very different mechanism of action and different technology compared to Optune therapy. The effect is very powerful, and unlike Optune, can be seen within hours after initiation of treatment. We believe that this technology holds great promise for new, effective and nontoxic treatment of glioblastoma.

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