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Controlled Clinical Trial
English Abstract
Journal Article
[The effect of melatonin on oxidative DNA damage in gastric mucosa cells of patients with functional dyspepsia].
UNLABELLED: The oxidative damage of DNA expresses severe cell lesion. The excess of oxygen free radicals is one of the causes of this type of disorders. Such a situation could occur in the course of H. pylori infection. Melatonin is a natural and very active antioxidant compound.
AIM OF STUDY: To establish weather an administration of melatonin decreases oxidative DNA damage in gastric mucosa cells.
MATERIAL AND METHODS: The study comprised 80 subjects, divided into two groups: group I (n=30)--patients with functional dyspepsia, H. pylori positive (+), with Epigastric Pain Syndrome, with H. pylori infection; group II (n=30)--patients H. pylori negative (-) with the same form of functional dyspepsia. The control group (0) comprised 20 subjects, aged 21-60 years.
RESULTS: In healthy subjects, non-infected with H. pylori the level of oxidative DNA damage in gastric mucosa cells was 6.95 +/- 2.98. In both study groups the percentage of oxidative DNA damage was respectively: 12.12 +/- 5.48% and 13.62 +/- 4.58% (p < 0.001). The differences in the results obtained in both study groups, that is H. pylori (+) and H. pylori (-) were similar (p > 0.05). In group of patients with functional dyspepsia and H. pylori infection the level of oxidative DNA damage in gastrocytes was 12.12 +/- 5.48%, and after 3 months administration of melatonin it decreased to the value 10.55 +/- 0.63% (p < 0.001). In patients with functional dyspepsia, without H. pylori infection the decrease of the level of oxidative DNA damages after melatonin administration was statistically significant and it was respectively: 13.62 +/- 4.58% (p < 0.001).
CONCLUSIONS: In functional dyspepsia, especially with coexisting H. pylori infection the oxidative DNA damage in gastric mucosa cells is observed. The melatonin administration changes the above mentioned oxidative DNA damage significantly.
AIM OF STUDY: To establish weather an administration of melatonin decreases oxidative DNA damage in gastric mucosa cells.
MATERIAL AND METHODS: The study comprised 80 subjects, divided into two groups: group I (n=30)--patients with functional dyspepsia, H. pylori positive (+), with Epigastric Pain Syndrome, with H. pylori infection; group II (n=30)--patients H. pylori negative (-) with the same form of functional dyspepsia. The control group (0) comprised 20 subjects, aged 21-60 years.
RESULTS: In healthy subjects, non-infected with H. pylori the level of oxidative DNA damage in gastric mucosa cells was 6.95 +/- 2.98. In both study groups the percentage of oxidative DNA damage was respectively: 12.12 +/- 5.48% and 13.62 +/- 4.58% (p < 0.001). The differences in the results obtained in both study groups, that is H. pylori (+) and H. pylori (-) were similar (p > 0.05). In group of patients with functional dyspepsia and H. pylori infection the level of oxidative DNA damage in gastrocytes was 12.12 +/- 5.48%, and after 3 months administration of melatonin it decreased to the value 10.55 +/- 0.63% (p < 0.001). In patients with functional dyspepsia, without H. pylori infection the decrease of the level of oxidative DNA damages after melatonin administration was statistically significant and it was respectively: 13.62 +/- 4.58% (p < 0.001).
CONCLUSIONS: In functional dyspepsia, especially with coexisting H. pylori infection the oxidative DNA damage in gastric mucosa cells is observed. The melatonin administration changes the above mentioned oxidative DNA damage significantly.
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