Superoxide dismutase Ameliorates the Bowel Alterations Induced by diabetes Mellitus – An Experimental Study
Henrique Fillmann1★, Juliana Tieppo1, Nélson Alexandre Kretzmann Filho1, Graziella Rodrigues1, Jaqueline Nascimento Picada2, Julian Panés3, Norma Possa Marroni1,2★ Corresponding author
- 1Hospital de Clínicas de Porto Alegre, Brazil.
- 2Universidade Luterana do Brasil, ULBRA, Brazil.
- 3Hospital Clínic. University of Barcelona, Spain.
CORRESPONDENCE
Henrique Fillmann
Hospital de Clínicas de Porto Alegre, Brazil.
Volume 1, Issue 3 · pp. 19–26 · PUBLISHED · DOI: 10.5530/ax.2011.3.4
View on Free Rad. Antiox. original site ↗
ABSTRACT
Introduction:The gastrointestinal system is frequently affected in patients with diabetes mellitus (DM). Some of these alterations are due to oxidative stress and the production of free radicals. The present study was designed to evaluate whether treatment with superoxide dismutase (SOD) exerts protection on established bowel alterations in experimental diabetes mellitus induced by streptozotocin. We measured the lipid peroxidation, the superoxide dismutase activity and the DNA damage. Materials and Methods:We used the anorectal pressure to evaluate the nitrosative stress and used an inflammatory score to measure the macroscopic and microscopic bowel alterations. Results: The oxidative stress and the DNA damage was elevated in DM group and reduced with the SOD administration. The use of SOD also ameliorates the inflammatory bowel alterations and the anorectal pressure. Conclusion: SOD administration showed beneficial effects in all parameters of large bowel alterations in DM rats.
KEYWORDS
REFERENCES
As publishedShowing references and in-text citations exactly as published.
Cite this article
SELECT FORMAT
Fillmann, H., Tieppo, J., Filho, N. A. K., Rodrigues, G., Picada, J. N., Panés, J., & Marroni, N. P. (). Superoxide dismutase Ameliorates the Bowel Alterations Induced by diabetes Mellitus – An Experimental Study. Free Radicals and Antioxidants, 1(3), 19–26. https://doi.org/10.5530/ax.2011.3.4
