Oxidative stress and metabolism in animal model of colitis induced by dextran sulfate sodium.
OBJECTIVE
Ulcerative colitis is a chronic inflammatory disease of the gastrointestinal tract. Its etiology remains unclear, but it appears to result from a dysregulated immune response, with infiltration of phagocytic leukocytes into the mucosal interstitium. The production and release of reactive oxygen species by immune cells seems to play a crucial role in physiopathology of colitis. The aim of this work was to evaluate the effects of N-acetylcysteine (NAC) and deferoxamine (DFX) in the treatment of colitis induced by dextran sulfate sodium (DSS).


METHODS
The effects of NAC and DRX on rats with DSS-induced colitis were determined by measuring intestinal parameters of oxidative stress and mitochondrial function, inflammatory response and bowel histopathological alterations.


RESULTS
DSS increased white blood cells count and NAC and DFX did not prevent this effect. However, DSS increased mitochondrial respiratory chain complex IV in colon of rats and NAC and DFX prevented this alteration. In addition, thiobarbituric acid reactive substances were increased in colon of DSS-treated rats. NAC and DFX, when taken together, prevented this effect. Complex II and succinate dehydrogenase were not affected by DSS, as protein carbonyl content.


CONCLUSIONS
It is speculated that NAC and DFX might be useful for treatment of colitis, but further research is necessary to clarify these effects.
Damiani
Carlos R
CR
Laboratory of Experimental Biochemistry, Universidade do Extremo Sul Catarinense, Criciúma, Brazil.
Benetton
César A F
CA
Stoffel
Cristhopher
C
Bardini
Katrine C
KC
Cardoso
Vilson H
VH
Di Giunta
Gabriela
G
Pinho
Ricardo A
RA
Dal-Pizzol
Felipe
F
Streck
Emilio L
EL
D000111:Acetylcysteine / Q000494:pharmacology* / Q000627:therapeutic use; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology* / Q000627:therapeutic use; D000975:Antioxidants / Q000494:pharmacology* / Q000627:therapeutic use; D003093:Colitis, Ulcerative / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D003106:Colon / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism / Q000473:pathology; D003676:Deferoxamine / Q000494:pharmacology* / Q000627:therapeutic use; D016264:Dextran Sulfate; D004195:Disease Models, Animal; D042963:Electron Transport Complex II / Q000378:metabolism; D003576:Electron Transport Complex IV / Q000378:metabolism; D005765:Gastrointestinal Agents / Q000494:pharmacology* / Q000627:therapeutic use; D007958:Leukocyte Count; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D008928:Mitochondria / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D051381:Rats; D017208:Rats, Wistar; D013385:Succinate Dehydrogenase / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
D000893:Anti-Inflammatory Agents; D000975:Antioxidants; D005765:Gastrointestinal Agents; D017392:Thiobarbituric Acid Reactive Substances; D016264:Dextran Sulfate; D042963:Electron Transport Complex II; D013385:Succinate Dehydrogenase; D003576:Electron Transport Complex IV; D003676:Deferoxamine; D000111:Acetylcysteine