Int J Colorectal Dis. 2004 Apr 6 [Epub ahead of print]
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Effects of iron deprivation or chelation on DNA damage in
experimental colitis.
Barollo M, D'Inca R, Scarpa M, Medici V, Cardin R, Fries W,
Angriman I, Sturniolo GC.
Department of Surgical and Gastroenterological
Sciences, University of Padua, Via Giustiniani 2,
Italy, 35128, Padova.
BACKGROUND AND AIMS. In inflammatory bowel diseases iron
contributes to the formation of DNA adducts through the
production of hydroxyl radicals. The aim of our study was to
evaluate the effects of dietary or pharmacological iron
deprivation in an experimental model of colitis in the rat
and its potential protective effect against DNA damage.
METHODS. Colitis was induced in rats by intracolonic
instillation of dinitrobenzene sulphonic acid. Rats were
assigned to an iron-deprived diet or to desferrioxamine
preceding the induction of colitis. The severity of colitis
was assessed by the presence of bloody diarrhea, colonic
macroscopic damage score, body-weight variations and the
amount of DNA colonic adducts. Hepatic and colonic iron
concentrations were measured. RESULTS. Treated rats
experienced less diarrhea and did not lose weight in
comparison to untreated animals. The macroscopic damage
score was significantly reduced in the iron-deprived diet
for the 5-week group ( P=0.03). Liver and colonic iron
levels were significantly more reduced in the iron-deprived
groups than in the standard diet group ( P<0.03 and P<0.01
after a 3- and 5-week iron-deprived diet, respectively). DNA
adduct formation was significantly reduced in the groups
deprived of iron for 5 weeks ( P<0.001) or treated with
desferrioxamine ( P<0.01). CONCLUSIONS. The degree of
colitis caused by DNBS is macroscopically improved by
dietary iron deprivation and to a lesser extent by
pharmacological chelation; genomic damage is reduced by
dietary iron deprivation or chelation, and this may have
clinical implications on cancer prevention.
PMID: 15067556 [PubMed - as supplied by publisher]
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