pharmacological chelation / colitis

2004-04-08 03:24:39 AM
Int J Colorectal Dis. 2004 Apr 6 [Epub ahead of print] Related Articles, Links
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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