摘要
AIM: Trace elements (TE) metabolism is altered in inflammatory bowel diseases. TE (zinc and copper) are constituents of antioxidant enzymes. Iron is involved in the pathogenesis of chronic inflammation. The aim was to evaluate zinc and copper status and the effects of iron manipulation in experimental colitis.METHODS: Twenty-four male Sprague-Dawley rats were divided into four groups: standard diet, iron-deprived diet,iron-supplemented diet, and sham-treated controls.Macroscopic damage was scored. DNA adducts were measured in the colon. Liver and colonic concentration of TE were measured.RESULTS: Macroscopic damage was reduced in irondeprived groups and increased in iron-supplemented rats.Damage to the DNA was reduced in iron-deprived groups and increased in iron-supplemented groups. Liver and colonic iron concentrations were reduced in iron-deprived and increased in iron-supplemented rats. Liver zinc concentration was reduced after supplementation whereas colonic levels were similar in controls and treated rats. Liver copper concentration was reduced in all the colitic groups except in the iron-supplemented group whereas colonic concentration was increased in iron-deprived rats.CONCLUSION: Iron deprivation diminishes the severity of DNBS colitis while supplementation worsens colitis. Zinc and copper status are modified by iron manipulation.
AIM： Trace elements （TE） metabolism is altered in inflammatory bowel diseases, TE （zinc and copper） are constituents of antioxidant enzymes. Iron is involved in the pathogenesis of chronic inflammation, The aim was to evaluate zinc and copper status and the effects of iron manipulation in experimental colitis.
METHODS： Twenty-four male Sprague-Dawley rats were divided into four groups： standard diet, iron-deprived diet, iron-supplemented diet, and sham-treated controls. Macroscopic damage was scored. DNA adducts were measured in the colon. Liver and colonic concentration of TE were measured.
RESULTS： Macroscopic damage was reduced in iron-deprived groups and increased in iron-supplemented rats. Damage to the DNA was reduced in iron-deprived groups and increased in iron-supplemented groups. Liver and colonic iron concentrations were reduced in iron-deprived and increased in iron-supplemented rats. Liver zinc concentration was reduced after supplementation whereas colonic levels were similar in controls and treated rats. Liver copper concentration was reduced in all the colitic groups except in the iron-supplemented group whereas colonic concentration was increased in iron-deprived rats.
CONCLUSION： Iron deprivation diminishes the severity of DNBS colitis while supplementation worsens colitis. Zinc and copper status are modified by iron manipulation.
基金
Supported by the MIUR 60% 2000
