beta-carotene and Colitis

Supplementation of 5-aminosalicylic acid (5-ASA) and of iron are among the principal therapies in patients with inflammatory bowel disease. Therapeutic iron, as well as heme iron from chronic mucosal bleeding, can increase iron-mediated oxidative stress in colitis. This study was designed to examine the influence of iron supplementation on histological expression and oxidative status relative to 5-ASA treatment and antioxidant treatment.. Colitis was induced using the iodoacetamide rat model, and rats were divided into different dietary groups of 6 rats each: 1, normal chow diet (control); 2, diet supplemented with iron; 3, iron supplementation and lycopene; 4, iron and Beta-carotene; 5, 5-ASA; 6, 5-ASA and lycopene; 7, 5-ASA and iron; 8, 5-ASA, iron, and lycopene. The animals were killed after 3 days and the weight of the ulcerated area recorded. Mucosal specimens were histologically evaluated. Myeloperoxidase (MPO) was measured to evaluate inflammatory status (U/g). Malondialdehyde (MDA) was measured in colonic tissue ( micro mol/g) and superoxide dismutase (SOD) in erythrocytes to assess the degree of tissue oxidative stress.. Significantly more severe colitis, including necrosis, ulceration, and hemorrhage, was seen in colonic biopsies of rats with colitis when iron was supplemented. This pathology was attenuated when iron was given in combination with 5-ASA and/or lycopene. There was no significant benefit from adding Beta-carotene.. Iron supplementation can amplify the inflammatory response and subsequent mucosal damage in a rat model of colitis. We suggest that the resultant oxidative stress generated by iron supplementation leads to the extension and propagation of crypt abscesses, either through direct membrane disruption by lipid peroxidation or through the generation of secondary toxic oxidants. Simultaneous treatment with 5-ASA and/or lycopene minimizes the potential hazard of iron. Therefore, we suggest giving iron supplementation with 5-ASA or lycopene or both.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Antioxidants; beta Carotene; Carotenoids; Colitis; Disease Models, Animal; Iron; Lipid Peroxidation; Lycopene; Male; Mesalamine; Oxidative Stress; Peroxidase; Rats; Rats, Wistar

The aim of this study was to examine the influence of lycopene and beta-carotene on the inflammatory status in a rat model of induced-colitis. Using the 2,4,6-trinitrobenzenesulfonic acid (TNBS) model, colitis was induced in thirty-two male Wistar rats divided into four groups. Each group received a different diet regime in parallel with the induction of colitis and was sacrificed after seven days. The groups were divided as follows: Group A: without colitis and fed a normal chow diet; Group B: induced with colitis and fed a diet supplemented with lycopene (300 micrograms/rat/day); Group C: induced with colitis and fed a diet supplemented with beta-carotene (300 micrograms/rat/day); Group D: induced with colitis and fed a normal chow diet. Colonic inflammation following TNBS induction was characterized by hemorrhagic necrosis and fibrosis of the mucosa, increased colonic wall thickness, infiltration of inflammatory cells, and increased myeloperoxidase (MPO) activity. Supplementation of lycopene in the diet had a beneficial effect on the various macroscopic parameters examined including: colonic thickness, colon weight, and total area of inflammation. Furthermore, the level of myeloperoxidase (MPO) was significantly lower in the lycopene-treated group compared to the control group. In terms of microscopic changes, a more attenuated inflammatory reaction was observed in the group fed a diet supplemented with lycopene. No significant effect was noted in the beta-carotene-supplemented group. Therefore, we propose that the dietary supplementation of lycopene may be an effective approach for reducing the level of oxidative stress and improving the inflammatory status of colitis.

Topics: Analysis of Variance; Animals; Antioxidants; beta Carotene; Carotenoids; Colitis; Colon; Inflammation; Lycopene; Male; Peroxidase; Rats; Rats, Wistar; Trinitrobenzenesulfonic Acid