Reifen, R., School of Nutritional Sciences, Hebrew University of Jerusalem, Rehovot, Israel
Nur, T., School of Nutritional Sciences, Hebrew University of Jerusalem, Rehovot, Israel
Ghebermeskel, K., Institute of Brain Chemistry and Human Nutrition, University of North London, London, United Kingdom
Zaiger, G., School of Nutritional Sciences, Hebrew University of Jerusalem, Rehovot, Israel
Urizky, R., School of Nutritional Sciences, Hebrew University of Jerusalem, Rehovot, Israel
Pines, M., The Volcani Center, Agricultural Research Organization, Bet Dagan, Israel

Inflammatory bowel disease is characterized by oxidative stress, inflammation and tissue damage. Vitamin A is an antioxidant, a regulator of epithelial proliferation and differentiation and vital for optimal immune function. To investigate the effect of vitamin A on the course of colitis, it was induced by administration of trinitrobenzene sulfonic acid (TNBS) into the colons of rats fed for 7 wk vitamin A-deficient (VAD), sufficient (VAS) or supplemented (VASUP) diet, or VAS pair-fed (PF) to the VAD rats. Inflammation and fibrosis were examined by hematoxin and eosin, and Sirius red staining. Activation of nuclear factor-κB (NF-κB) and oxidative stress were determined by electrophoretic mobility shift and plasma malondialdehyde (MDA) and RBC Cu/Zn-superoxide dismutase activity, respectively. Vitamin A deficiency in the noncolitic rats impaired food consumption and weight gain (P < 0.05) and increased plasma MDA, (P = 0.01) activity of NF-κB (P < 0.05) and deposition of collagen in the colon. Our data suggest that vitamin A deficiency induces colonic inflammation. Colitis is amplified by deficiency and ameliorated by supplementation of the vitamin. These findings have implications for the management of inflammatory bowel disease.