No abstract

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-kappaB (NF-kappaB) 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-kappaB (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.

1. The effect of vitamin A on the small intestine was examined in vitamin-A-deficient meat-type chickens. 2. Maturation and activity of the small intestinal cells were assayed by detection of proliferating cells with proliferating cells nuclear antigen, goblet cells with Alcian blue, mature cells with alkaline phosphatase and extent of RNA expression with dot blot analysis. 3. Vitamin A deficiency caused hyperproliferation of enterocytes, a decrease in the number of goblet cells, decreased alkaline phosphatase activity and decreased expression of 2 brush-border enzymes. 4. Our findings suggest that the absence of vitamin A interferes with the normal growth rate in chickens because it influences functionality of the small intestine by altering proliferation and maturation of cells in the small intestinal mucosa.

The effect of vitamin A on chicken intestinal mucosal morphology and functionality was tested in relation to severe and mild vitamin A deficiency and vitamin A repletion. Compared with rats and mice, chickens have a very quick response to a deficient dietary intake. Severe vitamin A deficiency altered the small intestine of chickens at both the biochemical and the morphological levels. It caused the loss of mucosal protein, reduced villus height and crypt depth and diminished activities of disaccharidases, transpeptidase and alkaline phosphate (EC 3.1.3.1). The ratios RNA-.DNA, RNA:protein and protein:DNA, and the DNA concentrations in 1 g intestinal tissue, together with morphological measurements, provided knowledge about the pattern of lesion. The results indicated that (1) lack of vitamin A influenced cellular hyperplasia as it caused an increase in DNA content and in the number of enterocytes per villus; (2) lack of vitamin A influenced cellular hypertrophy as it decreased the protein:DNA ratio. There was no difference in mucosal enzyme activity between the two deficient groups. The repletion group exhibited a remarkable increase in mucosal enzyme activity only 4 d after switching to the control diet. The evidence presented in our paper suggests that the low vitamin A supply interferes with the normal activity of chicken intestinal mucosa as it influences the processes of proliferation and maturation of enterocytes.

No abstract