Erythrocyte antioxidant enzymes and plasma antioxidant vitamins in Sudanese women with pre-eclampsia.

This case-control study was conducted in Khartoum hospital, Sudan to investigate the levels of antioxidant enzymes (glutathione peroxidase, catalase and superoxide dismutase) in erythrocytes and plasma antioxidant vitamins (retinol and alpha-tocopherol) in Sudanese women with pre-eclampsia (37), in comparison with well-matched pregnant controls women with normal pregnancy (38). Enzymes were measured using ELISA and vitamins were measured using HPLC. There were no significant differences in the levels of these three antioxidant enzymes in pre-eclamptic women compared with the controls. Women with mild pre-eclampsia (diastolic blood pressure, DBP < 110) have slightly higher levels of erythrocyte glutathione peroxidase, and lower levels of catalase and superoxide dismutase compared with women with severe pre-eclampsia (DBP > or = 110). A significantly negative correlation was observed between the levels of glutathione peroxidase and DBP, r = -0.371, p = 0.02. There was no significant correlation between catalase (r = -0.033, p = 0.840) or superoxide dismutase levels (r = 0.067, p = 0.6) and DBP. While retinol levels were not different, levels of alpha-tocopherol were significantly higher in women with pre-eclampsia than the control group, p = 0.026. The plasma levels of both vitamins were not statistically significantly different when women with mild and severe pre-eclampsia were compared.

Vitamin A deficiency reduces liver and colon docosahexaenoic acid levels in rats fed high linoleic and low alpha-linolenic acid diet.

Studies indicate that the transcription factor peroxisome proliferator-activated receptors (PPARs) regulate the activity of delta-6 and -5 desaturases and several key enzymes of peroxisomal beta-oxidation, including acyl-CoA oxidase. These enzymes are vital for the synthesis of docosahexaenoic (22:6 omega 3; DHA) and osbond (22:5 omega 6, OA) acids. An activated PPAR must form a hetrodimer with the obligate cofactor retinoid X receptor (RXR) to interact with a peroxisome proliferator responsive element (PPRE) of a target gene and to regulate transcriptional expression. The vitamin A metabolite, 9-cis retinoic acid, is the most potent ligand of RXR. We have tested the possibility that deficiency of vitamin A would compromise tissue levels of both DHA and OA in rats. Two groups of male Wistar rats were randomly distributed to receive vitamin A deficient (VAD) or sufficient (VAS) diet. After seven weeks of feeding, the rats were killed and colon and liver tissues removed for the analysis of fatty acids and antioxidant status. The VAD compared to the VAS rats had elevated levels of arachidonic (AA, P<0.001), adrenic acid (22:4 omega 6, P<0.005) and OA (P<0.0001) and reduced proportions of eicosapentaenoic (EPA, docosapentaenoic (DPA), DHA and total omega 3 fatty (P<0.0001) in colon choline phosphoglycerides (CPG). Similarly, liver CPG of the VAD rats had higher AA and adrenic acid and OA (P<0.0001), and lower EPA, DPA and DHA (P<0.0001) than the VAS rats. There was a similar fatty acid pattern in ethanolamine phosphoglycerides of the colon and liver tissues. These differences could not be explained by the conventional microsomal-peroxisomal pathway of the synthesis of the long-chain omega 6 and omega 3 polyunsaturated fatty acids. We postulate that deficiency of dietary vitamin A and the consequential depletion of retinoids inhibits DHA, and enhances OA, synthesis by differential effects on the independent synthetic pathways of the two fatty acids in the mitochondria. Various studies have documented that both DHA and vitamin A are vital for optimal visual and neural development and function. There is a need for further investigations to elucidate how vitamin A deficiency reduces membrane DHA level, and to delineate the synergistic effect of the two nutrients on vision, learning and memory.

Vitamin A deficiency exacerbates inflammation in a rat model of colitis through activation of nuclear factor-kappaB and collagen formation.

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.

Vitamin A deficiency interferes with proliferation and maturation of cells in the chicken small intestine.

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.

Effect of vitamin A on small intestinal brush border enzymes in a rat.

Weanling male rats fed a vitamin A deficient (VAD) diet were compared with rats fed the same diet supplemented with vitamin A. Half of the VAD group was repleted with vitamin A at the age of 70 days. There was a decline in weight in the VAD group after 45 days. Serum and liver retinol concentrations were negligible in the VAD groups at 70 days of age. These levels returned to normal in the repleted group within 20 days of supplementation. Histological observations in the intestinal tissues of the experimental animals exhibited reduced villus height (p < 0.05) compared with the vitamin A supplemented group (VAS), reduced number of mucous secreting goblet cells and total enterocytes. In addition, a significantly higher number of proliferating cells was found along the crypt. Disaccharidases (sucrase and maltase), peptidases (gamma GT) and alkaline phosphatase activities were markedly lower along the brush border (p < 0.05) in the VAD group compared to the VAS group. We also determined the total DNA, RNA and protein in the jejunal tissues per 0.1 mg/tissue in both groups. The RNA production per cell in the VAD groups was notably lower than that of the controls (p < 0.05). Our observation indicates that brush border enzyme levels are altered in animals with vitamin A deficiency, and that phenomenon is augmented when calculated per single cell. This change may be attributed to direct effects of vitamin A on the rate of proliferation and differentiation of the epithelial tissue along the jejunum rather than to gross structural changes along the small intestine.

Vitamin A deficiency induces morphometric changes and decreased functionality in chicken small intestine.

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.