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1 Institute of Medical Pharmacology II,
University of Pavia, 27100 Pavia, Italy.
2 A. Cesaris Institute of Industrial Chemistry, I-20071
Casalpusterlengo, Milano, Italy.
3 Camillo Golgi Institute of General Pathology, Centro di
Ricerca Prevenzione Tumori, University of Pavia, I-27100 Pavia,
Italy.
Summary
Beta-carotene (BC) storage was measured in liver and its subcellular fractions (plasma membranes, mitochondria, microsomes and nuclei) of rats fed BC added to diet. The BC supplementation dose was about 350 mg/week/rat. After 15 weeks of this supplementation, rats were killed and their livers were immediately excised and processed to obtain total liver tissue and its subcellular fractions. Their BC contents were measured by HPLC as pmols/mg protein. Intact BC was found to be stored in all the above subcellular fractions, thus showing that BC is probably taken up by liver cell lipid moiety. Interestingly, the mean BC concentrations in plasma membranes and mitochondria were significantly higher than that in total liver tissue. Our data confirmed that rodents are a good animal model for the study of BC metabolism and its effects on several pathologies, and cancer prevention and treatment in humans in spite of the fact that rodents are classified as white-fat animals because of their poor BC absorption and storage in fat and blood plasma, whereas humans are classified as yellow-fat organisms because of their opposite behavior in BC uptake and organ distribution.
Keywords
Beta-carotene, rat liver, subcellular fractions, storage
International Journal for Vitamin and Nutrition Research,
Band 69, 1999, Heft 1 © Verlag Hans Huber AG, Bern
1 Graduate Institute of Nutrition and
Health Science, Taipei Medical College, Taipei 110, Taiwan,
R.O.C.
2 Department of Nutritional Sciences, University of
California, Berkeley, CA 94720-3104
Summary
This study was carried out to choose between two hypotheses with respect to the regulation of b-carotene (BC) conversion to retinol in the whole animal: uptake of BC into intestinal mucosa is limited by saturation of an intestinal receptor; or the conversion to retinol is limited by saturation of the conversion enzyme(s). Groups of rats were given five different dose levels of labeled BC by stomach tube. Labeled and total BC and retinol were isolated from tissues and intestinal contents after 4 h. Results showed a positive linear relationship between BC in the intestinal wall and the dose administered, with no saturation level up to 1440 mg administered. Per cent formation of newly formed retinol from newly absorbed (i.e., labeled) BC was 20-26% of the three lower dose groups, 10% for the highest dose. No retinyl esters could be detected in the intestine. Most of the administered BC was in the intestinal contents, about 100-times more than in the intestinal wall and mucosa. Newly formed retinol in plasma was about 10-times that in liver. Small amounts of newly absorbed BC were found in liver, but no labeled retinyl esters. These results suggest that the absorption of BC is very inefficient; that it does not occur through an intestinal receptor; that the formation of retinol is regulated at the level of the conversion enzyme(s).
Keywords
b-Carotene, retinol, retinyl esters, intestinal wall
International Journal for Vitamin and Nutrition Research,
Band 69, 1999, Heft 1, © Verlag Hans Huber AG, Bern
Dr. B.R. Ambedkar Center for Biomedical Research,
University of Delhi, P.O. Box: 2148, Delhi 110 007, India
Summary
In the current study we report the perturbation of key enzymes of the heme metabolic pathway, i.e. d-amino levulinic acid synthase, heme oxygenase and biliverdin reductase, in vivo by administration of retinoic acid (RA) and retinoic acid in association with tin-metalloporphyrins, viz., tin-protoporphyrin (SnPP) and tin-mesoporphyrin (SnMP) in the liver, spleen, heart and lung of rats. RA at a dosing regimen of 50,000 I.U. stimulated splenic ALA-S activity, whereas co-administration of tin-metalloporphyrins with RA antagonised the RA mediated induction of ALA-S. In the other tissues viz., liver, heart and lung our results showed a diminution of ALA-S activity on RA administration, the level of repression was further attenuated when tin-metalloporphyrins were co-administered with RA. This marked suppression of ALA-S brought forth by concurrent administration of RA and tin-metalloporphyrins is suggestive of the beneficial effect of this formulation in acute attacks of porphyria, similar to heme. Furthermore, our results emphasize that the combined dosing of RA with tin-metalloporphyrins leads to a substantial decline in bilirubin levels due to a profound inhibition of HMOX in the probed tissues. The features of the combined action of RA and tin-metalloporphyrins in vivo lead to a substantial suppression of formation of the potentially toxic metabolite bilirubin, and the enhancement of disposal of the untransformed substrate (heme) of the enzyme that is inhibited. These results define some of the characteristics of a therapeutically useful formulation and represent a new therapeutic approach for the amelioration and management of hyperbilirubinemia.
Keywords
Retinoic acid, heme metabolism, d-amino levulinic acid synthase, heme oxygenase, biliverdin reductase, metalloporphyrins, hyperbilirubinemia, acute intermittent porphyria
International Journal for Vitamin and Nutrition Research,
Band 69, 1999, Heft 1, © Verlag Hans Huber AG, Bern
Department of Clinical Chemistry, Hoshi College of
Pharmacy, Tokyo 142, Japan
Summary
The comparative effects of vitamin K2 and vitamin E on aortic calcium (Ca) and inorganic phosphorus (P) levels in the aorta and the elastin fraction (fr.) were investigated in male rats after experimental arteriosclerosis was induced by vitamin D2 with atherogenic diet. Both vitamin K2 (100 mg/kg b.w.) and vitamin E (40 mg/kg b.w.) inhibited the increase of Ca and P in the aorta and the elastin fr. from the arteriosclerotic rats. Vitamin K2 (50 mg/kg b.w.) also suppressed the deposition of Ca and P in the aorta, but there was no change due to vitamin K3 or geranylgeraniol (side chain of vitamin K2) administration. Both vitamin K2 and vitamin E showed lipid radical scavenging activity in the in vitro experiment. However, neither vitamin K3 nor geranylgeraniol exhibited anti-arteriosclerotic or radical scavenging activity under the above experimental conditions. It is suggested that vitamin K2 and vitamin E promoted an antiarteriosclerotic effect by radical scavenging activity. These actions of vitamin K2 are required in the structure of 2-methylnaphthoquinone and its side chain (geranylgeraniol).
Keywords
Vitamin K2, vitamin E, vitamin D2, arteriosclerosis, calcification, calcinosis
International Journal for Vitamin and Nutrition Research,
Band 69, 1999, Heft 1, © Verlag Hans Huber AG, Bern
Department of Hygiene, Hyogo College of Medicine, 1-1
Mukogawa-cho, Nishinomiya, Hyogo 663, Japan
Summary
To investigate the effects of vitamin K (VK) on pancreatic function, intravenous glucose tolerance tests were performed in rats fed with and without low VK diet (inclucing less than 20% required vitamin K1). Plasma glucose and immuno-reactive insulin (IRI) were determined. It was found that at 0 min., plasma glucose and IRI levels in low VK group were slightly less than in the control (glucose, 204.5 ± 21.7 vs. 229 ± 19.6 mg/dl, IRI, 6.6 ± 1.3 vs. 9.3 ± 1.8 ng/ml mean ± SEM). At 3 min. after glucose administration, plasma glucose was higher (391.8 ± 25.6 vs. 371.8 ± 18.7 mg/dl) and IRI, lower (11.8 ± 2.1 vs. 18.2 ± 3.6 ng/ml) in the low VK group. The disappearance rate of plasma glucose in the low VK group at 5-10 min. was significantly less than in the control (6.7 ± 2.2 vs. 11.9 ± 1.8 mg/ dl/min.). Incremental IRI area at 0 to 5 min. in the low VK group is less than in the control (15.2 ± 4.4 vs. 25.0 ± 9.1 ng/ml/min.), but at 5-60 min. and 0-60 min., it was found to be significantly higher compared to the control (210.3 ± 55.2 vs. 32.5 ± 47.1 ng/ml/min. at 5-60 min.). Dietary low VK intake would thus appear to induce a tendency of poor early insulin response, and late hyperinsulinemia to the glucose load in rats.
Keywords
Vitamin K, deficiency, glucose tolerance test, insulin, pancreas, rats
International Journal for Vitamin and Nutrition Research,
Band 69, 1999, Heft 1, © Verlag Hans Huber AG, Bern
Departments of Animal and Poultry Science, University
of Saskatchewan, Saskatoon, SK, Canada S7N 5B5
Summary
The response of broiler chickens to a wide range of dietary
supplementation of thiamine to broiler breeder diet was studied in
order to understand the effects of maternal thiamine nutrition on the
status of thiamine indices in the offspring. Thiamine, and thiamine
pyrophosphate (TPP) content, and a-ketoglutarate dehydrogenase (KGDH)
activity were measured in hearts from 20 day old chicken embryos and
from chickens at 1, 7, 14, and 21 days of age and in blood at 21 days
of age.
Total thiamine content in the heart of day old chicks was higher in
comparison to 20 day old embryos. Maternal supplementation of
thiamine increased heart thiamine in the offspring (p < 0.001),
and increased the activity of KGDH in the hearts of day old chicks (p
< 0.001), but not in the embryo. The TPP content in the heart
increased in response to both maternal and offspring thiamine
supplementation (p < 0.001), however the effect of broiler
thiamine supplementation was largely independent from the maternal
effect. The effect of maternal thiamine nutrition on the offspring's
heart KGDH activity was apparent, but the responses to broiler
supplementation were dependent largely on the maternal effect. Blood
TPP content was not affected by maternal thiamine supplementation (p
= 0.39), but thiamine supplementation in the offspring diets
increased blood TPP (p < 0.001). Both maternal and offspring
thiamine supplementation increased blood free base thiamine content
(both p < 0.001). It is concluded from this study that maternal
thiamine nutrition affects thiamine status indices and thiamine
metabolism of the offspring.
Keywords
Thiamine, maternal, transfer, nutrition, broiler
International Journal for Vitamin and Nutrition Research,
Band 69, 1999, Heft 1, © Verlag Hans Huber AG, Bern
1 Department of Family Resources and Human
Development and
2 Department of Exercise Science and Physical Education,
Arizona State University, Tempe, AZ 85287
Summary
A placebo-controlled, depletion-repletion protocol was utilized to examine the effect of vitamin C status on substrate utilization during a 90 min walk at 50% maximal oxygen consumption (VO2max). Nine vitamin C depleted subjects (plasma vitamin C < 28 mmol/L) agreed to participate in the 5-week study (aged, 27.6 ± 2.5 years , mean ± SE; 5 females, 4 males). Subjects were apparently healthy but unaware of their vitamin C status. Prior to the experimental period, VO2max was measured using open-circuit spirometry during a graded walking protocol. Subjects ingested a placebo capsule daily during weeks 1-3 and a 500 mg vitamin C capsule daily during weeks 4-5 of the experimental study. Mean plasma vitamin C rose nearly 3-fold and mean plasma carnitine fell by nearly 20% at repletion (week 5) versus depletion (week 3). At the end of weeks 3 and 5, subjects completed a 90 minute treadmill walk at an exercise intensity of 50% VO2max. The relative contribution of fat utilized for energy during walking did not differ in the vitamin C depleted versus repleted states. However, work performed by subjects and gross efficiency during exercise increased significantly at repletion versus depletion (10% and 15%, respectively). These data indicate that vitamin C depletion is associated with reduced work efficiency during submaximal exercise.
Keywords
Vitamin C status, substrate utilization, work efficiency, exercise performance
International Journal for Vitamin and Nutrition Research,
Band 69, 1999, Heft 1, © Verlag Hans Huber AG, Bern
Dept. of Medicine, University of Toronto, Toronto,
Ontario, Canada
Summary
The ability of vitamin C supplement to influence lipid peroxidation and pulmonary function tests in healthy smokers was investigated. In this randomized double blind controlled trial, 56 smokers (S) received either 500 mg of vitamin C (C) or placebo (P) daily for 4 weeks. All completed the trial. Both groups were comparable and the number of cigarettes smoked were C: 14.2 ± 1.8 and P: 18.3 ± 2.0 pack-years. Plasma vitamin C concentrations increased significantly (p < 0.005) only in the group supplemented with vitamin C. Lipid peroxidation measured by breath pentane output (BPO) (C: 7.5± 1.4 vs P: 7.0 ± 1.3 pmol.kg-1.min-1) and plasma HPLC-separated malondialdehyde (MDA) (C: 0.58 ± 0.05 vs P: 0.47 ± 0.05 nmol.ml-1) were not significantly different between the 2 groups at baseline and did not change after four weeks of vitamin C supplementation (BPO: C: 5.3 ± 0.9 vs P: 5.5 ± 0.9 pmol.kg-1.min-1; HPLC-MDA: C: 0.50 ± 0.07 vs P: 0.42 ± 0.07 nmol.ml-1). No changes were detected in pulmonary function tests even in heavy smokers. Therefore, 4 week supplementation with 500 mg of vitamin C did not change lipid peroxidation indices and had no effect on pulmonary function tests.
Keywords
Breath pentane, antioxidant, smoking, vitamin C, lipid peroxidation
International Journal for Vitamin and Nutrition Research,
Band 69, 1999, Heft 1, © Verlag Hans Huber AG, Bern
1 Department of Physiology, School of
Pharmacy.
2 Institute of Nutrition and Food Technology, University
of Granada, E-18071 Granada, Spain.
3 Scientific Department, Nutrexpa SA, E-08013 Barcelona,
Spain
Summary
Epidemiological studies have reported that Western diets are often deficient in Mg. We investigated the ability of a cocoa-derived product, used in some European countries as a dietary complement added to milk, to aid recovery from chronic Mg deficiency in rats. The animals were divided into three groups, each of which received a different amount of dietary Mg. Rats in the Mg-deficient (D) group received an Mg-deficient diet (0.225 g Mg/kg food) during 8 weeks. In the cocoa-supplement group (D+ CC), the rats consumed the Mg-deficient diet for 5 weeks, and were then switched for 3 further weeks to the same diet supplemented with 3% (wt/wt) cocoa product, so that the Mg content of the diet was 0.27 g/kg food. Rats in the control group (C) were given the same diet as in group D, except that the amount of Mg was 0.56 g Mg/kg food. We measured the concentration of Mg, Ca and P from ten rats in plasma, whole blood, skeletal muscle, heart, kidney and femur in rats that were fed the diets for 35, 42, 49 or 56 days. In animal fed the cocoa-supplemented diet (D + CC) significant improvements were found between days 35 and 56 in the alterations in Mg, Ca and P caused by Mg deficiency in all tissues studied. On day 56, kidney and bone concentrations of Mg and Ca had returned to normal. Our findings show that the habitual use of the cocoa product as a dietary supplement favors correction of the negative effects of long-term feeding with a diet moderately deficient in Mg.
Keywords
Cocoa, Mg deficiency, calcium, phosphorus
International Journal for Vitamin and Nutrition Research,
Band 69, 1999, Heft 1, © Verlag Hans Huber AG, Bern
Facultad de Ciencias Veterinarias, Universidad
Nacional de La Plata CC296, 1900 La Plata, Argentina
Summary
Studies were carried out to determine the effect of rat liver cytosolic protein enriched in fatty acid binding protein on the microsomal and mitochondrial ascorbate-Fe++ lipid peroxidation and to determine how vitamin A influences the inhibitory effect of this protein in the peroxidation process. The inhibition of light emission (maximal induced chemiluminescence) by the fatty acid binding protein containing fraction was protein concentration dependent. The inhibition of chemiluminescence produced by the addition of cytosolic protein on rat liver microsomes or mitochondria was more evident when the soluble protein obtained from the vitamin A treated group was used. The results indicated that vitamin A plays a role in protecting rat liver microsomes and mitochondria against the harmful effect of lipid peroxidation.
Keywords
Lipid peroxidation, microsomes, mitochondria, vitamin A, liver
International Journal for Vitamin and Nutrition Research,
Band 69, 1999, Heft 1, © Verlag Hans Huber AG, Bern