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Results for “zinc deficiency”

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At least 19 recordsLinked to original sources
PubMed1975

Alteration of porcine skin acid mucopolysaccharides in zinc deficiency.

Zinc deficiency is overtly manifested as a dermatitis in swine; therefore, the purpose of this investigation was to determine possible zinc-related alterations in the metabolism of the skin acid mucopolysaccharides (AMPs). Eighteen 4-week-old Yorkshire pigs were randomly allocated to one of three dietary treatments. Six animals were fed a semipurified, zinc-deficient, basal diet containing 20 ppm zinc. Six animals served as pair-fed controls and were fed the basal diet supplemented with 90 ppm zinc as zinc carbonate. The remaining six animals were fed the zinc-supplemented diet on and ad libitum schedule. All animals were killed after 36 days when overt deficiency symptoms were apparent in those animals fed 20 ppm zinc. Skin AMPs were isolated. Total hexosamine and galactosamine indicated no alteration in total AMPs. Fractionation of total AMPs into consitituent sulfated and nonsulfated components revealed a significant increase in hyaluronic acid. No statistical difference in sulfated AMPs was found in skin from deficient and pair-fed animals, which was in accord with an in vitro sulfur-35 uptake study.

Animal Nutritional Physiological Phenomena↗
PubMed1991

Recurrent aphthous ulceration with zinc deficiency and cellular immune deficiency.

Zinc deficiency (serum zinc level 65 micrograms/dl) and cellular immune deficiency (confirmed by lymphoblastic transformation assay) were found in a 15-year-old boy who had had recurrent aphthous ulceration for 6 years. Despite the previous therapy (orally administered steroid, isoprinosine, interferon, lysozyme, and local treatment), the ulcers recurred monthly. After 3 months of zinc therapy (50 mg zinc sulfate orally three times daily) the aphthae disappeared and did not reappear for 1 year. The lymphoblastic transformation activity and serum zinc levels were also normalized with this treatment.

Child↗
PubMed1990

Zinc deficiency and zinc repletion: effect on the response of rats to infection with Trichinella spiralis.

The expulsion of a primary infection of Trichinella spiralis was studied in rats fed diets containing (per kg diet) either 3 mg Zn [zinc deficient (Zn-)] or 40 mg Zn [zinc adequate (Zn+)]. A dose of 2000 muscle larvae (ML) impaired weight gain (mg/g body wt) in all groups compared with uninfected controls [eg, 0-7 d postinfection (dpi): infected Zn-, -105 +/- 10 (means +/- SEM); uninfected Zn-, 54 +/- 19 (p less than 0.001)]. In a study with 20.5 ML/g body wt, some Zn- rats were transferred at the time of infection to the zinc-adequate diet. [This was the zinc-repleted group (ZnR).] Both groups retained a group of pair-fed controls (Zn-PF and ZnRPF). The percentage dose established at 7 dpi was similar in all groups (32.5-39.3%) but at 13 dpi recoveries were 19.4 +/- 2.2% for Zn-, 0.1 +/- 0.1% for Zn-PF, 1.6 +/- 0.9% for ZnR, 0.6 +/- 0.2% for ZnRPF, and 4.1 +/- 2.2% for Zn+ (p less than 0.001). Up to 13 dpi, all groups except ZnR lost weight. These results show that zinc deficiency impairs the expulsion of T spiralis in rats.

Animals↗
PubMed1992

Symptomatic zinc deficiency in experimental zinc deprivation.

An evaluation of indices of poor zinc status was undertaken in five male subjects in whom dietary zinc intake was reduced from 85 mumol d-1 in an initial phase of the study to 14 mumol d-1. One of the subjects developed features consistent with zinc deficiency after receiving the low zinc diet for 12 days. These features included retroauricular acneform macullo-papular lesions on the face, neck, and shoulders and reductions in plasma zinc, red blood cell zinc, neutrophil zinc and plasma alkaline phosphatase activity. Alcohol induced hepatitis, which was suspected in this subject, may have caused a predisposition to altered zinc metabolism and possible zinc deficiency which was exacerbated by subsequent zinc deprivation. The report supports the value of neutrophil zinc concentration as an indicator of poor zinc status.

Adult↗
PubMed1977

Effects of zinc deficiency and zinc repletion during pregnancy on parturition in two strains of rats.

The effects on parturition of a low zinc diet during pregnancy and of three levels of zinc repletion late in pregnancy were compared in two strains of rats, Sprague Dawley and Long Evans. Long Evans rats had a higher hematocrit and higher plasma protein levels than did Sprague Dawley rats. Long Evans rats also had heavier mammary glands and tended to deliver somewhat later than the Sprague Dawley rats. Weight gains during pregnancy and weights of the liver, spleen, adrenal glands, and pups did not vary between strains. No differences were detectable in the degree of stress at parturition between the unsupplemented females of the two strains. Injection of 300, 600, or 900 microgram zinc on day 18 of pregnancy increased female weight gains, pup weight, and spleen and mammary gland weights, and decreased hematocrit level. Three females in the unsupplemented groups died about the expected time of parturition; none died in the supplemented groups. Although there were some differences between the strains, the effects of a low zinc diet and the requirement for zinc for normal parturition were the same in the two strains. An injection of 900 microgram zinc on day 18 resulted in normal parturition in both strains.

Adrenal Glands↗
PubMed1977

Implications of the inhibition of animal tumors by dietary zinc deficiency.

Because zinc is an essential nutrient for tissue growth, cellular division, protein synthesis, and DNA and RNA replication, it also ought to play a critical role in the growth of tumors. To test this thesis, a series of experiments were performed to test the effect of zinc deficiency on the lethality of a variety of solid and ascites tumors in mice and rats. Specifically, the following models were tested: Walker 256 carcinosarcomas, solid and ascites forms in rats; three mouse leukemias (L5178yf, L1210, and P388) in CDF, male mice; and Lewis lung carcinoma in C57BI/6 male mice. Rats receiving a zinc-deficient diet showed marked reduction of tumor growth, both of solid or ascites models, and this was accompanied by striking increase in survival. Survival of mice with transplanted leukemia was also significantly prolonged by zinc deficiency. In addition, growth of the Lewis lung carcinoma was inhibited, but the survival through increased, was probably limited by the adverse effects of zinc deficiency. The results suggest that tumor inhibition is a general effect of zinc deficiency, irrespective of cell type, cell growth rate, species, or site of growth. There are numerous potential applications of zinc metabolism to the diagnosis, therapy, and understanding of cancer.

Animals↗
PubMed1978

Regeneration of T-cell helper function in zinc-deficient adult mice.

Diets deficient in zinc cause rapid atrophy of the thymus and loss of T-cell helper function in the young adult A/J mouse. Because zinc deficiency, as well as other nutritional deficiences, causes extensive damage to the immune system, the question arose as to whether zinc-deficient mice could repair the thymus and fully regenerate T-cell helper function if returned to diets containing adequate amounts of zinc. Five-week-old A/J female mice were fed either a zinc-deficient (<1 mug of Zn per g) or a zinc-adequate (50 mug of Zn per g) diet for 31 days. Histological examination of thymuses from the zinc-deficient mice revealed that the cortex was preferentially involuted and the thymus was about one-third of normal size. The direct plaque-forming cells produced per mouse spleen in response to immunization with sheep erythrocytes was 34% of normal; indirect plaque-forming cells were 18% of normal (Jerne plaque assay). After the deficient mice had been fed a zinc-adequate diet for 1 week, their response was nearly normal, except that the indirect response was 68% of controls; in this same period, the thymuses of these mice had quadrupled in size and exhibited a greatly enlarged cortex repopulated with immature thymocytes. By 2 weeks, the thymuses of the previously zinc-deficient mice were normal in size and appearance; however, there was a slight increases in numbers of indirect plaque-forming cells. By 4 weeks, the thymus weights, direct and indirect plaque-forming cell counts, and secondary response of the previously deficient mice were normal. Mice that were nearly athymic after 45 days of dietary zinc deficiency were also able to fully reconstruct the thymus and regenerate T-cell helper function. The data show that the zinc-deficient young adult mouse has the capacity to fully restore the T-cell-dependent antibody-mediated responses upon nutritional repletion.

Animals↗
PubMed1979

Mesenteric lymph proteins in zinc-deficient rats.

Because zinc apparently has a role in amino acid utilization, we have studied possible consequences of zinc deficiency on the metabolism of amino acids in the intestinal mucosa by examining proteins transported via the mesenteric lymph in zinc-deficient and zinc-supplemented rats. Mesenteric lymph ducts were cannulated under pentobarbital, and on recovery the animals were fed [14C]leucine as a pulse dose by duodenal infusion. Protein output via intestinal lymph was generally constant over the infusion range studied. Total lymph protein output was not affected by zinc deficiency or supplementation. The electrophoretic pattern of the lymph protein revealed a protein band that migrated with the alpha2-globulins coincidental to zinc deficiency; the band disappeared after zinc supplementation. There was an inverse zinc-copper relationship in mesenteric lymph; duodenal infusion of zinc to deficient rats was followed by a decrease in lymph copper. Deficiency of zinc seems to have little influence on the quantitative aspect of protein carried in mesenteric lymph but seems to be involved with the nature of the protein in this body fluid.

Animals↗
PubMedDate not supplied

Studies on iron deficiency anemia, rickets and zinc deficiency and their prevention among Chinese preschool children.

The incidence of iron deficiency anemia, rickets, and zinc deficiency is very high in Chinese preschool children and a method for prevention is urgently needed. From our studies, it can be seen that a soft drink powder is a convenient vehicle for the supplementation of iron, zinc, calcium, vitamin D, riboflavin, and ascorbic acid. Table salt is also a good, low-cost carrier for iron and zinc, and cow's milk can only be used for the enrichment of vitamins A and D. In our study the therapeutic dose of iron was lower than 3 mg/kg body weight recommended by the WHO Expert Committee. As ascorbic acid can enhance the absorption of iron in the body, so 300 mg vitamin C was added to 100 g of soft drink powder containing 100 mg of elemental iron. Ten g of powder is not only enough for the prevention of iron deficiency anemia but it can also cure iron deficiency anemia within 3 months. One hundred mg of iron in 100 g of table salt is an adequate level, because an adult or a child taking 10 or 5 g of salt will receive 10 and 5 mg of elemental iron respectively. This dosage is adequate for the prevention of anemia. From our results, 10 mg of zinc daily is enough for the prevention and treatment of zinc deficiency in preschool children. Four hundred IU of vitamin D (from fortified soft drink powder or enriched fresh cow's milk) orally-administered daily, is a good way to prevent rickets in infants and young children.

Anemia, Hypochromic↗
PubMed1979

Effect of glucocorticoids and zinc deficiency on femur and liver zinc in rats.

Male weanling rats were fed diets containing less than 1, 3, 6 oor 13 ppm zinc or stock rat diet for 3 weeks. Each dietary group was subdivided into a control group and a prednisolone-treated group (5 mg pred/kg body weight). Femur and liver zinc contents were determined by flame atomic absorption spectrophotometry. Prednisolone caused growth retardation at all levels of dietary zinc. A marked increase was seen in femur zinc content of prednisolone-treated rats fed zinc-deficient diets. No such increase was seen in rats fed diets adequate in zinc. No significant change was seen in liver zinc content of zinc-deficient rats due to prednisolone. By comparing femur zinc in rats fed zinc-deficient diets with femur zinc in weanling rats, it appears that prednisolone causes an increase in femur zinc in rats fed deficient diets by (a) preventing bone resorption, and (b) increasing femur uptake of dietary zinc. Because the effects of glucocorticoids in rats appear to differ from effects in man, similar studies in other species are recommended.

Animals↗
PubMed1992

Influence of low dietary lipid content on anorexia and [14C]glucose uptake in the intestine of zinc-deficient mice.

Zinc deficiency was induced in adult male mice by feeding them for 8 weeks on a purified semi-synthetic Zn-deficient diet (ZD) containing 90 g lipid/kg (60 g maize oil plus 30 g cod-liver oil). One group was then fed on a low-lipid Zn-deficient diet (ZDLR) containing 30 g cod-liver oil/kg as the sole lipid source for a further 8 weeks. At the end of the experiment the stomach clearance rate, daily food intake, body-weight gain and [14C]glucose uptake in the intestine were significantly higher in group ZDLR than in mice that continued eating the Zn-deficient lipid-adequate diet ZD, and were comparable to results for a group given a Zn-supplemented diet. These results suggest that the pathogenesis of anorexia, nutrient malabsorption and growth retardation are secondary to lipid malabsorption resulting from Zn deficiency.

Animals↗
PubMed1992

Zinc uptake by blood cells of rats in zinc deficiency and inflammation.

In zinc deficiency, the function of leukocytes is impaired. However, the results of studies on the zinc concentration of blood cells in zinc deficiency are conflicting, probably in part because of technical and analytical problems. The aim of this study was to investigate, under standard conditions, the uptake of 65Zn-labeled zinc by blood cells, taken from zinc-deficient rats and from rats in which an inflammation is induced. In both conditions, the serum zinc concentration is reduced. In clinical practice, this makes it difficult to determine whether the decrease in serum zinc is the result of a real or an apparent zinc deficiency. In stress, like an inflammatory disease, the decrease of zinc reflects an apparent zinc deficiency because of redistribution of serum zinc into the liver and because of decrease in serum albumin concentration. Over 70% of the serum zinc is bound to albumin. Blood cells from zinc-deficient and control rats were isolated using a discontinuous Percoll gradient and incubated under nearly physiological conditions in a 65Zn-containing medium. A significant increase in the in vitro uptake of 65Zn-labeled zinc by the blood cells of zinc-deficient rats was seen: erythrocytes 1.3, mononuclear cells 2.0, and polymorphonuclear cells 2.6 times the control values. During inflammation, no change in 65Zn-labeled zinc uptake by erythrocytes and mononuclear cells was demonstrated after 2 d, although the serum zinc and albumin concentrations were decreased, but a small but significant increase in zinc uptake by polymorphonuclear cells was observed. This study of 65Zn uptake in vitro under standard conditions may prove of value for distinguishing in patients real zinc deficiency from apparent zinc deficiency owing to, e.g., stress, although additional experiments should be performed.

Animals↗