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PubMed1986

Zinc tolerance tests in zinc deficient and zinc supplemented diets.

Seven men consumed a low-zinc (3.3 mg/day) diet for 8 wk, followed by zinc-repletion (+15 mg/day) for 12 days. Zinc tolerance tests (50 mg) were administered initially and following depletion and repletion periods. Plasma zinc after 2 h in the zinc tolerance test was marginally higher after both the depletion (p less than 0.06) and repletion (p less than 0.001) periods as compared to the initial test. No changes were seen in parotid zinc tolerance tests or fasting levels of zinc in plasma or parotid saliva. In a subsequent study, zinc tolerance tests were given to normal subjects before and after 12 days of zinc supplementation (15 mg/day). Again, zinc levels in plasma were increased following zinc supplementation at the 2nd h post-zinc dose, but levels in saliva did not change. The elevation of plasma zinc curves with both zinc deficiency and supplementation suggests that this test is not a reliable indicator of zinc status.

Adult↗
PubMed1995

Maternal zinc deficiency, but not copper deficiency or diabetes, results in increased embryonic cell death in the rat: implications for mechanisms underlying abnormal development.

The mechanisms underlying the teratogenicity of maternal copper deficiency, zinc deficiency, and diabetes are largely unknown. Here we investigated whether these insults are associated with altered patterns of cell death in gestation day (GD) 11.0 rat embryos. Four weeks prior to mating, rats in the copper-deficient group (CuD) were fed a copper-deficient diet supplemented with the chelator, triethylenetetramine, to facilitate the depletion of tissue copper stores. Rats in this group were switched to a triethylenetetramine-free copper-deficient diet 1 week prior to mating. Dams in the diabetic and control groups were fed a control (8 micrograms copper, 25 micrograms zinc/g) diet throughout the study. On GD 3.0, one subset of the control dams was assigned to the zinc-deficient group (ZnD) and fed a zinc-deficient diet. A second subset of control dams was assigned to a restricted fed group and fed the control diet in quantities consumed by the zinc-deficient dams. Litters were taken by cesarean section on GD 11.0. Embryos were examined for gross morphology and assessed for patterns of cell death using Nile blue sulfate. Embryos from the CuD dams were characterized by edematous hindbrain. Embryos from the diabetic group were characterized by delayed development. Altered patterns of cell death were only detected in embryos from the ZnD dams. Within the ZnD group, embryos were either characterized by small size, edematous head region, and control patterns of cell death, or normal size, normal morphology, and increased cell death. These different patterns of morphology and cell death in the embryos of ZnD dams were associated with different patterns of maternal food intake.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Transient partial growth hormone deficiency due to zinc deficiency.

We present here a 13-year-old boy with partial growth hormone deficiency due to chronic mild zinc deficiency. When zinc administration was started, his growth rate, growth hormone levels, and plasma zinc concentrations increased significantly. His poor dietary intake resulted in chronic mild zinc deficiency, which in turn could be the cause of a further loss of appetite and growth retardation. There was also a possibility of renal zinc wasting which may have contributed to zinc deficiency. Zinc deficiency should be carefully ruled out in patients with growth retardation.

Adolescent↗
PubMed1983

Zinc absorption, intraluminal zinc and intestinal metallothionein levels in zinc-deficient and zinc-replete rodents.

Zinc absorption, endogenous luminal zinc and intestinal metallothionein were examined in rats and mice fed zinc-deficient and zinc-replete diets for 5-7 days. Small intestinal luminal washings from undosed rodents fed the replete diet contained 18- to 20-fold more zinc than those from zinc-deficient animals. Isotope dilution by this endogenous zinc could account for apparent differences between the groups in absorption of 65Zn from oral doses of 0.1-0.2 mumol 65Zn. With larger (1-2 mumol) oral doses of 65Zn in mice, no difference between the dietary groups was found, although zinc-deficient rats still absorbed more zinc than zinc-replete controls. In mice, zinc absorption from perfused duodenum, jejunum and ileum also was not increased by zinc deficiency. With oral doses, food generally lowered zinc absorption where endogenous or exogenous zinc was present in the gastrointestinal tract; food in perfusates lowered uptake more than transfer. Polarographically determined metallothionein was highest in duodenum of mice. It was lowered by feeding the deficient diet for 5 days without an increase in zinc absorption. It was concluded that zinc absorption is homeostatically increased by zinc deficiency in rats but not in mice and that intestinal metallothionein levels do not affect zinc absorption in mice.

Administration, Oral↗
PubMed2006

Correction of interleukin-2 gene expression by in vitro zinc addition to mononuclear cells from zinc-deficient human subjects: a specific test for zinc deficiency in humans.

A nutritional deficiency of zinc in humans is widespread in the developing world, and a conditioned zinc deficiency is observed in many diseased states, the elderly population, and pregnant women of both developed and developing nations. It was recently reported that zinc is required for Nuclear Factor-kappaB (NF-kappaB) activation and gene expressions of both interleukin-2 (IL-2) and interleukin-2 receptor alpha (IL-2Ralpha) and beta in HUT-78, a Th0 human malignant lymphoblastoid cell line. In this study, it has been reported for the first time that zinc is also required for gene expression of IL-2 and IL-2Ralpha in primary cells. Isolated peripheral blood mononuclear cells (MNCs) from zinc-deficient elderly subjects was used for this study. NF-kappaB activation was shown to have decreased in the MNCs from zinc-deficient subjects, which was corrected by in vivo zinc supplementation. It was further shown that either in vivo zinc supplementation or the addition of zinc in vitro to MNCs from zinc-deficient subjects results in correction of the gene expression of IL-2 and IL-2Ralpha. Therefore, it was proposed that in vitro addition of zinc to MNCs for correction of gene expression of IL-2 in humans may be used as a specific test for zinc deficiency. Although currently no known specific laboratory test exists for the diagnosis of zinc deficiency in humans, the use of correction of IL-2 messenger RNA (mRNA) with in vitro zinc addition to MNCs from zinc-deficient subjects may be very useful.

Aged↗
PubMed1986

Release of zinc from maternal tissues during zinc deficiency or simultaneous zinc and calcium deficiency in the pregnant rat.

Earlier studies have shown that diets that increase tissue catabolism reduce the teratogenic effects of zinc deficiency. The hypothesis that zinc may be released from body tissues when the metabolic state is altered was further tested. Nonpregnant Sprague-Dawley females were injected with 65Zn; after equilibration, the two major pools of zinc, bone and muscle had different specific activities, muscle being much higher. Females were mated and fed diets adequate in zinc and calcium, deficient in zinc alone or deficient in both zinc and calcium. Calculations using weight loss, zinc content of maternal bone and muscle and total zinc content of the fetus at term indicated that most of the zinc in the fetus at term in both the zinc-deficient and zinc-calcium-deficient groups came from breakdown of maternal muscle in the last 3 d of pregnancy. The relatively small amount of additional zinc released from bone in the zinc-calcium-deficient rats early in pregnancy was sufficient to prevent abnormal organogenesis. Specific activity of zinc in the zinc-deficient and zinc-calcium-deficient fetuses was equal and high, indicating that most zinc in these fetuses came from maternal tissues and from the same maternal sources in both groups. In contrast, specific activity of zinc in the fetuses from rats fed adequate zinc and calcium was less than 30% of that in either of the deficient groups; this is consistent with the hypothesis that most zinc accrued by these fetuses came directly from the diet.

Animals↗
PubMed2001

Zinc homeostasis in the brain of adult rats fed zinc-deficient diet.

Zinc concentration and (65)Zn uptake in the brain of rats fed zinc-deficient diet for 12 weeks were examined, based on a previous finding of the impairment of learning behavior by the zinc deprivation. Zinc concentrations in the brain, except for the hippocampal formation, did not decrease significantly in zinc-deficient rats, whereas zinc concentration in the liver of the zinc-deficient rats was approximately half that of control rats. When zinc-deficient rats were subjected to brain autoradiography with (65)Zn, (65)Zn concentration in any brain region of zinc-deficient rats was significantly higher than in control rats 6 days after injection of (65)ZnCl(2). The increase rate of (65)Zn concentration in the brain by the zinc deprivation was approximately 150%, and was similar to those in the liver and serum, suggesting that dietary zinc deprivation may cause a scarcity of zinc in the brain, in addition to the peripheral tissues such as the liver. These results indicate that the adult brain is responsive to dietary zinc deprivation. In the brain of zinc-deficient rats, the increase rate of (65)Zn concentration in the hippocampal formation seemed to be low compared to those in other brain regions. The hippocampal formation may be the most responsive to dietary zinc deprivation in the adult brain. The present finding demonstrates that zinc homeostasis in the brain is altered by chronically dietary zinc deprivation.

Animal Feed↗
PubMed1982

Zinc deficiency and the kidney. II. Response of zinc-deficient rats to three diuretic drugs.

Carbonic anhydrase is a zinc metalloenzyme whose activity may be affected by zinc deficiency. This investigation was designed to evaluate the effect of zinc deficiency on the response to three diuretic drugs which vary in their capacity to inhibit carbonic anhydrase: acetazolamide, furosemide and hydrochlorothiazide. The response of the zinc-deficient rats was compared to that of pair-fed and ad libitum zinc-supplemented controls. The pattern of electrolyte excretion by zinc-deficient rats in response to the three diuretics was qualitatively similar to that of the pair-fed and zinc-supplemented rats. When corrected for differences in body weight between the three groups, the natriuretic response to the diuretics in zinc-deficient rats was greater than that of either the pair-fed or zinc-supplemented controls. Although administration of the diuretics increased potassium excretion in all groups, the response of the zinc-deficient rats was attenuated. These differences in the response of zinc-deficient rats to diuretics did not appear to be related to the capacity of these drugs to inhibit carbonic anhydrase.

Acetazolamide↗
PubMed2003

Effects of oyster extract on the reproductive function of zinc-deficient mice: bioavailability of zinc contained in oyster extract.

Zinc is a vital nutrient in the normal reproductive function and embryonic development of mammals, and it is well known that oyster extract contains significant amounts of zinc. The effects of oyster extract on reproductive function, such as embryonic development, serum levels of zinc and sperm maturation were examined in zinc-deficient mice. Zinc deficiency in dams during pregnancy induced a decrease in the successful pregnancy rate, maternal weight gain, the number of live fetuses and fetal body weight. Zinc deficiency for 12 weeks in male mice induced a decrease in body weight, testis weight and sperm count in the epididymis. However, reproductive failure, embryonic defects and decreased sperm motility in zinc-deficient mice were improved by supplementation with oyster extract. Some nutrients contained in oyster extract, such as taurine and glycogen, may be related to the recovery of reproductive function. There were significantly lower serum concentrations of zinc in dams fed a zinc-deficient diet. However, the serum zinc concentration was normal in the oyster extract-supplemented group. No difference in the concentration of serum zinc was observed between the oyster extract- and zinc carbonate-supplemented groups. From these findings, it is suggested that oyster extract is a useful supplement that can prevent reproductive defects from zinc deficiency, and the bioavailability of zinc may be identical to zinc carbonate.

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↗