Spontaneous occurrence of Angiostrongylus costaricensis in marmosets (Saguinus mystax)

Two marmosets imported from Iquitos, Peru, were found to be infected with Angiostrongylus costaricensis. Both animals had large solitary granulomas involving the wall and adjacent mesentery of the small intestine. Histopathologic examination showed the adult nematodes in the lumina of the mesenteric arteries that coursed through these granulomas. The inflammatory reaction was associated with numerous degenerating eggs and larvae. This is the first report of this parasite in nonhuman primates and extends its geographic range to Peru. In addition, in one animal, Dipetalonema sp were seen free in the abdominal cavity, and pleroceroid larvae (spargana) were in the loose connective tissue of the left axilla. This animal also had microgranulomas associated with eggs and larvae of Angiostrongylus in the kidney, liver, lung, and heart.     

Tetrapeltalonema (t.) mystaxi sp. n. (Nematoda: Filarioidea) from Brazilian moustached marmosets, Saguinus m. mystax.

Tetrapetalonema (T.) mystaxi sp. n. is described from the subscapular connective tissues of Saguinus mystax. The parasite is placed in the subgenus Tetrapetalonema and most closely resembles Tetrapetalonema atelensis, from which it can be differentiated by its long esophagus, size and shape of the spicules, and the size and arrangement of nuclei in the tail of the microfilaria.     

Dietary phytate,zinc and hidden zinc deficiency

Epidemiological data suggest at least one in five humans are at risk of zinc deficiency. This is in large part because the phytate in cereals and legumes has not been removed during food preparation. Phytate, a potent indigestible ligand for zinc prevents it's absorption. Without knowledge of the frequency of consumption of foods rich in phytate, and foods rich in bioavailable zinc, the recognition of zinc deficiency early in the illness may be difficult. Plasma zinc is insensitive to early zinc deficiency. Serum ferritin concentration ≤ 20 μg/L is a potential indirect biomarker. Early effects of zinc deficiency are chemical, functional and may be “hidden”. The clinical problem is illustrated by 2 studies that involved US Mexican-American children, and US premenopausal women. The children were consuming home diets that included traditional foods high in phytate. The premenopausal women were not eating red meat on a regular basis, and their consumption of phytate was mainly from bran breakfast cereals. In both studies the presence of zinc deficiency was proven by functional responses to controlled zinc treatment. In the children lean-mass, reasoning, and immunity were significantly affected. In the women memory, reasoning, and eye-hand coordination were significantly affected. A screening self-administered food frequency questionnaire for office might help caregiver's identify patients at risk of zinc deficiency.     

Soil-sodicity-induced zinc deficiency in maize

Summary Maize (Zea mays L. cv. Ganga-2) plants were grown in pot culture on a loamy alluvial soil of Lucknow district (India) alkalinized to graded levels of ESP (Exchangeable Sodium Percentage) ranging from 15.5 to 55.3. Before sowing maize seeds the soil was fertilised with NPK, Fe, Mn and Cu. At and above ESP 34 Zn-deficiency symptoms first appeared at 30 days. The symptoms gradually became pronounced with increase in age and at 60 days they were found even at ESP 15.5. The severity of symptoms was related to increase in sodicity. Alkalinization of soils depressed available soil Zn and tissue Zn and increased tissue ratios of Na/Zn and P/Zn. It also decreased the total plant content of Zn, Fe, Mn, Cu and even Na. Increase in soil sodicity increased both tissue concentration and total content of P in plants upto ESP 34 beyond which it decreased it. Among different extractants, 0.1N HCl, DTPA pH 7.3 and EDTA-(NH₄)₂ CO₃ pH 8.6, for measuring available soil Zn the latter showed best correlations with soil ESP (−), tissue P (−), P/Zn ratio (−), dry matter yield (+) and tissue Zn (+). Tissue Zn was related to yield (+), tissue Na (−) and soil ESP (−). Mild, moderate, severe and very severe Zn deficiency in maize was induced by soil ESP levels, 18, 25, 33 and 45, respectively.     

Skeletal effects of zinc deficiency in growing rats.

There is ample evidence that zinc plays an important role in bone metabolism and zinc deficiency has been implicated as a risk factor in the development of osteoporosis. It was the aim of the present study to investigate the skeletal effects of alimentary zinc deficiency in growing rats using quantitative bone histomorphometry. Twenty-four male Sprague Dawley rats with a mean initial body weight of 101 +/- 2 g were allocated in two groups of 12 rats each and had free access to a semi-synthetic, casein-based, zinc-deficient diet (0.76 mg zinc/kg) or to the same diet supplemented with 60 mg zinc per kg. All rats were sacrificed 42 days after the start of the experiment and the right distal femur was removed for bone histomorphometry. Relative to controls (+Zn), the zinc-deficient rats (-Zn) had a significantly lower body weight and about an 80% reduction in plasma and femur zinc concentration. The histomorphometric evaluation of the distal femoral metaphysis showed that zinc deficiency led to a 45% reduction (p < 0.01) in cancellous bone mass and to a deterioration of trabecular bone architecture, with fewer and thinner trabeculae. The osteopenia in -Zn rats was accompanied by significant reductions in osteoid perimeter (-31%, p < 0.05), osteoblast perimeter (-30%, p < 0.05), and osteoclast number (-38%, p < 0.01) relative to +Zn controls. We conclude that zinc deficiency induced low turnover osteopenia in femoral cancellous bone of growing rats. These results support the hypothesis that zinc deficiency during growth may impair the accumulation of maximal bone mass in humans; additionally, they suggest that zinc deficiency may play a role as a risk factor in the pathogenesis of osteoporosis.     

Mechanism of phosphorus-induced zinc deficiency in cotton. II. Evidence for impaired shoot control of phosphorus uptake and translocation under zinc deficiency

Cotton (Gossypium hirsutum L. cv. Deltapine 15/21) plants were precultured for 19 to 25 days under controlled climatic conditions in nutrient solutions with different levels of Zn. With the onset of visual Zn-deficiency symptoms the pH of the nutrient solution decreased from 6.0 to about 5.0. In contrast, Zn-sufficient plants raised the pH of the nutrient solution to about 7.0. In short-term studies it could be demonstrated that the Zn nutritional status of the plants remarkably influenced the uptake and translocation rates of mineral nutrients. Compared to Zn-sufficient plants, P uptake rate in severely Zn-deficient plants was increased by a factor of 2 to 3, whereas the uptake rates of K, Ca and particularly NO₃ decreased. The accumulation of P in the roots of Zn-deficient plants was either not affected or even lower than in Zn-sufficient plants. Thus, Zn deficiency had a specific enhancement effect on root to shoot transport of P. This enhancement effect of Zn deficiency on uptake and transport of P was similar at nutrient solution pH values of 7.0 and 5.8; i.e. it was not the result of acidification of the nutrient solution. After application of ³⁶CI, ⁸⁶Rb and ³²P to plant stems, basipetal transport of ³⁶CI and ⁸⁶Rb was not affected by the Zn nutritional status of the plants. However, in Zn-deficient plants, only 7.8% of the ³²P was translocated basipetally compared to 34% in the Zn-sufficient plants. A resupply of Zn for 19 h to Zn-deficient plants enhanced basipetal ³²P transport. The results indicate that a feedback mechanism in the shoots is impaired in Zn-deficient plants which controls the P uptake by roots and especially the P transport from roots to shoots. As a result of this impairment toxic concentrations of P accumulate in the leaves. The mechanism responsible is likely the retranslocation of P in the phloem from shoots to roots.     

Kinetics of zinc status and zinc deficiency in Berardinelli-Seip syndrome

Berardinelli-Seip syndrome (BSS) is a very rare disorder characterized by near-complete absence of adipose tissue from birth or early infancy, hypoleptinemia, hypertriglyceridemia, insulin resistance, diabetes mellitus, and other clinical signals. It is caused by mutations in AGPAT2 or Gng3lg. We evaluated 10 BSS patients and 10 healthy subjects. A single dose of 382.43 μmol zinc was administered intravenously before and after 3 months of oral zinc supplementation. Blood samples were collected from the contralateral arm at 0, 30, 60, 90, and 120 min after zinc injection. Plasma and serum were obtained to measure hematological and biochemical parameters. Urine was collected to measure creatinine, protein, and zinc. Basal serum zinc levels were similar in controls and BSS patients. However, serum zinc profiles were significant reduced in BSS patients in comparison with controls. The change in total-body zinc clearance was more significant in BSS patients, indicating that these patients had suboptimum zinc deficiency.     

Histone formation, gene expression, and zinc deficiency in Euglena gracilis

Histones, and other basic proteins, have been isolated from zinc-sufficient (+Zn) Euglena gracilis by standard chromatographic methods. These cells contain 2.46 micrograms of histones and 1.96 micrograms of DNA per 10(6) organisms. Each of the histones, H1, H3, H2A, H2B, and H4, is present in both log- and stationary-phase +Zn cells and has been characterized according to its electrophoretic mobility and molecular weight. H1 has been further identified on the basis of its amino acid composition and its cross-reactivity with calf thymus histone H1 antibodies. Similarly, H3 has been recognized as well by its specific reaction with an H3 antibody. In contrast, log-phase zinc-deficient (-Zn) cells contain H1 and H3 while H2A, H2B, and H4 are absent. All of the histones vanish in stationary-phase-Zn organisms. The DNA content increases as the -Zn cells progress from log to stationary phase, reaching a value of 4.40 micrograms/10(6) cells, double that of comparable stationary-phase +Zn organisms. A 2000-3000-dalton polypeptide whose electrophoretic behavior differs from that of the known histones constitutes over 90% of the total basic proteins of -Zn cells. On addition of zinc to stationary -Zn cells, cell division resumes, and all the histones and other basic proteins reappear. Together with previous results, the data demonstrate that zinc significantly affects the metabolism of all major chromatin components, i.e., the RNA polymerases, DNA, and histones of E. gracilis [Vallee, B.L., & Falchuk, K.H. (1981) Philos. Trans. R. Soc. London, Ser. B 294, 185-197]. The implications of these effects of zinc on chromatin structure and function are discussed.     

Spontaneous pathology of the common marmoset (Callithrix jacchus) and tamarins (Saguinus oedipus, Saguinus mystax)

Background  Marmosets and tamarins are increasingly used in research, but their pathology remains poorly defined compared with Old World primates.

Methods  Necropsy records of 129 marmosets and 52 tamarins were reviewed; none was used experimentally.

Results  The most common marmoset lesions were dehydration, emaciation, nephritis, colitis, and inanition. The most common tamarin lesions were dehydration, ascites, emaciation, and congestive heart failure. Colitis and heart disease were the most common cause of death in marmosets and tamarins, respectively. Immature marmoset and tamarin deaths often occurred within the first month of life. Immature marmosets usually died from inanition, stillbirth, and colitis; immature tamarins from atelectasis, stillbirth, heart failure, and colitis. Lymphoma was the most common neoplasm for both marmosets and tamarins.

Conclusion  The findings were similar to prior reports with differences in frequency and severity. We report the first case of endometriosis in a marmoset.     

Copper excess, zinc deficiency, and cognition loss in Alzheimer's disease

In this special issue about biofactors causing cognitive impairment, we present evidence for and discuss two such biofactors. One is excess copper, causing neuronal toxicity. The other is zinc deficiency, causing neuronal damage. We present evidence that Alzheimer's disease (AD) has become an epidemic in developed, but not undeveloped, countries and that the epidemic is a new disease phenomenon, beginning in the early 1900s and exploding in the last 50 years. This leads to the conclusion that something in the developed environment is a major risk factor for AD. We hypothesize that the factor is inorganic copper, leached from the copper plumbing, the use of which coincides with the AD epidemic. We present a web of evidence supporting this hypothesis. Regarding zinc, we have shown that patients with AD are zinc deficient when compared with age-matched controls. Zinc has critical functions in the brain, and lack of zinc can cause neuronal death. A nonblinded study about 20 years ago showed considerable improvement in AD with zinc therapy, and a mouse AD model study also showed significant cognitive benefit from zinc supplementation. In a small blinded study we carried out, post hoc analysis revealed that 6 months of zinc therapy resulted in significant benefit relative to placebo controls in two cognitive measuring systems. These two factors may be linked in that zinc therapy significantly reduced free copper levels. Thus, zinc may act by lowering copper toxicity or by direct benefit on neuronal health, or both.     

An effect of zinc deficiency on dental caries.

Rat pups suckled by dams fed a zinc-deficient diet developed higher levels of dental caries following a caries-test challenge than pups suckled by dams fed a zinc-adequate diet. The zinc deficient treatment was administered during the mineralization stage of tooth development before the molars erupted. The data shows that suboptimal zinc nutriture was associated with an increase in dental caries.Fluoride, a trace element, is recognized as a factor in preventing dental caries and its use has had a significant impact on dental health in this country. However, the possible roles of other trace elements have not been closely examined. Zinc is a trace element important to bone mineralization as well as in general nutrition.The effects on dental caries produced by the addition of zinc to rat diets have been reported (1, 2, 3). In those investigations, however, zinc supplements were added to diets that were adequate in zinc. Moreover, zinc supplements were fed after the teeth had appeared in the oral cavity. Because the critical period of tooth maturation occurs before eruption (4), post-eruptive zinc supplements probably should not markedly influence the development and, specifically, the mineralization of the tooth. Therefore, we investigated the influence of pre-eruptive zinc deficiency on caries development in rats.     

Effect of zinc deficiency and zinc supplementation on adrenals,plasma steroids and thymus in rats

Weanling rats were given diets deficient in or supplemented with zinc. Within a few weeks there were increases in the weight of the adrenal glands and in the concentration of cholesterol and 11-hydroxycorticosteroids in the adrenal glands of the zinc deficient animals. The decrease in cholesterol concentration due to ACTH administration was greater in zinc-deficient than in supplemented rats. After four weeks on the zinc-deficient diet rats had smaller thymus glands than zinc-supplemented rats but zinc-deficient diets had no such effect on adrenalectomised rats. The addition of 2 mg zinc/ml drinking water had no effect on adrenal weight or thymus weight but increased plasma 11-hydroxysteroids after 30 days. The possible connection between zinc intake and resistance to injury and disease is discussed.     

The establishment of specified-pathogen-free marmosets, Callithrix jacchus.

The establishment of 3 specified-pathogen-free marmosets (Callithrix jacchus) during the period May 1969 to January 1973 is described. A brief history of the conventional breeding colony from which the animals were derived is given and hysterotomy and hand-rearing techniques are described.     

Mechanism of phosphorus-induced zinc deficiency in cotton. III. Changes in physiological availability of zinc in plants Is mail

The effect of varied supply of P (2.5× 10⁻⁵ to 6× 10⁻⁴ M) and Zn (0 to 10⁻⁶ M) on uptake and concentrations of P and Zn was studied in cotton ( Gossypium hirsutum L. cv. Deltapine 15/21) grown in nutrient solution under controlled environmental conditions. At a given Zn supply, increasing levels of P had no significant effect on the concentrations of total Zn in plants. However, increasing levels of P induced or enhanced visual Zn deficiency symptoms when the Zn concentration in the nutrient solution was low. The concentrations of water-soluble Zn in roots and shoots constituted 60% of the total Zn concentrations for plants grown with low P and 30% for plants grown with high P. The concentration of water-soluble Zn in leaves, but not total Zn, was closely correlated with visual Zn deficiency symptoms, levels of chlorophyll, super oxide dismutase and membrane permeability. The critical deficiency concentration of water-soluble Zn in cotton leaves was in the range of 6 to 7 μg (g dry weight)⁻¹ or about 1.0 μg (g fresh weight)⁻¹. The results show that high P concentrations in plant tissue decrease the physiological availability of Zn. Water-soluble Zn in the tissue appears to be a suitable indicator for Zn nutritional status in general and phosphorus-induced Zn deficiency in particular. Also in field-grown orange trees (Citrus sinensis) visual Zn deficiency symptoms in leaves were closely related to the concentration of water-soluble Zn.     

Circulating thymic hormone levels in zinc deficiency

The effect of zinc deficiency (Zn^?) on the circulating thymic hormone (FTS) levels in A/J mice was studied. After 3 weeks of feeding the mice a Zn^? diet, FTS levels were markedly reduced and after 17 weeks, FTS was undetectable. By contrast, the zinc-supplemented (Zn⁺) group seemed to maintain FTS levels better than the normal diet group with aging. On the other hand, spleen spontaneous rosette-forming cells (sRFC) were studied for their azathioprine (AZ) sensitivity in A/J mice on different diets. The Zn^? mice had fewer sRFC than did the normally fed or Zn⁺ mice. The role of zinc in controlling levels of FTS and thus thymic function is discussed.     

Moderate zinc deficiency in rhesus monkeys. An intrinsic defect of neutrophil chemotaxis corrected by zinc repletion

Experimental animals fed zinc-deficient diets are well known for susceptibility to infections and impaired mitogen response and Ig production. However, the levels of zinc deficiency used have generally been severe, not comparable to human populations, and have not addressed neutrophil function. To address this issue we have studied the effect in rhesus monkeys of a well defined moderately zinc-deficient (MZ) diet on polymorphonuclear leukocyte (PMN) function. Female adult rhesus monkeys were fed either a control (100 micrograms Zn/g) or MZ (2 micrograms Zn/g) diet for 9 mo with quantitation of PMN chemotaxis, and phagocytosis of opsonized yeast. In addition, membrane potential and secretion responses (changes in 90 degrees light scatter) and changes in PMN shape (forward light scatter shifts) were also measured. When compared to the PMN of animals fed control diets, there was a significant reduction in chemotaxis to FMLP of MZ-fed monkey PMN. Although shape change, cell membrane depolarization, as well as phagocytosis were not significantly different among the two groups, the PMN of MZ animals had significantly lower relative loss of orthogonal light scatter (degranulation) due primarily to a lower resting orthogonal light scatter and also a smaller loss when stimulated with FMLP. In vitro addition of zinc to the cells (25 microM) did not improve chemotaxis, and in fact, was inhibitory for most control and zinc-deficient cells. However, after 2 wk of dietary zinc repletion (100 micrograms Zn/g), chemotaxis in the low zinc group was higher and comparable to the control response. These data indicate that zinc deficiency is associated with an intrinsic PMN defect that specifically affects chemotaxis and is corrected with dietary zinc repletion.