Search

Iron deficiency anemia, zinc and vitamin A deficiencies are serious public health problems in Cameroon, as in many developing countries. Local vegetables which are sources of provitamin A carotenoids (PACs) can be used to improve vitamin A intakes. However, traditional meals are often unable to cover zinc and iron needs. The aim of this study was to determine the bioavailability of 3 PACs (α-carotene, β-carotene, and β-cryptoxanthin) in young men, who were fed with a vitamin A-free diet and received iron and zinc supplementation. Twelve healthy participants were divided into three groups and were supplemented with elemental iron (20 mg of iron fumarate), 20 mg of zinc sulfate or iron+zinc (20 mg of iron in the morning and 20 mg of zinc in the evening) for 11 d. They were given a vitamin A- and PAC-free diet from the 6th to the 11th day, followed by a test meal containing 0.55 kg of freshly peeled papaya as a source of PACs. Blood samples were collected four times successively on the 11th day (the test meal day), at T0 (just after the test meal), after 2 h (T2), after 4 h (T4) and after 7 h (T7). Ultracentrifugation was used to isolate serum chylomicrons. Retinol appearance and PAC postprandial concentrations were determined. The supplementation with zinc, iron and iron+zinc influenced the chylomicron appearance of retinol and PACs differently as reflected by retention times and maximum absorption peaks. Iron led to highest retinol levels in the chylomicron. Zinc and iron+zinc supplements were best for optimal intact appearance of α-carotene, β-carotene and β-cryptoxanthin respectively. Supplementation with iron led to the greatest bioavailability of PACs from papaya and its conversion to retinol.

In developing countries, complementary foods are based on local cereal porridges. These foods are poor in trace elements, with a high risk of inducing micronutrient deficiencies-the primary cause of mortality in children under the age of five. Inappropriate feeding of complementary foods is the major factor creating malnutrition and micronutrients deficiencies in Cameroon children, as well as in other developing countries. This study determined the zinc and phytate content of 30 complementary foods that were based on maize or Irish potatoes. The foods were blended or treated by dehusking, fermentation and germination. Zinc was measured by flame atomic absorption spectrophotometry and phytates by high pressure-liquid chromatography; then phytates/zinc molar ratios were calculated. Concentrations (mg/100g dry matter) ranged, respectively, from 0.20 to 2.58 (0.12 ± 0.67) for zinc and from 0.00 to 6.04 (1.87 ± 1.7) for phytates. The phytate/zinc ratio varied from 0.00 to 51.62 (11.12 ± 11.53). It appears that germination and fermentation reduced the level of phytates: however, zinc levels in the samples did not change significantly. The traditional, local complementary foods were not only poor in zinc, but contained very high levels of phytates. These phytates have the potential to considerately reduce the acid extraction of zinc, and could impair its bioavailability., (Copyright © 2012 Elsevier GmbH. All rights reserved.)

Zinc (Zn) deficiency in animals became of interest until the 1950s. In this paper, progresses in researches on physiology of Zn deficiency in animals, phytate effect on bioavailability of Zn, and role of phytase in healing Zn deficiency of animals were reviewed. Several studies demonstrated that Zn is recycled via the pancreas; the problem of Zn deficiency was controlled by Zn homeostasis. The endogenous secretion of Zn is considered as an important factor influencing Zn deficiency, and the critical molar ratio is 10. Phytate (inositol hexaphosphate) constituted up to 90% of the organically bound phosphorus in seeds. Great improvement has been made in recent years on isolating and measuring phytate, and its structure is clear. Phytate is considered to reduce Zn bioavailability in animal. Phytase is the enzyme that hydrolyzes phytate and is present in yeast, rye bran, wheat bran, barley, triticale, and many bacteria and fungi. Zinc nutrition and bioavailability can be enhanced by addition of phytase to animal feeds. Therefore, using phytase as supplements, the most prevalent Zn deficiency in animals may be effectively corrected without the mining and smelting of several tons of zinc daily needed to correct this deficiency by fortification worldwide.

A column liquid chromatographic method that uses a spectrophotometric detector for the analysis of phytate and other inositol phosphates in foodstuffs and seeds is described. It has been tested thoroughly and sent to 6 other laboratories where there was an interest in such an analytical method and the equipment was available for performing it. These samples were blinded to the individual collaborators. Also sent was a standard wheat bran sample available from the American Association of Cereal Chemists with a standard phytate value reported as 3.2%. The postcolumn sulfosalicylic acid reaction was developed in the 1950s as an analytical method for ferric ion. All reagents are aqueous solutions and the specific pH values of each are important. The column separation is at pH 4, which dissociates all phosphate analogs. The ferric sulfosalicylate is at pH 1.8. The postcolumn reaction is then at pH 2.0-2.3. At this pH, the sulfosalicylate complexes one ferric ion and will yield it to a stronger complexing agent such as a phosphate ester. At higher pH values, sulfosalicylate complexes 2 ferric ions and will yield neither to these anions. The method sensitivity is 8-12 nmoles/injection.

A method is described that accurately and rapidly quantifies the free and total phosphorous content of a commercially available, purified, phytic acid preparation. This allows its use as a standard for phytic acid determinations in foods. The method involves a wet ashing step followed by phosphorous measurement with a 1-amino-2-naphthol-4-sulfonic acid-molybdate reagent in a microplate reader at 660 nm. The procedure can be performed in 3 h with as little as 50 mg sample.

Homeostatic equilibrium of a nutrient is characteristic of a healthy body. For zinc, phytate has been shown to alter that equilibrium in several monogastric species including man. The pancreas is an important organ in the maintenance of zinc homeostasis. Elevated calcium has been shown to be a synergistic agent in affecting the rate of onset and rate of homeostatic change. In the studies described, rats were depleted of zinc to differing extents, zinc was injected intraperitoneally to label the endogenous zinc pool. Phytate- and nonphytate-containing protein diets were fed and feces were collected. Feces were counted for radioactivity. The ratios of radioactivity (phytate:nonphytate) indicated that the major effect of phytate was on the endogenous secreted pool. Evidence is included to indicate that two, pancreatic labile pools of zinc are secreted, one is stable complexes not affected by phytate and two, a labile pool of zinc readily available for complexation. A mathematical model is included that fits all nutritional models for zinc homeostasis.

Sixty 3-wk-old female Sprague-Dawley rats were randomly divided into six groups of 10 animals each. Group 1 was fed for 8 wk purified AIN-76A diet (basal diet) containing 0.025 mg molybdenum/kg diet. Groups 2-6 were fed the same basal diet supplemented with sodium molybdate to provide total dietary Mo of 0.050, 0.100, 0.200, 0.400 and 0.800 mg/kg diet, respectively. Molybdenum concentration in liver and brain increased linearly up to the 0.200 mg Mo/kg diet level. Beyond this level, no further significant increase occurred. Dietary Mo of 0.100 mg/kg elevated the Mo concentration in heart to its maximal level. Supplementation with 0.025 mg Mo/kg to a total of 0.05 mg Mo/kg diet significantly increased Mo concentration in spleen and kidney; higher levels of dietary Mo did not result in further significant responses. Molybdenum supplementation significantly increased the activities of xanthine dehydrogenase/oxidase (XDH), sulfite oxidase and superoxide dismutase in the liver, and of XDH in small intestinal mucosa. Maximal activities were attained at 0.050, 0.050, 0.200 and 0.100 mg Mo/kg diet, respectively. Dietary Mo of 0.200 mg/kg diet was estimated as the Mo requirement of rats fed the AIN-76A diet.

Phytate, a naturally occurring organic compound found in plant seeds, roots, and tubers, was determined in a collaborative study using a modified anion-exchange method. Seven samples (peanut flour, oats, rice, isolated soybean protein, a vegetarian diet composite, wheat bran, and whole wheat bread), supplied as blind duplicate samples, were analyzed in triplicate by 7 collaborators. Phytate concentrations in the samples ranged from 2.38 to 46.70 mg/g. Relative standard deviations (RSD = CV) for repeatability ranged from 2.5 to 10.1%, and for reproducibility, from 4.5 to 11.0%. The method has been adopted official first action.

The phytate content of several foods is presented. Published zinc values were used to calculate phytate:zinc molar ratios. These ratios can be used to estimate the relative risk of having an inadequate intake of zinc. They may be used in planning menus to select the combination of foods that will supply the most available zinc to the daily diet. On the basis of animal experiments to date, a daily phytate:zinc molar ratio of 10 or less is thought to be acceptable in providing adequate dietary zinc, and daily ratios consistently above 20 may jeopardize zinc status. Many factors other than the daily dietary phytate:zinc molar ratio influence zinc nutriture, but the ratio concept is a tool which may contribute to a more accurate assessment of zinc status.

Clinical similarities between patients with sickle cell anemia and zinc-deficient subjects suggested a secondary zinc deficiency in sickle cell anemia. Zinc was assayed in various biological fluids and tissues by atomic absorption spectrophotometry. Zinc in the plasma, erythrocytes, and hair was decreased and urinary zinc excretion was increased in anemia patients as compared to controls. Erythrocyte zinc and daily urinary zinc excretion were inversely correlated in the anemia patients (r equal to minus .63, P smaller than 0.05), suggesting that hyperzincuria may have caused zinc deficiency in these patients. Carbonic anhydrase, a zinc metalloenzyme, correlated significantly with erythrocyte zinc (r equal to plus 0.94, P smaller than 0.001). Plasma RNase activity was significantly greater in anemia subjects than in controls. We administered zinc sulfate, 660 mg per day, orally, to seven men and two women with sickle cell anemia. Two 17-year-old males gained 5 cm and 7 cm in height during 49 and 42 weeks of zinc therapy, respectively. All but one patient gained weight (0.5 kg to 4.1 kg). Five of the males showed increased growth of pubic, axillary, facial, and body hair, and in one a leg ulcer healed in six weeks on zinc and in two others some benefit of zinc therapy on healing of ulcers was noted.

The sleep-wake cycle of 12 tryptophan dietary deficient rats and their non-deficient paired controls were observed for a 8:00 a.m. to 8:00 p.m. period. EEG, EMG and body activity were continuously monitored on polygraphic recordings throughout the 12 hr observation period. The results indicate no significant difference between the tryptophan deficient and sufficient animals in time spent awake, slow-wave or parodoxical sleep. There was a non-significant trend among the tryptophan deficient animals to be less active and spend more time in both slow-wave and paradoxical sleep, which is in contrast to an expected insomnia effect. The results do not support the suggested relationship between reduced serotonin levels and the occurrence of insomnia, questioning the serotonergic theory of sleep.

A pooled sample of hair was divided and portions prepared for analysis by three washing procedures, to evaluate the effect of washing procedure on the subsequent trace-element (Zn, Cu, Mg) content. The methods selected were a detergent wash, a hexane-ethanol wash, and an acetone-ether-detergent wash. For all elements, there was a significant difference among the results after these wash procedures. Magnesium content of hair was most affected by washing, containing less than half of the magnesium of the unwashed hair. The detergent wash removed the most zinc and magnesium; the acetone-ether-detergent wash removed the most copper. Our results indicate that the trace-element analysis of hair is sensitive to the preparation technique and therefore is an unreliable source of information about trace-element status.

The study involved three levels of dietary zinc (deficient, marginal, and adequate) and four hormonal conditions; namely, no steriods, norethindrone, mestranol, and norethindrone plus mestranol. The steroids were incorporated into diets and fed to 11-wk-old female Sprague-Dawley rats. After 10 wk of treatment, various tissues were excised for mineral assays by atomic-absorption spectrophotometry. Both steroids, reduced weight gain. Mestranol depressed plasma zinc, tibia copper and magnesium, and liver iron, but elevated the zinc levels in liver and erythrocytes, plasma copper, liver magnesium and calcium, and iron content of tibia and heart. In general, the effect was most prominent with adequate zinc but diminished in magnitude with the reduction of zinc intake. In addition, norethindrone increased heart iron and tibia calcium. Mestranol appeared to be the main causative factor and may have induced a possible shift of minerals from one pool to another. As expected, zinc deficiency resulted in the reduction of zinc concentrations of plasma, tibia, kidney, and pancreas, and the elevation of copper, iron, magnesium, and calcium concentrations of various tissues.

Oral contraceptive steroids, norethynodrel and mestranol, were fed to 11-wk-old female Sprague-Dawley rats, in combination and in quantities proportional to those used by women for contraceptive purposes. Three experiments were performed. The first experiment, demonstrated that 10 wk of treatment, impaired the animal's glucose tolerance, but not its insulin response to glucose. The second experiment demonstrated that 6 wk of steroid feeding, decreased the in vivo conversion of blood U-14C-labeled glucose into adipose tissue fatty acids and into diaphragm glycogen, although the effect on the diaphragm was not statistically significant. In the third experiment, it was found that the uptake of 2-deoxyglucose-1-14C by the adipose tissue removed from rats after 6 wk of treatment, was not different from that of control tissue, but the uptake by the hemidiaphragms was slightly lower.

Thirty-two adult patients with sickle cell anemia were evaluated endocrinologically. Secondary sex characteristics were abnormal in 29, and eunuchoidal skeletal proportions were present in all except one. The age at which different stages of pubic hair growth were attained in these patients was delayed in comparison to normals (P less than 0.005). Hormonal assays were carried out in 14 patients. Basal serum testosterone, dihydrotestosterone, and androstenedione values were lower (P less than 0.02) in patients than controls. Serum LH and FSH levels before and after stimulation with gonadotropin-releasing hormone were consistent with primary testicular failure. Erythrocyte and hair zinc concentrations were significantly decreased, and there was positive correlation between erythrocyte zinc and serum testosterone (r = 0.61, P less than 0.01) in sickle cell anemia. Our study shows that androgen deficiency in this disease is a result of primary rather than secondary hypogondadism. Further studies are required to establish the role of zinc in the pathogenesis of testicular failure in sickle cell anemia.

Clinical, biochemical and nutritional data were collected from a large population of women using oral contraceptive agents. Higher incidence of abnormal clinical signs related to malnutrition were observed in the lower (B) as compared to the higher (A) socioeconomic groups, and also in the nonsupplemented groups as compared to the supplemented groups in the B subjects. As a rule the intake of oral contraceptive agent subjects of vitamin A, C, B6 and folic acid did not differ from that of the controls As expected, subjects from the supplemented groups had higher intake of vitamin A, C, B6, thiamin, riboflavin and folic acid, and A groups had higher intake of vitamin C, B6, riboflavin and folic acid. Increased plasma vitamin A and decreased carotene levels were observed in oral contraceptive agent users. In general oral contraceptive agents had little or no effect on plasma ascorbic acid. Urinary excretion of both thiamin and riboflavin in subjects using oral contraceptive agents were lower in A groups. Erythrocyte folate and plasma pyridoxal phosphate was decreased in A groups due to oral contraceptive agents. Subjects who took supplements had higher levels of plasma vitamin A, ascorbic acid and folate. But urinary thiamin and riboflavin were higher only in group A subjects who took supplements.

The interactions of oral contraceptive agents (OCA's) with vitamins were studied in a large population of women. In the upper socioeconomic groups, higher incidences of abnormal clinical signs related to vitamin deficiencies were seen in OCA users than in the control subjects. Plasma pyridoxal phosphate and red cell and serum folate were lower in subjects using OCA's in the upper socioeconomic group as compared to levels in the control subjects. Reduction in erythrocyte glutamic oxalacetic transaminase (EGOT) activity and elevation in the EGOT-stimulation test were observed in subjects using OCA's in both upper and lower socioeconomic groups. These observations suggest a relatively deficient state with respect to vitamins B6 and folic acid in OCA users. No significant effect on serum vitamin B12 was observed as a result of OCA administration.

Trace elements in 84 adult patients (38 men and 46 women) with sickle cell disease (SCD) were reflected in clinical and biochemical data. Height was retarded in six men and five women. Eighty percent of the SCD patients in this sample were below the 50th percentile from the normal mean for weight. Twenty-eight men showed a lack of facial and body hair, and five additional subjects showed only scanty facial hair. Whereas zinc in plasma, red blood cells, and hair was decreased, the excretion of zinc in urine was increased in SCD patients as compared to the controls. We believe that one of the mechanisms accounting for zinc deficiency in SCD may be hyperzincuria and that growth retardation and hypogonadism in men so commonly seen in SCD may be related to zinc deficiency.

The epidemiological aspects of oral contraceptive agents on nutrient metabolism were studied in a large population of women. Incidence of clinical abnormalities, related to malnutrition, were more frequently observed in the lower (B) as compared to the higher (A) socioeconomic groups. In the A groups some clinical signs were more common in the nonsupplemented groups of subjects. In general, the intake of oral contraceptive agent subjects for calories, protein, calcium, magnesium, iron, copper and zinc did not differ from the controls. The intake of the above nutrients in group A subjects were higher than those of group B except for calories. The subjects who took supplements had higher intakes of calcium, iron, magnesium and copper. No effect of oral contraceptive agents was seen on hemoglobin, hematocrit and erythrocyte count. Serum iron was increased due to "Norinyl." Total iron binding capacity was increased as a result of oral contraceptive agent administration. Total iron binding capacity values were higher in group B as compared to group A and in the nonsupplemented as compared to the supplemented groups. Plasma copper was increased and plasma zinc was decreased as a result of oral contraceptive agent administration. An increase in erythrocyte zinc was observed due to "Norinyl." No effect of oral contraceptive agents on plasma calcium, magnesium and erythrocyte magnesium was observed. Although no effect of oral contraceptive agents on plasma total protein was found, serum albumin was decreased.

As the number of factors which affect zinc absorption and homeostasis increase, it becomes more apparent that the relative zinc status of the population cannot be estimated from the analyzed zinc content of foods. The environment of the small intestine at the time of absorption can only be estimated from the diet fed. Even then since both endogenous and exogenous factors determine the zinc absorbed, the precision of these estimations should allow for large individual variation.

Zinc content of testes, bones, esophagus, kidneys, and muscles was decreased, whereas iron content was increased in the testes of zinc-deficient rats compared to restrictedly fed control rats. Histochemical enzyme determinations revealed reduced activities of certain enzymes in the testes, bones, esophagus, and kidneys. In the testes, lactic dehydrogenase (LDH), malic dehydrogenase (MDH), alcohol dehydrogenase (ADH), and NADH diaphorase; in the bones, LDH, MDH, ADH, and alkaline phosphatase; in the esophagus, MDH, ADH, and NADH diaphorase; and in the kidneys, MDH and alkaline phosphatase were decreased in zinc-deficient rats compared to restrictedly fed controls. Succinic dehydrogenase (SDH) revealed no significant changes under the conditions of our experiments in various groups of rats that were investigated. In a "repleted" group of rats, content of zinc in testes and bones increased significantly, compared to the deficient group. The iron content of the testes decreased after repletion with zinc. In the testes, bones, esophagus, and kidneys, the activities of various enzymes increased after repletion with zinc. Inasmuch as the major manifestations of zinc deficiency syndrome in the rat include growth retardation, testicular atrophy, and esophageal parakeratosis, our results suggest that the content of zinc in the above tissues most likely controls the physiological processes through the formation of zinc-dependent enzymes.