Food preference of young rhesus monkeys fed marginally zinc deficient diets

Zinc deprivation has been shown to produce hypogeusia in rhesus monkeys but the possible consequences of altered taste sensitivity for food preference and selection is not known. We studied 13 rhesus monkeys (2.5 to 3 years of age) for food preference in a structured choice situation. These animals were fed two levels of dietary zinc: marginally zinc deprived (fed 4 μg zinc/g diet from conception and throughout development;N=6), or control (fed a 100 μg zinc/g diet throughout the study;N=7). Preference for familiar vs unfamiliar food items, order of food preferences, persistence in retrieval of preferred and nonpreferred foods, and preference under four deprivation periods were examined. Animals were offered a choice of two food items, both containing minimal zinc levels, and food choice and latency of choice were measured. Results indicate that animals fed the marginal zinc diets had reduced preference for unfamiliar foods relative to controls and different patterns of food preference. These results may be relevant to maintenance of appropriate food selection in marginally zinc deprived populations.     

Effects in chicks of arsenic,arginine, and zinc and their interaction on body weight,plasma uric acid,plasma urea,and kidney arginase activity

The interaction among arsenic, zinc, and arginine was studied in chicks using two fully crossed, three-way, two-by-two-by-two experiments. Arsenic at levels of 0 and 2 μg/g zinc at levels of 2.5 (zinc-deficient) and 25 (zinc-adequate) μg/g, and arginine at levels of 0 and 16 mg/g were supplemented to the diet. After 28 d in both experiments, growth was depressed in chicks fed diets either supplemented with arginine or deficient in zinc. Arsenic deprivation depressed growth of chicks fed diets containing the basal level of arginine and 25 μg supplemental Zn/g. Arsenic deprivation had little or no effect on growth of zinc-deprived chicks fed diets containing the basal level of arginine, or in zinc-deprived or zinc-adequate chicks fed supplemental arginine. Zinc-deficiency elevated urea in plasma and arginase activity in kidney. Those elevations, however, were more marked in arsenic-supplemented than in arsenic-deprived chicks. Also, plasma urea and kidney arginase activity were markedly elevated in chicks fed supplemental arginine; the elevations were more marked in zinc-deficient chicks. These findings support the concept that arsenic has a physiological role, associated with zinc, that can influence arginine metabolism in the chick.     

Renal metallothionein responds rapidly and site specifically to zinc repletion in growing rats

Metallothionein (MT) is important for heavy metals and free radical protection in the kidney. MT is responsive to zinc and primarily localized within the renal cortex. However, site-specific renal responses to dietary zinc repletion are understudied. The objective of this study was to examine the effects of dietary zinc deficiency and repletion on renal MT concentration and immunolocalization in rats. Weanling male Sprague Dawley rats were randomly assigned to either a zinc-deficient, zinc control, or pair-fed to zinc-deficient group. Half of the zinc-deficient and pair-fed rats were repleted with the control diet ad libitum for an additional 24 h. Renal tissue samples were assessed for total zinc, MT concentrations and MT immunostaining. Dietary zinc deficiency reduced renal zinc and MT concentrations, and attenuated intensity and localization of MT. Dietary zinc repletion for 24 h restored renal zinc and MT concentrations, the latter primarily in the proximal convoluted tubules of the cortex. Concentrations of renal MT, but not zinc, were elevated by diet restriction and MT (μg/mg protein) and partially normalized by 24 h diet repletion. In conclusion, renal MT modification due to zinc deficiency or diet restriction can be rapidly normalized in a site-specific manner with normal dietary zinc intake. The results support a role for MT in kidney homeostasis, in particular at the level of the proximal tubules in the cortex. The speed of MT repletion may have clinical implications for dietary zinc in the treatment of acute and chronic renal pathology due to toxins and free radicals.     

Dietary zinc deficiency decreases plasma concentrations of vitamin E

Experiments were conducted to examine the effects of dietary zinc (Zn) upon plasma vitamin E (E) concentrations to test the hypothesis that there may be a significant dietary interaction between these two nutrients. Weanling female Sprague-Dawley rats were fed diets that were (i) Zn-deficient (less than 0.9 micrograms Zn/g diet) ad libitum; (ii) Zn-adequate (50.9 micrograms Zn/g diet), pair-fed to the Zn-deficient group; and (iii) Zn-adequate (50.9 micrograms Zn/g diet) ad libitum. Plasma E in Zn-deficient animals (4.02 +/- 1.20 micrograms/ml) was significantly reduced (P less than or equal to 0.05) compared with results in both Zn-adequate pair-fed (9.21 +/- 0.70 micrograms/ml) and Zn-adequate ad libitum-fed (9.47 +/- 0.90 micrograms/ml) animals. Zn deficiency in this model system also resulted in significant (P less than or equal to 0.05) reductions in femur and plasma Zn concentrations as well as in plasma retinol, plasma triglyceride, and plasma cholesterol concentrations. Plasma albumin and total plasma protein concentrations were normal in Zn-deficient animals. With dietary Zn deficiency, the decrease in plasma E appeared to be out of proportion to associated decreases in plasma triglyceride and plasma cholesterol concentrations. Since E is associated with plasma lipoproteins, these data suggest that lipid and/or E malabsorption may be a consequence of Zn deficiency. In response to increased dietary intake of E, increments of plasma E were lower in Zn-depleted than in Zn-adequate, pair-fed animals. These findings suggest that dietary Zn deficiency possibly may increase the nutritional requirement for E necessary to maintain adequate plasma concentrations.     

Effects of dietary zinc on free radical generation, lipid peroxidation, and superoxide dismutase in trained mice.

The purpose of this study was to investigate the effects of dietary zinc on free radical generation, lipid peroxidation, and superoxide dismutase (SOD) in exercised mice. In the first part of the study, 48 male weanling mice were randomly divided into three groups. They were fed a zinc-deficient diet containing 1.6 mg/kg zinc or were pair-fed or fed ad libitum a zinc-adequate diet supplemented with 50 mg/kg zinc. Half of each group received an exercise training program that consisted of swimming for 60 min per day in deionized water. The diets and exercise program persisted for 6 weeks. In the second part of the study, 64 mice were fed zinc-deficient diets for 6 weeks, and then one group was fed the zinc-deficient diet for an additional 3 weeks, and the other three groups were fed diets supplemented with 5, 50, and 500 mg/kg zinc, respectively. Half of each group also received the exercise program. Both blood and liver samples were examined. Free radicals in liver were directly detected by electron spin resonance techniques and the extent of lipid peroxidation was indicated by malonic dialdehyde (MDA). Both CuZn-SOD and Mn-SOD were measured. The results showed that exercise training increased the metabolism of zinc, and zinc deficiency induced an increased free radical generation and lipid peroxidation and a decreased hepatic CuZn-SOD activity in exercised mice. Furthermore, although exercise training had no effect on the level of free radicals in zinc-adequate mice, it could increase the hepatic mitochondrial MDA formation further in zinc-deficient animals and zinc deficiency would eliminate the exercise-induced increase in SOD activities which existed in zinc-adequate mice. A total of 50 mg/kg zinc supplemented in the diet was adequate to correct the zinc-deficient status in exercised mice while 5 mg/kg zinc had a satisfactory effect on the recovery of only sedentary zinc-deficient mice. However, 500 mg/kg zinc had a harmful effect on both sedentary and exercised zinc-deficient animals.     

Effect of dietary copper and zinc levels on tissue copper,zinc, and iron in male rats

The interaction between dietary copper and zinc as determined by tissue concentrations of trace elements was investigated in male Sprague-Dawley rats. Animals were fed diets in a factorial design with two levels of copper (0.5, 5 μg/g) and five levels of zinc (1, 4.5, 10, 100, 1000 μg/g) for 42 d. In rats fed the low copper diet, as dietary zinc concentration increased, the level of copper decreased in brain, testis, spleen, heart, liver, and intestine. There was no significant effect of dietary copper on tissue zinc levels. In the zinc-deficient groups, the level of iron was higher in most tissues than in tissues from controls (5 μg Cu, 100 μg Zn/g diet). In the copper-deficient groups, iron concentration was higher than control values only in the liver. These data show that dietary zinc affected tissue copper levels primarily when dietary copper was deficient, that dietary copper had no effect on tissue zinc, and that both zinc deficiency and copper deficiency affected tissue iron levels.     

In vivo effects of zinc deficiency on calmodulin concentrations in selected rat tissues

Two groups of male Sprague-Dawley rats, one fed zinc-deficient diet, ad libitum, the other, pair-fed with the same diet, but given supplemental zinc in the drinking water (8 mg Zn++/ml) were studied. After ten weeks of diet, rats were exsanguinated and zinc and calmodulin concentrations in brain and testis were measured. Mean zinc concentration in testis was significantly decreased in rats fed zinc-deficient diet without supplemental Zn++, but mean zinc concentration in brain was not different. Similarly, mean calmodulin concentration in testis was decreased in rats fed zinc-deficient diet without supplemental Zn++ whereas mean calmodulin concentration in brain was not different. Distribution studies of zinc and calmodulin showed that both zinc and calmodulin were released more freely into soluble fractions of testis in rats fed zinc-deficient diet without supplemental Zn++. These results indicate, for the first time in in vivo studies, that zinc influences the calmodulin content of testis.     

The effect of zinc deficiency and food restriction on prostaglandin E2 and thromboxane B2 in saliva and plasma of rats

Zinc has been implicated in the regulation of prostaglandins and other arachidonic acid derivatives. Studies of zinc-deficient animals, however, are compromised by concomitant reduction in food intake that may also alter eicosanoid levels in body tissues and fluids. In this study, three groups of rats, designated as zinc-deficient, pair-fed and control, were fed diets containing 1 ppm, 15 ppm (in amounts paired to deficient rats) and 15 ppm Zn ad libitum, respectively, for 6 weeks. Saliva and blood were analyzed for PGE2 and TXB2 by radioimmunoassay. Saliva concentrations of both eicosanoids were lower (p less than 0.05) in the pair-fed animals, but not significantly altered by zinc deficiency. Plasma levels of PGE2 and TXB2 were unchanged by either zinc deficiency or food restriction. The results of this study support the contention that the effect of zinc on these prostaglandins is not mediated by altered rates of synthesis or degradation but rather by effects on eicosanoid function.     

Effects of dietary zinc deficiency on gonadotrophin secretion and testicular growth in young male sheep.

The hypothesis that the secretion of gonadotrophins would be reduced by zinc deficiency was tested in five groups of four young Merino rams (initial liveweight 22 kg). Four groups were fed ad libitum with diets containing 4, 10, 17 or 27 micrograms Zn g-1. The effects of loss of appetite on the deficient diet was controlled by feeding a fifth group (pair-fed control) at a rate of 27 micrograms Zn g-1, but the amount of feed offered was restricted to that eaten voluntarily by the deficient (4 micrograms Zn g-1) group. Blood was sampled every 20 min for 32 h on two occasions before the treatments were imposed and 96 days later, at the end of the experiment. The rams were injected with gonadotrophin-releasing hormone (GnRH; 10 ng kg-1 i.v.) after each serial sampling, and with naloxone (1 mg kg-1 i.v.) 24 h after the end of the final GnRH test. In the group that were fed the diet with the lowest zinc content, the concentration of zinc in blood plasma was reduced to 18% of that in the pair-fed controls (P < 0.05) and was within the deficient range. The appetite of the deficient rams was half that of the controls fed 27 micrograms Zn g-1 ad libitum and there was no increase in liveweight or testicular diameter during pubertal development. Similar, but smaller, effects were observed in the pair-fed controls. There were no significant differences between pair-fed and deficient groups in the frequency of the luteinizing hormone (LH) pulses or in the concentration of follicle-stimulating hormone (FSH), but the secretion of gonadotrophins was markedly lower in both groups than in the control rams fed ad libitum. The response to GnRH was not affected by treatment, but the increase in LH pulse frequency evoked by naloxone was lower in the deficient animals than in other groups. The animals fed zinc at intermediate rates (10-17 micrograms g-1) showed similar responses to the controls fed ad libitum. It is concluded that the specific effects of zinc deficiency on testicular function were small. Most of the reduction in testicular growth in rams fed a deficient diet was not specifically related to the trace element, but was due to the fall in energy and protein intake caused by the loss of appetite. This leads to a reduction in the frequency of GnRH pulses secreted by the hypothalamus, and to low rates of gonadotrophin secretion by the pituitary gland.     

The mobility and reactivity of maleimide-binding proteins in the rat erythrocyte membrane. Effects of dietary zinc deficiency and incubation with zinc in vitro

Erythrocyte ghosts, prepared from rats fed zinc-deficient diets, were analyzed for the mobility of membrane proteins by electron spin resonance spectroscopy of the sulfhydryl-binding spin probe, 4-maleimido-2,2,6,6-tetramethylpiperidine-N-oxyl. Compared with erythrocyte membranes from rats fed zinc-adequate diets ad libitum or pair-fed, erythrocyte membranes from zinc-deficient rats had a significantly increased ratio of weakly immobilized to strongly immobilized probe-binding proteins. This suggests that dietary zinc deficiency causes a conformational change in erythrocyte membrane proteins. Dietary zinc deficiency did not significantly affect N-ethylmaleimide (NEM)-induced thermal sensitivity or NEM-induced mechanical fragility in rat erythrocytes; however, the addition of zinc in vitro to red cells significantly inhibits NEM-induced mechanical fragility.     

Influence of zinc depletion and zinc status on serum growth hormone levels in rats

In a preceding trial, the growth hormone concentrations in the serum of zinc-deficient rats were greatly reduced compared to thead libitum- fed control animals. The same reduction, however, was also noted in the case of the pair-fed control animals with strongly diminished feed intake. Therefore, it was not possible to distinguish between the effects of zinc deficiencyper se and the effects resulting from restricted feed intake. A new study with 136 young male Sprague-Dawley rats showed again that zinc deficiency as well as strongly restricted feed intake reduced the growth hormone content in the serum. But in a marginal zinc deficiency status, when feed intake was only slightly or not reduced, there were lowered serum growth hormone levels in comparison to pair-fed control rats. A 1-wk zinc repletion did not increase the serum growth hormone content of the rats to a normal level, although the serum zinc concentration was normalized.     

The effect of zinc defficiency and food restriction on prostaglandin E2 and thromboxane B2 in saliva and plasma of rats

Zinc has been implicated in the regulation of prostaglandins and other arachidonic acid derivatives. Studies of zinc-deficient animals, however, are compromised by concomitant reduction in food intake that may also alter eicosanoid levels in body tissues and fluids. In this study, three groups of rats, designated as zinc-deficient, pair-fed and control, were fed diets containing 1 ppm, 15 ppm (in amounts paired to deficient rats) and 15 ppm Zn adlibitum, respectively, for 6 weeks. Saliva and blood were analyzed for PGE₂ adn TXB₂ by radioimmunoassay. Saliva concentrations of both eicosanoids were lower (p<0.05) in the pair-fed animals, but not significantly altered by zinc deficiency. Plasma levels of PGE₂ and TXB₂ were unchanged by either zinc deficiency or food restriction. The results of this study support the contention that the effect of zinc on these prostaglandins is not mediated by altered rates of synthesis or degradation but rather by effects on eicosanoid function.     

Effects of zinc deficiency and supplementation on plasma leptin levels in rats

The effects of zinc deficiency and supplementation on plasma leptin levels were studied in Sprague-Dawley rats. After 6 wk on a zinc-deficient diet containing 0.65 ppm Zn/g, the mean body weight was significantly lower than that of normal or zinc-supplemented rats, which showed no difference among them. The plasma leptin and zinc levels were lowest in zinc-deficient animals and highest in those that received a normal diet and daily intraperitioneal injections of 3 mg Zn/kg. These results indicate that zinc deficiency leads to a significant inhibition in plasma leptin levels, whereas zinc supplementation significantly increases plasma leptin.     

Gestational zinc deficiency amplifies the regulation of metallothionein induction in adult mice

To determine if prenatal zinc deficiency has a persistent effect on metallothionein (MT) regulation, Swiss-Webster mice were mated and fed a diet containing either control (100 micrograms Zn/g) or low levels of zinc (5 micrograms Zn/g) from Day 7 of gestation to parturition. After birth all mice were given the control diet. Liver zinc and MT levels were 50% lower in newborn pups from dams fed the low zinc diets than in control pups. In control pups, liver zinc and MT concentrations were relatively stable during the first week of postnatal life. In contrast, in pups prenatally deprived of zinc, liver levels of zinc and MT increased such that by Day 3 of postnatal life, the levels were not significantly different from controls. At Day 56, serum IgM concentrations were significantly lower in the low zinc offspring. Liver zinc concentrations in the two groups of mice were similar at Day 70 postnatal, and in both groups liver MT levels were below detection limits. However, when Day 70 mice were given zinc injections to stimulate MT synthesis, the prenatally zinc deprived offspring showed markedly higher liver MT levels than did control mice given similar injections, despite similar liver zinc concentrations in the two groups. These results show that prenatal zinc deficiency has pronounced effects on postnatal MT metabolism which can persist into adulthood.     

Maternal zinc deficiency reduces NMDA receptor expression in neonatal rat brain, which persists into early adulthood

Prenatal and early postnatal zinc deficiency impairs learning and memory and these deficits persist into adulthood. A key modulator in this process may be the NMDA receptor; however, effects of zinc deficiency on the regulation of NMDA receptor activity are not well understood. Female Sprague-Dawley rats were fed diets containing 7 (zinc deficient, ZD), 10 (marginally zinc deficient, MZD) or 25 (control) mg Zn/g diet preconception through postnatal day (PN) 20, at which time pups were weaned onto their maternal or control diet. Regulation of NMDA receptor expression was examined at PN2, PN11, and PN65. At PN2, expression of whole brain NMDA receptor subunits NR1, NR2A, and NR2B was lower in pups from dams fed ZD and MZD compared to controls, as analyzed using relative RT-PCR and immunoblotting. At PN11, whole brain and hippocampi NR1, NR2A, NR2B and PSA-NCAM (polysialic acid-neural cell adhesion molecule) expression and the number of PSA-NCAM immunoreactive cells were lower in pups from dams fed ZD compared to controls. Whole brain brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) concentrations were lower in pups from dams fed ZD or both low zinc diets, respectively. Whole brain NR1 expression remained lower in previously zinc-deficient rats at PN65. These data indicate potential mechanisms through which developmental zinc deficiency can impair learning and memory later in life.     

Absorption,endogenous excretion,and balance of zinc in growing rats on diets with various sugars replacing starch

The effect of partially replacing starch for various sugars on the apparent and true absorption, endogenous excretion, and balance of zinc was investigated in a study with growing rats. Six groups of five or six animals with an initial live weight of 39.4 +/- 2.7 g were fed diets that had the same Zn content (22 mg/kg), but differed in the sugar content: 1. Starch only (56%); 2. Glucose (15%); 3. Fructose (15%); 4. Sucrose (30%); 5. Galactose (15%); and 6. Lactose (30%). At the start of a 15-d fecal and urinary collection period, each animal was given an intramuscular injection of 380 kBq 65Zn for estimating endogenous Zn excretion by isotope dilution. The ratio of the specific activity of fecal Zn (after 12 d) to that of urinary Zn (after 9 d) was applied to reflect the ratio of endogenous to total fecal Zn collected from day 10 to 15. This ratio averaged 0.59, without significant differences among treatments. For this period, apparent and true absorption averaged 87.1 and 94.7% of Zn intake, respectively, and did not significantly differ among diets. Urinary excretion of 65Zn and of stable zinc by the galactose-fed rats was markedly higher than that by the other animals. Their Zn balance was, per unit weight gain, comparable with that of the other groups (30.7 vs 28.2 to 30.2 micrograms/g).     

Long-term effects of lactational zinc deficiency on bone mineral composition in rats fed a commercially modified Luecke diet

The purpose of this study was threefold: 1. to determine the long-term effects of interactions between lactational zinc deficiency and gender on bone mineral composition in repleted rat offspring, 2. to determine the nutritional efficacy of the second of two commercially designed, modified Luecke diets (ML2) during the gestational and lactational stress, and 3. determine the ultratrace element contents of Ralston Rodent Laboratory Chow #5001. The ML2 basal diet, based on dextrose, sprayed egg white, and corn oil contained 0.420 μg Zn/g, was supplemented with Zn (as zinc acetate) at 0 (diet 0ML2) or 30 (diet 30ML2) μg/g, and was mixed and pelleted commercially. all rat dams were fed the 30ML2 diet ad libitum during gestation. Beginning at parturition, the dams were fed either the 1. 0ML2, 2. 30ML2 (food restricted), or 3. 30ML2 (ad libitum) diets. All pups were fed the 30ML2 diet ad libitum from 23 to 40 d of age. From d 40 to 150, all pups were fed Ralston Rodent Laboratory Chow. The 30ML2 diet was found to be nutritionally efficacious; litter size and pup growth were normal and pup mortality was only 1.2%. Pups (ZD) with access to the 0ML2 diet until 23 d of age and nursed by dams fed the 0ML2 diet, when compared to pups (PF) fed restricted amounts of the 30ML2 diet, exhibited increased mortality and decreased concentrations of tibial zinc but no change in growth. Inadequate zinc nutriture during infancy, despite postlactational zinc repletion, induced imbalances in adult bone mineral metabolism. Thus, at 150 d of age, the ZD pups exhibited increased levels of bone P and Mg and decreased concentrations of K as compared to the PF pups.     

Levels and distribution of zinc,copper, magnesium,and calcium in rats fed different levels of dietary zinc

Effects of altered dietary zinc on levels of zinc, copper, magnesium, and calcium in organ and peripheral tissues were studied. When rats fed a zinc-deficient diet (1.3 μg Zn/g) for 28 d were compared with rats fed a control diet (37.5 μg Zn/g), levels of zinc were slightly lower in plasma, hair, and skin and 50% lower in femur and pancreas, whereas the levels of copper were higher in all tissue except plasma. Magnesium levels were higher than controls in the heart and lower in the spleen, whereas the calcium levels were lower in plasma, lung, spleen, kidney, and skin and strikingly higher in brain, hair, and femur. When rats fed a zinc-supplemented diet (1.0 mg Zn/g) were compared to the same conrols, levels of zinc in these were higher in all organs and peripheral tissues studied, except heart, lung, and liver; copper levels were higher in liver, kidney, and spleen; magnesium levels were significantly higher in the spleen, but were little affected in other tissues, although calcium levels were higher in pancreas, spleen, kidney, and skin and lower in plasma and hair. These data indicate that overall copper organ and peripheral tissue levels are affected inversely, and zinc and calcium levels directly, by zinc nutriture.     

Zinc availability and digestive zinc solubility in piglets and broilers fed diets varying in their phytate contents, phytase activity and supplemented zinc source

The study was conducted to evaluate the effects of dietary zinc addition (0 or 15 mg/kg of Zn as inorganic or organic zinc) to three maize-soybean meal basal diets varying in their native Zn, phytic P contents and phytase activity (expressed in kg of feed: P- with 25 mg Zn and 1.3 g phytic P, P+ with 38 mg Zn and 2.3 g phytic P or P+/ENZ being P+ including 500 units (FTU) of microbial phytase per kg) in two monogastric species (piglets, broilers). Measured parameters were growth performance, zinc status (plasma, and bone zinc) and soluble zinc in digesta (stomach, gizzard and intestine). The nine experimental diets were fed for 20 days either to weaned piglets (six replicates per treatment) or to 1-day-old broilers (10 replicates per treatment). Animal performance was not affected by dietary treatments (P > 0.05) except that all P- diets improved body weight gain and feed conversion ratio in piglets (P < 0.05). Piglets fed P- diets had a better Zn status than those fed P+ diets (P < 0.05). In both species, Zn status was improved with supplemental Zn (P < 0.05), irrespective of Zn source. Phytase supplementation improved piglet Zn status to a higher extent than adding dietary Zn, whereas in broilers, phytase was less efficient than supplemental Zn. Digestive Zn concentrations reflected the quantity of ingested Zn. Soluble Zn (mg/kg dry matter) and Zn solubility (% of total Zn content) were highest in gizzard contents, which also presented lower pH values than stomach or intestines. The intestinal Zn solubility was higher in piglet fed organic Zn than those fed inorganic Zn (P < 0.01). Phytase increased soluble Zn in piglet stomach (P < 0.001) and intestine (P = 0.1), but not in broiler gizzard and intestinal contents. These results demonstrate (i) that dietary zinc was used more efficiently by broilers than by piglets, most probably due to the lower gizzard pH and its related higher zinc solubility; (ii) that zinc supplementation, irrespective of zinc source, was successful in improving animal's zinc status; and (iii) suggest that supplemented Zn availability was independent from the diet formulation. Finally, the present data confirm that phytase was efficient in increasing digestive soluble Zn and improving zinc status in piglets. However, the magnitude of these effects was lower in broilers probably due to the naturally higher Zn availability in poultry than in swine.     

Effects of zinc deficiency on morphogenesis of the fetal rat eye

Maternal zinc deficiency during pregnancy results in a high frequency of fetal eye malformations in the Long-Evans rat. In this study we examine the development of the eye from days 12 through 21 of gestation in conceptuses of dams fed deficient or adequate levels of zinc and also examine maternal plasma and conceptus zinc concentrations during this period. Dams were fed diets containing 0.5 (0.5 Zn group), 4.5 (4.5 Zn group), or 100 (100 Zn AL group) micrograms zinc per gram diet ad libitum, or 100 micrograms zinc g-1 diet in amounts restricted on a daily basis to the intake of matched animals from the 0.5 Zn group (100 Zn RI group). Conceptuses were removed and maternal plasma was collected on days 12, 14, 16, 19 and 21 of gestation. Maternal plasma and conceptus zinc concentrations reflected maternal dietary zinc level, with dam plasma Zn concentrations in the order of 0.5 Zn group less than 4.5 Zn group less than 100 Zn group on all days. A similar pattern held for embryo/fetus zinc, except for days 19 and 21, at which times the 0.5 Zn and 4.5 Zn fetuses had similar zinc concentrations. Histological examination of the developing eye of 0.5 Zn fetuses on days 12 and 14 revealed that invagination of the optic cup was often deficient, and that closure of the choroid fissure did not occur, resulting in colobomata and retinal folding visible at term. A very few fetuses were found at term to be anophthalmic or have only remnants of ocular tissue.(ABSTRACT TRUNCATED AT 250 WORDS)