Effects Of Marginal Zinc Deficiency Research Articles

Marginal zinc deficiency alters the heart proteome of rats.

Zinc deficiency is closely related to cardiovascular diseases (CVDs), but the effects of marginal zinc deficiency (MZD) after birth on the heart are unknown. In this study, 4-week-old male rats were fed a low zinc diet (10 mg kg-1, 1/3 recommended nutrient intake, RNI) for 8 weeks. Echocardiography and histopathology were performed to assess the functional and morphological alterations of the heart. High-throughput proteomics was used to study the effects of MZD on cardiac protein expression. We found that MZD reduced food intake, body weight, serum zinc, and heart weight; however, the coefficient, zinc concentration, function, and histopathology of the heart were not changed. The heart proteome was altered in the marginal zinc-deficient diet group (MZG), compared with the normal zinc diet group (NZG). A total of 310 differentially expressed proteins (P < 0.05) were significantly changed by MZD, among which 163 proteins were up-regulated and 147 were down-regulated. Of these, 43 proteins are related to CVDs and 18 proteins are zinc-associated proteins. Gene Ontology and Pathway analysis revealed that 74 biological processes (BPs) and 37 pathways were significantly changed by MZD. This included six CVD-related BPs, such as regulation of heart rate, cardiac muscle contraction, regulation of ventricular cardiac muscle cell action potential, and regulation of blood pressure, and eight CVD-related pathways, such as dilated cardiomyopathy, diabetic cardiomyopathy, and hypertrophic cardiomyopathy. Our data show that marginal zinc deficiency after birth significantly alters cardiac protein expression and pathways related to CVDs.

Effects of marginal zinc deficiency on learning and memory ability after birth.

Zinc deficiency during pregnancy and severe zinc deficiency after birth both impaired learning and memory ability, but the effects of marginal zinc deficiency (MZD) after birth on learning and memory are unclear. In the first experiment, 4-week-old male rats were randomly divided into three groups: the marginal zinc-deficient group (MZG, 10 mg kg-1, 1/3 RNI), normal zinc group (NZG, 30 mg kg-1, RNI), and paired zinc group (PZG, 30 mg kg-1). After a 4-week feeding period, the brain weight, brain coefficient, and serum zinc concentration were measured, and hippocampal proteomics analysis was performed. In the second experiment, 4-week-old male rats were fed the same diet for 8 weeks. In addition to the previously mentioned indicators, the Morris water maze results, brain pathology, post-translational modifications (PTMs) of hippocampal proteins, and the concentrations of indicators known to be related to learning and memory were analyzed. In both experiments, compared with those of the NZG, the food intake, body weight and serum zinc of the MZG were significantly decreased, and the brain weight was unchanged, but the brain coefficient was increased. Two hippocampal proteomics analyses and PTM screening showed that MZD did not change the expression and PTM of proteins. The brain pathology, learning, memory and the concentrations of indicators known to be related to learning and memory were not changed by MZD. Our study confirmed that marginal zinc deficiency (10 mg kg-1, 1/3 RNI) had no effect on the learning and memory abilities of rats after birth.

Marginal Zinc Deficiency in Mice Increased the Number of Abnormal Sperm and Altered the Expression Level of Spermatogenesis-Related Genes

Marginal zinc deficiency is more common than severe zinc deficiency, and the effect of marginal zinc deficiency on male reproduction is unknown. This study investigated the effect of marginal zinc deficiency on spermatogenesis and its mechanism. Male ICR mice were fed normal zinc (30mg/kg) and marginal zinc deficiency (10mg/kg) diets for 35days. Zinc-dependent proteins and enzymes were measured as biomarkers of zinc levels in the body. Metallothionein and Cu-Zn SOD levels in the control group were higher than those in the marginal zinc deficiency group. Hematoxylin and eosin staining showed that the marginal zinc deficiency diet caused histopathological changes in the testis and destruction of the sperm head under scanning electron microscopy. Sperm parameters and sex hormone levels were also affected by marginal zinc deficiency. In addition, marginal zinc deficiency led to alter expression level of several important spermatogenesis-related genes in the epididymis and testes. These results indicate that although zinc intake in marginal zinc deficiency is close to the recommended reference value, low zinc intake interferes with the expression of genes related to spermatogenesis and may lead to sperm abnormalities in mice.

Effects of zinc status on age-related T cell dysfunction and chronic inflammation

Age-related T cell dysfunction contributes to immunosenescence and chronic inflammation. Aging is also associated with a progressive decline in zinc status. Zinc is an essential micronutrient critical for immune function. A significant portion of the older populations are at risk for marginal zinc deficiency. The combined impact of dietary zinc deficiency and age on immune dysfunction has not been well explored despite the common occurrence together in the elderly population. We hypothesize that age-related zinc loss contributes to T cell dysfunction and chronic inflammation in the elderly and is exacerbated by inadequate dietary intake and improved with zinc supplementation. Using an aging mouse model, the effects of marginal zinc deficiency and zinc supplementation on Th1/Th17/proinflammatory cytokine profiles and CD4+ T cell naïve/memory phenotypes were examined. In the first study, young (2 months) and old (24 months) C57BL/6 mice were fed a zinc adequate (ZA) or marginally zinc deficient (MZD) diets for 6 weeks. In the second study, mice were fed a ZA or zinc supplemented (ZS) diet for 6 weeks. MZD old mice had significant increase in LPS-induced IL6 compared to ZA old mice. In contrast, ZS old mice had significantly reduced plasma MCP1 levels, reduced T cell activation-induced IFNγ, IL17, and TNFα response, as well as increased naïve CD4+ T-cell subset compared to ZA old mice. Our data suggest that zinc deficiency is an important contributing factor in immune aging, and improving zinc status can in part reverse immune dysfunction and reduce chronic inflammation associated with aging.

Marginal Zinc Deficiency and Environmentally Relevant Concentrations of Arsenic Elicit Combined Effects on the Gut Microbiome.

Extensive research shows that dietary variation and toxicant exposure impact the gut microbiome, yielding effects on host physiology. However, prior work has mostly considered such exposure-microbiome interactions through the lens of single-factor exposures. In practice, humans exposed to toxicants vary in their dietary nutritional status, and this variation may impact subsequent exposure of the gut microbiome. For example, chronic arsenic exposure affects 200 million people globally and is often comorbid with zinc deficiency. Zinc deficiency can enhance arsenic toxicity, but it remains unknown how zinc status impacts the gut microbiome's response to arsenic exposure and whether this response links to host toxicity. Using 16S amplicon sequencing, we examined the combinatorial effects of exposure to environmentally relevant concentrations of arsenic on the composition of the microbiome in C57BL/6 mice fed diets varying in zinc concentration. Arsenic exposure and marginal zinc deficiency independently altered microbiome diversity. When combined, their effects on microbiome community structure were amplified. Generalized linear models identified microbial taxa whose relative abundance in the gut was perturbed by zinc deficiency, arsenic, or their interaction. Further, we correlated taxonomic abundances with host DNA damage, adiponectin expression, and plasma zinc concentration to identify taxa that may mediate host physiological responses to arsenic exposure or zinc deficiency. Arsenic exposure and zinc restriction also result in increased DNA damage and decreased plasma zinc. These physiological changes are associated with the relative abundance of several gut taxa. These data indicate that marginal zinc deficiency sensitizes the microbiome to arsenic exposure and that the microbiome associates with some toxicological effects of arsenic.IMPORTANCE Xenobiotic compounds, such as arsenic, have the potential to alter the composition and functioning of the gut microbiome. The gut microbiome may also interact with these compounds to mediate their impact on the host. However, little is known about how dietary variation may reshape how the microbiome responds to xenobiotic exposures or how these modified responses may in turn impact host physiology. Here, we investigated the combinatorial effects of marginal zinc deficiency and physiologically relevant concentrations of arsenic on the microbiome. Both zinc deficiency and arsenic exposure were individually associated with altered microbial diversity and when combined elicited synergistic effects. Microbial abundance also covaried with host physiological changes, indicating that the microbiome may contribute to or be influenced by these pathologies. Collectively, this work demonstrates that dietary zinc intake influences the sensitivity of the microbiome to subsequent arsenic exposure.

Effect of dietary zinc intake on N-methyl-N-nitrosourea-induced mammary tumorigenesis in rats.

Numerous studies have shown that zinc nutrition influences the growth of several types of tumor. However, the influence of zinc nutrition on mammary tumorigenesis is not known. To study the effects of dietary zinc intake on N-methyl-N-nitrosourea (MNU)-induced mammary tumorigenesis, female Sprague-Dawley rats were fed an egg-white-based diet providing 3 (Z3), 12 (Z12), or 31 (Z31) mg zinc/kg diet ad libitum. In addition, two pair-fed controls, PFZ12 and PFZ31, were also included. Fourteen weeks after MNU injection, cumulative tumor incidence and total number of tumors were lower in Z3 rats than in Z12 and Z31 rats. Cumulative tumor incidence and total number of tumors were lower in Z3 rats than in PFZ12 rats, but were the same as in PFZ31 rats. Cumulative tumor incidence and total number of tumors were also lower in pair-fed controls than in their corresponding ad libitum controls, but were the same between the ad libitum controls. Overall, the results showed that the effect of marginal zinc deficiency on MNU-induced mammary tumorigenesis in rats was primarily the result of a reduced feed intake associated with marginal zinc deficiency rather than zinc per se.

Effect of marginal zinc deficiency on human growth and development.

Growth and development disorders in humans caused by zinc (Zn) deficiency have been investigated for a long time. Although marginal Zn deficiency is a common nutritional problem around the world, especially in the children of developing countries where diets have less Zn available, it is difficult to identify. This review provides the progression of studies in the effect of Zn deficiency on human growth and development, and also explains the possible mechanisms of how Zn promotes these phenomena. These mechanisms involve the effects of Zn on DNA synthesis, RNA synthesis, and cell division. The concept of zn-finger proteins explains the role of Zn in gene expression and endocrine function. Findings indicate that Zn deficiency can result in delayed growth and development which can be corrected in part by Zn supplementation.

Oscillatory Potentials and Light Microscopic Changes Demonstrate an Interaction between Zinc and Taurine in the Developing Rat Retina , ,

Our objective was to investigate whether zinc interacts with taurine to influence the development of retinal structure and function. Virgin female Sprague-Dawley rats were bred overnight and assigned to one of four treatments in a 2 × 2 factorial design with two levels of zinc (50 μg/g through gestation and 50 μg/g after parturition; 15 μg/g through gestation and 7.5 μg/g after parturition) and two levels of taurine (2 or 0 μmol/g). The control diet contained 50 μg/g zinc and 2 μmol/g taurine. Guanidinoethyl sulfonate (10 g/L), a taurine transport inhibitor, was added to the drinking water of the rats receiving 0 μmol/g taurine. At postnatal d 23, male pups (n = 10) were weaned onto their respective diets. Pup eyes were examined by biomicroscope and indirect ophthalmoscope at 4 and 7 wk; retinal folds and choroidal atrophy were detected in the pups deficient in zinc and taurine. Analysis of plasma zinc and tibial zinc concentrations revealed a significant interaction in these tissues (P < 0.05). Dark-adapted oscillatory potentials (OP) were recorded at 7.5–8.5 wk. Two-way ANOVA showed a significant interaction between zinc and taurine for OP2 and OP3 amplitudes; marginal zinc deficiency decreased the amplitude of the OP only when rats were also deficient in taurine. A significant depressing effect of marginal zinc deficiency was noted for OP1 amplitude. Taurine deficiency significantly depressed the amplitude of OP1 and OP4 . Histological examination of the retinas from rats deficient in both zinc and taurine revealed photoreceptor degeneration and confirmed retinal dysplasia. These data provide evidence for an interaction between zinc and taurine in retinal morphology and function.

Effect of Marginal Zinc Deficiency on Human Growth and Development

Growth and development disorders in humans caused by zinc (Zn) deficiency have been investigated for a long time. Although marginal Zn deficiency is a common nutritional problem around the world, especially in the children of developing countries where diets have less Zn available, it is difficult to identify. This review provides the progression of studies in the effect of Zn deficiency on human growth and development, and also explains the possible mechanisms of how Zn promotes these phenomena. These mechanisms involve the effects of Zn on DNA synthesis, RNA synthesis, and cell division. The concept of Zn-finger proteins explains the role of Zn in gene expression and endocrine function. Findings indicate that Zn deficiency can result in delayed growth and development which can be corrected in part by Zn supplementation.

Effects of marginal zinc deficiency on microtubule polymerization in the developing rat brain

One of the possible mechanisms that has been proposed to underlie the deleterious effects of zinc deficiency on brain development is an impairment in the normal formation of the cytoskeletal network. In the current study, in vivo microtubule polymerization was characterized in brain supernatant fluids, from 20-d-old pups whose dams were fed diets containing control (50 micrograms zinc/g) or marginal levels of zinc (10 micrograms zinc/g) throughout pregnancy and lactation. Pup brain and body weights were similar between the groups; however, plasma zinc concentrations were lower (27%) in pups fed the marginal zinc diet than in controls. Tubulin concentrations in 100,000 g brain supernates were similar between the groups; however, tubulin polymerization in the brain supernates was significantly lower in pups fed the marginal zinc diet compared to controls. Primarily, the early events of polymerization were affected; the lag period of the reaction was doubled, and the initial velocity was slower (26%) in supernates from pups fed the marginal zinc diet than in controls. These findings support the idea that some of the negative effects of marginal zinc deficiency on brain development and function may be mediated by an alteration in microtubule formation.

Influence of marginal maternal zinc deficiency on pregnancy outcome and infant zinc status in rhesus monkeys.

To investigate the effects of marginal zinc deficiency on early development, rhesus monkeys were fed a diet marginally deficient in zinc (M; 4 micrograms/g) throughout pregnancy and during the first month of lactation. Despite the low concentration of zinc in the diet. M dams did not develop overt signs of zinc deficiency. However, compared to control dams fed diets adequate in zinc (C; 100 micrograms Zn/g), M dams showed a low response to the mitogens concanavalin A and phytohemagglutinin. Pregnancy outcome was similar in the two groups and all of the neonates were judged to be healthy at delivery. From birth until d 30 of age, the infants were closely monitored for signs of zinc deficiency, and at d 30, they were killed and tissues were removed and analyzed for a number of parameters reported to be affected by zinc status. At birth, M infants had low plasma zinc concentrations compared to controls; however, this difference was not observed at d 30. D 30 M infants showed a normal response to the mitogens concanavalin A and phytohemagglutinin, but showed a low response to pokeweed mitogen. Tissue (liver, brain, spleen, kidney, and heart) trace element concentrations were similar in the two groups of infants, as were liver metallothionein concentrations and 65Zn uptake/retention by isolated hepatocytes. Infant wt gain was inversely correlated with plasma zinc, liver zinc, and liver metallothionein concentrations in both the M and C groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of marginal zinc deficiency on lipoprotein lipase activities in postheparin plasma, skeletal muscle and adipose tissues in the rat.

The activities of lipoprotein lipase in postheparin plasma, retroperitoneal adipose and gastrocnemius muscle tissues were determined in the rats fed 2.8 ppm of dietary zinc for eight weeks, as compared with pair-fed and ad libitum-fed rats given 30.8 ppm of zinc. The postheparin lipoprotein lipase activity, as determined by using a lipid emulsion labeled with [3H]triolein as the substrate, was significantly lower in the first group of rats, relative to that in the second and third groups. Tissue lipoprotein lipase activities were compared using the lipid emulsion and activator serum obtained from the zinc-deficient rats and the ad libitum-fed rats. The activator sera were devoid of very low density and low density lipoproteins, but enriched in high density lipoproteins. Muscle lipoprotein lipase activities were significantly lower when assayed with the activator serum from the zinc-deficient compared with the activities determined with the activator serum from the ad libitum-fed. Similarly, muscle lipoprotein lipase activities were lower in all groups when [3H]-triolein-labeled chylomicrons from the zinc-deficient were used as the substrate, compared with the activities determined using the chylomicrons from the ad libitum-fed. Lipoprotein lipase activities in the adipose tissues were not affected by the different sources of the activator sera and chylomicrons. The results strongly suggest that the decrease in postheparin lipoprotein lipase activity in zinc deficiency is not due to changes in tissue lipoprotein lipase enzyme per se, but to compositional alterations in chylomicrons and high density lipoprotein, particularly, with regard to C apolipoproteins, modulators of lipoprotein lipase activity.

Effect of marginal zinc deficiency on humoral immunity in rats

The purpose of this experiment was to examine the effects of a marginal zinc deficiency on serum immunoglobulin (Ig) IgM and IgG1 levels. 60 weanling female Sprague-Dawley rats were divided into six groups of ten animals each. Two control groups (73.7 ppm Zn) and two zinc-deficient groups (4.3 ppm Zn) were fed a semisynthetic casein diet ad libitum. The animals of two further groups received the control diet (73.7 ppm Zn) pair-fed to the zinc-deficient animals. After 15 days the rats of one group of each treatment were infected i.m. with a single injection (0.2 ml) of a bovine enterovirus, apathogenous to rats. 3 weeks later, all rats were anesthetized with ether and decapitated. Infection of the rats with the bovine enterovirus had no effect on the serum immunoglobulin level. The marginal zinc deficiency did not alter the IgM and IgG1 serum concentrations at all either. It remains to be examined whether other Ig-classes will react to marginal zinc deficiency. Also, the effect of severe zinc deficiency on the humoral immune system must be studied.

Effect of marginal zinc deficiency on the apolipoprotein-B content and size of mesenteric lymph chylomicrons in adult rats.

To investigate the mechanisms underlining the impaired intestinal absorption of lipids in zinc deficiency, the apo-B content and chemical composition of chylomicrons from marginally zinc-deficient rats fed 2.8 ppm of dietary zinc (ZD) were compared with those from pair-fed (PF) and ad libitum control (CT) groups fed an adequate level (30.8 ppm) of zinc. Chylomicrons, obtained by cannulating the mesenteric lymph, were isolated by ultracentrifugation at 1.3 X 10(6) g/min at 12 C and purified by 2% agarose column chromatography. Apolipoprotein- (apo) B was separated by the method of isopropanol precipitation. The apo-B concentration of chylomicrons was lowered significantly in ZD group. The apo-B contents of chylomicrons in ZD, PF and CT rats, as expressed as % chylomicron protein, were 8.7 +/- 0.1, 11.5 +/- 0.5 and 10.7 +/- 0.7%, respectively. No significant differences were noted between ZD and PF groups in total protein (TP), phospholipid (PL), triglyceride (TG) and cholesterol (CH), although there was a slight decrease in TG and an increase in CH in CT rats compared with ZD and PF groups. The ratio of the core to surface constituents, as determined by TG/(TP + PL), was significantly higher in ZD group relative to the controls, suggesting that chylomicrons from ZD rats were larger. This finding was consistent with the appearance of larger chylomicron particles in the lacteal of the intestinal mucosa following lipid ingestion. These findings suggest that the intestinal synthesis of apo-B may be defective in zinc-deficient rats and may explain in part the impaired absorption of dietary lipids observed in zinc deficiency.

Effect of Marginal Zinc Deficiency on the Lymphatic Absorption of [14C]Cholesterol

The effect of zinc deficiency on intestinal absorption of cholesterol was investigated in adult male rats fed 3.6 ppm of dietary zinc (ZD) and compared with pair-fed (PF) and ad-libitum (CT) controls fed 30.6 ppm of zinc for 10 to 12 wk. The intestinal absorption of cholesterol was measured by collecting the mesenteric lymph at hourly intervals for 8 h after infusing a dose of [14C]cholesterol in a lipid emulsion through an indwelling duodenal catheter. Data on the hourly lymphatic output of [14C]cholesterol showed that the absorption of [14C]cholesterol plateaued at 4 h postdosing in all groups. The rate of the appearance of [14C]cholesterol in the mesenteric lymph significantly decreased in ZD rats at 5 h and thereafter. The cumulative absorption of [14C]cholesterol by ZD rats for the 8-h period was 4.4 ± 1.0% of the dose, compared with 11.8 ± 1.1% by PF and 10.7 ± 1.4% by CT rats. There were no differences in percent distribution of esterified [14C]cholesterol among the three groups. Also, no significant change in mucosal cholesterol esterase activity was observed due to zinc deficiency. The present data and previous findings taken together suggest that the primary mechanism responsible for the impaired absorption of cholesterol may be associated with defective formation of chylomicrons in the intestinal mucosa.

Effect of marginal zinc deficiency on the morphological characteristics of intestinal nascent chylomicrons and distribution of soluble apoproteins of lymph chylomicrons

Effects of marginal zinc depletion on the compositional and morphological characteristics of chylomicrons were investigated in adult male rats fed 3 ppm of dietary zinc, as compared with pair-fed and ad-libitum controls given 30 ppm of zinc for 6 to 8 wk. Lymph was collected by cannulating the intestinal lymphatic duct during infusion of a 1:1 mixture of Intralipid and 150 mM NaCl via a duodenal catheter. Lymph chylomicrons were isolated by ultracentrifugation and further purified by agarose column chromatography. A marginal level of zinc deficiency produced decreases in the relative concentrations of apolipoproteins C and E, with an increase in apoprotein A-I and no change in apoprotein A-IV and no significant alterations in the lipid components. Nascent chylomicrons in the intestinal absorptive cells were irregular and larger in shape and size, as determined by light and electron microscopy. The present results suggest that the changes in chylomicron apoproteins produced by zinc deficiency are due in part to postsynthetic modification of intestinal chylomicrons upon their release into the lymph.

Effects of Marginal Zinc Deficiency on Subclinical Lead Toxicity in the Rat Neonate

Influence of maternal dietary zinc intake on tissue distribution of lead and zinc in neonatal rats administered lead acetate by gavage during lactation was examined. Milk from dams fed a marginally deficient diet (6 µg Zn/g diet) contained a lower zinc concentration at the beginning of lactation than did that from control dams (30 µg Zn/g diet); no differences were seen by d 11 of lactation. Dams fed the deficient diet had lower plasma zinc values in comparison with pair-fed or ad libitum-fed dams and lower femur zinc concentration in comparison with pair-fed dams. Pups suckling marginally deficient dams had lower concentrations of zinc in plasma, femurs and kidneys although hippocampal and cerebellar zinc were unaltered. Body weights of pups from marginally zinc-deficient dams were lower than those from ad libitum-fed dams, but similar to those from pair-fed dams. Lead ingestion had no effect on body weight. Marginally zinc-deficient pups had greater lead accumulation in blood, femurs, hippocampi and cerebella, but not kidney, than did zinc-adequate pups. Marginal zinc deficiency during lactation increases the body lead burden of suckling rats, an effect not attributable to increased transfer of lead into milk in response to suboptimal maternal zinc status.

Placenta and maternal effects of marginal zinc deficiency during gestation in rats

Effects of a marginally zinc deficient diet (6 μg Zn/g diet) were investigated in the pregnant rat. In comparison to the control group (50 μg Zn/g diet), serum zinc concentration was significantly lower (P<0.01) in the marginal group on day 18 of gestation; serum decreased by about 45 μg/dl between days 18 and 22 of gestation in both groups, however. Dam cumulative weight gain increased 25% during the last four days of gestation in the marginal group, but it nearly doubled in the control group. Average fetal weight in the marginal group was 16% lower than controls, but placental weight, placental DNA, and protein concentration were not reduced. The total activity of the zinc metalloenzyme, leucine aminopeptidase (LAP) (E.C.3.4.11.3.) in the placenta and maternal serum was not affected by the marginal zinc diet. Apparent K m and relative V max of placental LAP were also unaffected. It appears that maternal zinc status and weight gain are reduced in a marginal zinc deficiency to support placental function and fetal growth.

Alteration of Antibody-Mediated Responses of Suckling Mice to T-Cell-Dependent and Independent Antigens by Maternal Marginal Zinc Deficiency: Restoration of Responsivity by Nutritional Repletion

To further characterize the effects of marginal zinc deficiency on the development of the immune system of the suckling A/J mouse, dams were fed marginal (1.6 μg Zn/g), intake restricted (30μg Zn/g) or adequate (30 μg Zn/g) levels of dietary zinc days 5–17 postpartum. Marginal levels of zinc had little effect on the body weight of dams; however, their pups were only 71–75% the weight of control pups. In response to two T-cell independent (TI) antigens pups of low zinc dams could produce only 49 and 44% as many antibody-producing cells per spleen as control pups. Pups of restricted-fed dams produced about 60% as many cells as controls for each TI antigen. The avidities of the plaques produced by pups of restricted and control dams in response to TI antigens were nearly the same but were 5.5 times higher than the relative avidities of the antibodies produced by pups of low zinc dams. The responses of the deficient pups to sheep red blood cells (SRBC), a T-dependent (TD) antigen, were 25–30% of response of control and 56–75% of that of restricted pups depending on whether direct (IgM) or indirect (IgG) plaques were enumerated. The data demonstrate that marginal deficiencies in zinc during lactation greatly reduce the ability of suckling pups to mount antibody-mediated responses and suggest that the kinds of lymphocyte subsets found in deficient pups are altered. However, antibody-mediated response capacity was normal in the deficient pups following a short period of zinc supplementation.

Normal levels of zinc and sulfhydryls in morphologically abnormal populations of spermatozoa from moderately zinc‐deficient rats

AbstractZinc is required for spermatogenesis in mammals and is concentrated in the dense outer fibers of the sperm tail, where it is associated with cysteine‐rich protein. To investigate the effects of marginal zinc deficiency upon dense fiber formation and upon sperm quality in general, weanling Sprague‐Dawley rats were administered a commercial low‐zinc diet, supplemented with phytate, for approximately 60 days, and were compared with controls fed the same diet plus 50 ppm zinc in their drinking water. The following characteristics of the zinc‐deficient rats were significantly lower than in the controls: body weight, testis weight, epididymis weight, seminal vesicle weight, sperm content of the cauda epididy‐midis, sperm motility, testis zinc, and hair zinc. By contrast, the levels of sperm zinc and sperm sulfhydryls were the same in the zinc‐deficient and control rats. The zinc‐deficient rats displayed a highly variable spectrum of sperm defects, which included decapitation, disorganized and redundant tail elements, and superfluous cytoplasm. However, abortive dense fiber development was only rarely observed. Apparently, even when availability of zinc is limited and reduced sperm production ensues, elaboration of dense fibers rich in zinc and sulfhydryls continues to be obligatory for the completion of spermiogenesis.