The effects of maternal zinc deficiency on myometrial contractility: an in vitro study

Aim: The aim of the study is to investigate the effects of zinc-supplemented or zinc-deficient diet on myometrial contractility during pregnancy. Material and Method: The patients were divided in four groups as Group 1 (n=5) fed with zinc-deficient diet, Group 2 (n=5) fed with zinc-supplemented diet, Group 3 (n=5) fed with normal diet, and Group 4 (n=5) as the control group and in vitro contractility study was conducted in the myometrial samples taken from these four groups, and intergroup comparison was performed for the results. The p<0.05 was accepted as significant. Results: In the evaluation of the contractility data, it was determined that the strength and period of contraction and also the frequencies increased in the zinc-supplemented group compared to the other groups. The difference was found to be significant only in frequency ( p<0.05). In the intergroup comparison, the frequency was found to be significantly higher in the zinc-supplemented group than all the other groups ( p<0.05). Conclusion: This in vitro finding can indicate the importance of zinc supplementation during pregnancy for postpartum bleeding.

Zinc Administration Affects Bronchial Mucosal NF-κB p105/p50, p-NF-κB p65, IL-8, and IL-1β of Zinc-deficient Rats

BACKGROUND: Risk of acute respiratory infections in children less than 5 years of age is up to 95%. Zinc deficiency is one of the main risk factors. This study aimed to explore the effect of zinc on the bronchial mucosae inflammatory status expressed by nuclear factor (NF)-κB p105/p50, NF-κB p65, interleukin (IL)-8, and IL-1β.METHODS: Twenty-four Wistar rats were divided into 4 groups: normal zinc diet group without zinc supplementation (Z1), normal zinc diet group with zinc supplementation (Z2), zinc deficient diet group without zinc supplementation (Z3), and zinc deficient diet group with zinc supplementation (Z4). NF-κB p105/p50, p-NF-κB p65, IL-8, and IL-1β were measured by immunohistochemical staining.RESULTS: The inflammatory status of bronchial mucosae between Z1 and Z2 groups showed no difference (p=0.055). However, the inflammatory status of bronchial mucosae between Z3 and Z4 groups showed significant difference (p<0.01). Multivariate factorial design showed that zinc supplementation was beneficial when given to zinc deficient diet group with regard to decrease p-NF-κB p65, IL-8 and IL-1β levels (p<0.001) and increase dendritic cell (p=0.022).CONCLUSION: Zinc administration under conditions of zinc deficiency affects the inflammatory status, as shown by the decrease of p-NF-κB p65, IL-8 and IL-1β and the increase of NF-κB p105/p50.KEYWORDS: zinc, NF-κB, p105/p50, p65, IL-8, IL-1β, rat

The Effects of Short-Term Zinc Feeding on Zinc Absorption and Zinc Transporter Expression in the Small Intestine of Mice

Objectives Zinc homeostasis is primarily maintained by zinc transporters that regulate zinc uptake and efflux in the small intestine; however, no study to date has comprehensively examined zinc transporter expression in the small intestine of mice fed varying levels of dietary zinc. The objective of this study was to determine the effects of zinc absorption and zinc transporter expression in the small intestine of mice fed varying levels of zinc for one week. Methods Seven-week-old male C57BL/6 J mice were randomized to either a standard AIN-93 G diet containing 30 ppm zinc (zinc adequate) or modified AIN-93 G diets containing &lt;1 ppm (zinc deficient) or 100 ppm zinc (zinc supplemented) for one week (n = 5–10/diet). Mice were given an oral gavage containing a slurry of zinc deficient feed and 10 μg 67 Zn; plasma isotope appearance was determined 6-h later by ICP-MS. Gene expression of Slc39a1–14 and Slc30a1–10 was determined in each intestinal segment (duodenum, jejunum, and ileum) by RT-qPCR. Results Plasma and liver zinc concentrations were not different after one week of feeding (P &gt; 0.05 for both). Plasma appearance of 67 Zn was greater in mice fed the zinc deficient (mean ± SD: 0.36 ± 0.03 ng/mL) compared to the zinc adequate (0.22 ± 0.03 ng/mL) and zinc supplemented (0.22 ± 0.03 ng/mL, P &lt; 0.0001 for both) diets. With the exception of Slc39a12, Slc30a3, and Slc30a8, the remaining zinc transporters were expressed across all diets and intestinal segments. Expression of Slc39a1, Slc39a4, Slc39a5, Slc39a7, Slc39a9, Slc39a11, Slc39a14, Slc30a2, Slc30a4, Slc30a5, Slc30a6, and Slc30a9 changed with diet (Pdiet &lt; 0.05 for all); expression of Slc39a3, Slc39a7, Slc39a9 and Slc30a5 changed by intestinal segment (Psegment &lt; 0.05 for all). Of those transporters expressed, Slc39a4 was positively associated with plasma appearance of 67 Zn (r = 0.645, P &lt; 0.0001) and increased 7-fold in mice consuming the zinc deficient diet compared to the zinc adequate and zinc supplemented diets (P &lt; 0.0001 for both). Conclusions Although most zinc transporters are expressed in the small intestine and likely function in concert, fluctuations in fractional zinc absorption are positively correlated with Slc39a4 expression in the small intestine. Funding Sources The views expressed herein are those of the authors and do not reflect official policy of the Army, DoD, or US Government. Supported by MRDC.

Zinc Supplementation Effect on the Bronchial Cilia Length, the Number of Cilia, and the Number of Intact Bronchial Cell in Zinc Deficiency Rats

BACKGROUND: Airway epithelium is the first line of defense against a variety of exposures. Inflammatory processes, hyperresponsiveness and zinc deficiency cause epithelial damage. Zinc is involved in apoptosis and microtubule formation. However, its role in the integrity of bronchial mucosa and cilia is unclear.METHODS: To assess the effect of zinc on the integrity of the bronchial epithelium, 24 male Rattus norvegicus strain Wistar rats were randomized into four experimental groups: normal zinc diet group without zinc supplementation, normal zinc diet group with 60 ppm zinc supplementation, zinc deficient diet group without zinc supplementation, and zinc deficient diet group with 120 ppm zinc supplementation. Bronchial mucosal integrity was measured with the number of epithelial cells, and the number and length of cilia.RESULTS: Number of cell in normal zinc diet group was 8.8±1.82, while it was only 8.1±1.08 in zinc deficient diet group (p<0.001). Number of cilia per cell was 4.6±1.08 in normal zinc diet group, compared to 4.0±0.79 in zinc deficient diet group (p<0.001). Ciliary length also differ by 7.68±0.66 μm in normal zinc diet group and only 5.16±0.91 μm in zinc deficient diet group (p<0.001).CONCLUSION: Zinc supplementation of the normal zinc diet group affected the length of bronchial cilia. Zinc supplementation of the zinc deficient diet group affected the integrity of the bronchial epithelium, which was shown by the number and length of cilia, and the number of epithelial cells.KEYWORDS: zinc, bronchial epithelial integrity, cilia length, number of cilia, epithelial cell

Lessons Learned from Experimental Human Model of Zinc Deficiency

Zinc is an essential element for humans, and its deficiency was documented in 1963. Nutritional zinc deficiency is now known to affect over two billion subjects in the developing world. Conditioned deficiency of zinc in many diseases has also been observed. In zinc-deficient dwarfs from the Middle East, we reported growth retardation, delayed sexual development, susceptibility to infections, poor appetite, and mental lethargy. We never found a zinc-deficient dwarf who survived beyond the age of 25 y. In an experimental model of human mild zinc deficiency, we reported decreased thymulin (a thymopoietic hormone) activity in Th1 cells, decreased mRNAs of IL-2 and IFN-gamma genes, and decreased activity of natural killer cells (NK) and T cytotoxic T cells. The effect of zinc deficiency on thymulin activity and IL-2 mRNA was seen within eight to twelve weeks of the institution of zinc-deficient diet in human volunteers, whereas lymphocyte zinc decreased in 20 weeks and plasma zinc decreased in 24 weeks after instituting zinc-deficient diet. We hypothesized that decreased thymulin activity, which is known to proliferate Th1 cells, decreased the proliferation differentiation of Th1 cells. This resulted in decreased generation of IL-2 and IFN-gamma. We observed no effect in Th2 cell function; thus, zinc deficiency resulted in an imbalance of Th1 to Th2 function resulting in decreased cell-mediated immunity. Zinc therapy may be very useful in many chronic diseases. Zinc supplementation improves cell-mediated immunity, decreases oxidative stress, and decreases generation of chronic inflammatory cytokines in humans. Development of sensitive immunological biomarkers may be more sensitive than an assay of zinc in plasma and peripheral blood cells for diagnosis of marginal zinc deficiency in human.

The Effect of Zinc Deficiency and Supplementation on Elements in the Kidney Tissue of Ovariectomized Rats: Histopathologic Changes

The objective of the present study is to determine the effects of zinc deficiency in and zinc supplementation to ovariectomized rats on some elements in kidney tissue. The study included 40 Sprague-Dawley type adult female rats. The experimental animals were randomized into four groups with equal numbers as follows: Group 1: Control (10). Group 2: Ovariectomized control (10). Group 3: Ovariectomized + zinc supplemented (10). Group 4: Ovariectomized + zinc deficient (10). After the animals were decapitated at the end of the experiment, element levels were determined by Atomic Emission (ICP-AES) as mg/g/wet tissue for calcium, phosphate, zinc, aluminum, copper, iron, lithium, and manganese and μg/g/wet tissue for magnesium in the kidney tissue. Additionally, the tissue samples were subjected to a histopathologic assessment. An examination of the study results showed that ovariectomy significantly reduced calcium, phosphorus, and zinc levels, while zinc supplementation to the rats following ovariectomy restored the reduced element levels to normal (0.10 ± 0.03, 0.85 ± 0.16, 0.11 ± 0.03 vs 0.19 ± 0.06, 1.86 ± 0.18, 0.52 ± 0.05). Group 4, which was both ovariectomized and fed on a zinc-deficient diet, had significantly lower aluminum, copper, and lithium values. Calcification, inflammation, and sclerotic changes in group 4, the group which was fed on a zinc-deficient diet, were greater in comparison to other groups (p < 0.05). Results of the study suggest that ovariectomy + zinc deficiency leads to calcification, inflammation, and sclerotic changes in renal tissue and significantly reduces element levels, whereas zinc supplementation after ovariectomy restores the lowered element levels to normal.