Effect Of Zinc Deficiency Research Articles

Zinc deficiency triggers hearing loss by reducing ribbon synapses of inner hair cells in CBA/N mice

Zinc plays a vital role in our metabolism, encompassing antioxidant regulation, immune response, and auditory function. Several studies have reported that zinc levels correlate with hearing loss. We have previously demonstrated that the auditory brainstem response (ABR) threshold increased in mice fed a zinc-deficient diet. However, the effects of zinc deficiency on hearing were not fully elucidated. The present study investigated whether zinc deficiency affects hearing in association with neuronal components or cochlear structures. CBA/N mice were fed a normal or zinc-deficient diet for 8 weeks and assessed for ABR and distortion product otoacoustic emissions (DPOAE). The cochlear sections were stained with hematoxylin and eosin solution. Also, we observed the expression of synaptic ribbons, neurofilaments, and alpha-synuclein (α-Syn). The 8-week zinc-deficient diet mice had an elevated ABR threshold but no changed DPOAE threshold or cochlear structures. A reduced number of synaptic ribbons of inner hair cells (IHCs) and impaired efferent nerve fibers were observed in the zinc-deficient diet mice. The number of outer hair cells (OHCs) and expression of α-Syn remained unchanged. Our results suggest that zinc-mediated hearing loss is associated with the loss of neuronal components of IHCs.

Zinc deficiency effect on clinical features of Coronavirus Disease 2019 patients: A scoping review

COVID-19 was declared a pandemic in March 2020. Various therapeutic guidelines have been established for treating COVID-19, such as anti-inflammatory, antiviral therapies, and zinc supplementation. Zinc deficiency is thought to worsen the condition of patients with COVID-19 infection. However, the effect of zinc deficiency on COVID-19 patients has not been widely reported. In this scoping review, we aim to explore the impact of zinc deficiency on the clinical features of COVID-19 patients. A comprehensive search was conducted across the databases, including PubMed, ScienceDirect, Springer Link, ProQuest, and Google Scholar, using the keywords “Zinc” AND “(COVID-19 or SARS-CoV-2)”. A total of 2,458 articles published between 2019 and 2020 were screened following the PRISMA guidelines and subjected to critical appraisal. Three articles were included, focusing on the effect of zinc deficiency on the clinical features of COVID-19 patients. As of 2022, two articles reported worsening symptoms, one described an increased hospitalization duration, and one reported worsening treatment outcomes in the zinc deficiency group. This review concludes that zinc deficiency worsens symptoms, increases the duration of hospitalization, and leads to worse outcomes in COVID-19 patients.

Zinc deficiency: an overlooked cause of poor health

Micronutrient deficiencies are common globally. George Winter looks at the effect of zinc deficiency on health in various groups of people

Effect of Zinc Deficiency on Gene Expression and Antioxidant Enzyme Activity in Barley Plants at Optimal and Low Temperatures

Effect of Zinc Deficiency on Gene Expression and Antioxidant Enzyme Activity in Barley Plants at Optimal and Low Temperatures

Effect of Zinc Deficiency in Substrate on Growth, Photosynthetic Apparatus and Seed Productivity of Barley

Effect of Zinc Deficiency in Substrate on Growth, Photosynthetic Apparatus and Seed Productivity of Barley

Zinc Deficiency Induces Autophagy in HT-22 Mouse Hippocampal Neuronal Cell Line

Zinc is a trace metal vital for various functions in nerve cells, although the effect of zinc deficiency on neuronal autophagy remains unclear. This study aimed to elucidate whether zinc deficiency induced by treatment with N, N, N′, N′-tetrakis (2-pyridylmethyl) ethylenediamine (TPEN), a zinc chelator, affects and alters autophagy activity. In cell viability assays, TPEN showed cytotoxicity in HT-22 cells. TPEN treatment also increased LC3-II levels and the ratio of LC3-II to LC3-I. Western blot analysis showed that phospho-AMP-activated protein kinase levels and the ratio of phospho-AMP-activated protein kinase to total AMP-activated protein kinase increased. Protein levels of the mammalian target of rapamycin and sirtuin 1 decreased following TPEN treatment. When TPEN-treated HT-22 cells were cotreated with autophagy inhibitors, 3-methyladenine (1 mM), or bafilomycin A1 (3 nM), the TPEN-induced decrease in cell viability was exacerbated. Cotreatment with chloroquine (10 μM) partially restored cell viability. The study showed that zinc deficiency induces autophagy and may be cytoprotective in neurons. We expect our results to add a new perspective to our understanding of the neuronal pathology related to zinc deficiency.

Zinc deficiency and associated factors among pregnant women's attending antenatal clinics in public health facilities of Konso Zone, Southern Ethiopia.

Zinc is an essential mineral known to be important for the normal physiological functions of the immune system. It is one of the basic nutrients required during pregnancy for the normal development and growth of the fetus. However, Zinc deficiency during pregnancy causes irreversible effects on the newborn such as growth impairment, spontaneous abortion, congenital malformations and poor birth outcomes. Even though, the effect of Zinc deficiency is devastating during pregnancy, there is scarcity of evidence on Zinc deficiency and related factors among pregnant women in the current study area. To assess Zinc deficiency and associated factors among pregnant women attending antenatal clinics in public health facilities of Konso Zone, Southern Ethiopia. Institution based cross-sectional study was conducted among randomly selected 424 pregnant mothers. Data were collected using pre tested questionnaire (for interview part), and 5 blood sample was drawn for serum zinc level determination. Data were entered to Epi-Data version 3.1 software and exported to SPSS version 25 for analysis. Binary logistic regression analysis was computed and independent variables with a p-value ≤ 0.25 were included in multivariable analysis. Serum zinc level was determined using atomic absorption spectroscopy by applying clean and standard procedures in the laboratory. Finally adjusted odds ratio with 95% confidence level, P-value < 0.05 was used to identify significant factors for Zinc deficiency. The prevalence of Zinc deficiency was found to be 128 (30.26%) with the mean serum zinc level of 0.56±0.12 g/dl. Age, 25-34 years [AOR 2.14 (1.19,3.82)], and 35-49 years [AOR 2.59 (1.15, 5.85)], type of occupation, farming [AOR 6.17 (1.36, 28.06)], lack of antenatal follow up during pregnancy [AOR 3.57 (1.05,12.14)], lack of freedom to purchase food items from market [AOR 3.61 (1.27, 10.27)], and inadequate knowledge on nutrition [AOR 3.10(1.58, 6.08)] were factors associated with Zinc deficiency. Zinc deficiency is a public health problem among pregnant mothers in the current study area. Improving maternal nutritional knowledge, motivating to have frequent antenatal follow up, and empowering to have financial freedom to purchase food items from market were the modifiable factors to reduce Zinc deficiency. Nutritional intervention that focused on improving nutritional knowledge and insuring access to Zinc sources food items should be delivered for pregnant mothers.

Effect of zinc deficiency on hair loss in pregnant women

Zinc and iron, for example, are crucial trace elements for pregnant women's health. This study has been conducted for the evaluation of zinc and ferritin status of pregnant women since these elements have significant effects on health of the pregnant women as well as the growing embryo in Al Muthanna Province/ Iraq. Seventy five samples of this study were gathered from the three studied groups (Control, pregnant women with Hair Losing and non-pregnant women with Hair Losing) in the Central Health Laboratory of Al Muthanna Province through the period from November 2020 to May 2021, blood samples were collected for further analysis Conclusions : According to the findings of this study, serum zinc and ferritin levels are frequently low in pregnant women who complain of hair loss. Overall, zinc and ferritin insufficiency in Iraq is a major public health concern. Improving nutritional diversity aids in solving the risk among the study participants.

Effects of Zinc Deficiency in Male Mice on Glucose Metabolism of Male Offspring.

As an essential metal, zinc is central to insulin biosynthesis and energy metabolism. Zinc can not only maintain the activity of insulin, but also has insulin-like effect. When zinc is sufficient, the body needs less insulin. Zinc can correct abnormal glucose tolerance and even replace insulin to improve glucose metabolism disorder in diabetic rats. However, the effect of paternal zinc deficiency on glucose metabolism of offspring is still unclear. In the present study, sixteen 8-week-old male mice were randomly allocated into low-zinc group and control group (8 mice in each group), which were fed with low zinc and standard diet for 6 weeks, respectively. The mice were mated with female mice fed with standard diet to get the first generation of mice (F1) to explore the effect zinc deficiency on the glucose metabolism of offspring. Glucose tolerance, insulin sensitivity and insulin secretion in mice were determined by oral glucose tolerance test (OGTT), insulin tolerance test (ITT) and glucose stimulated insulin secretion test (GSIS), respectively. Compared with the control group, the fasting blood glucose levels of F1 generation male mice in the low zinc group increased at 15 and 30 min after glucose injection. The blood glucose of F1 generation male mice in the low zinc group of mice decreased at 60, 90, 120, 180, 240 min after insulin injection. Compared with the control group, serum insulin of F1 generation male mice in the low zinc group decreased at 15 min after glucose injection (all p values <0.05). However F1 female mice in the low zinc group did not show abnormal glucose metabolism. Marginal zinc deficiency in male mice can cause abnormal glucose homeostasis in male offspring, but not in female offspring.

Effect of zinc deficiency and excess on catalase activity and HvCAT2 gene expression in barley

Effect of zinc deficiency and excess on catalase activity and HvCAT2 gene expression in barley

Zinc homeostasis in immunity and its association with preterm births.

Preterm birth is among the most common adverse pregnancy outcomes and is the leading cause of neonatal mortality and morbidity. While trace elements are essential for humans, their specific roles in the prenatal period remain unexplored. Zinc, a ubiquitous element, plays a pivotal role in protein synthesis, cell division, nucleic acid metabolism, apoptosis, ageing, reproduction, immunological and antioxidant defence mechanism. Although zinc quantities are very small in body tissue, it is involved in every conceivable biochemical pathway, which is critical for the performance of various functions necessary to sustain life. Owing to the multifactorial role of zinc, it is not possible to attribute a certain zinc-dependent mechanism in preterm births. Although the effect of zinc deficiency on immunity, its impact on maternal function and health as well as its role in the developing foetus is well documented, much less attention has been given to the understanding of micronutrient zinc homeostasis in immunity and its association with preterm births. Despite extensive research, the pathway by which zinc regulates pregnancy outcomes as well as the function of immune cells in controlling the delivery status (term/preterm) is still obscure. The present review aims to focus on the understanding of relationship of micronutrient zinc homeostasis in immunity and its association with preterm births.

Effect of Zinc Deficiency on Blood Glucose, Lipid Profile, and Antioxidant Status in Streptozotocin Diabetic Rats and the Potential Role of Sesame Oil.

Zinc is recognized to have a crucial function in insulin production. As a result, its absence may have a deleterious impact on the progression of diabetes and associated consequences. So, this study was undertaken to evaluate the effect of sesame oil on biochemical parameters, zinc status, and oxidative stress biomarkers in streptozotocin (STZ)-induced diabetic rats fed zinc-deficient diet. Rats were divided into four groups. The first group consisted of non-diabetic rats that were fed in a sufficient zinc diet, whereas the second was a diabetic group which received also sufficient zinc diet, while the third and fourth groups were diabetic rats fed in a deficient zinc diet, one was non-treated and the other was treated with sesame oil 6% diet for 27days. Zinc deficiency has affected the weight of the diabetic animals. It was also noticed that inadequate dietary zinc intake increased concentrations of glucose, cholesterol, triglycerides, malondialdehyde, and transaminases activities. Furthermore, zinc deficiency feed provoked a decrease in zinc level in tissues (femur, liver, and pancreas); glutathione concentration; and lactic dehydrogenase, amylase, catalase, superoxide dismutase, and glutathione-S-transferase activities. However, sesame oil treatment ameliorated all the previous parameters approximately to their normal values. It was found out that sesame oil supplementation is a potent factor in mitigating the oxidative severity of zinc deficiency in diabetes through its effective antioxidant potential.

Acute Diarrhea in Exclusively Breast Fed Infants in relation to Zinc Level

Background: Zinc deficiency is associated with alteration in gastrointestinal tract structure, function, and impaired immune function. Aim: To analyze the effects of zinc deficiency on the occurrence of acute diarrhea in exclusively breast-fed infants. Methods: In a case-control study, including a total of 72 exclusively breast-fed infants aged ≤ 6 months, 34 of them with acute diarrhea were in the study group and 38 infants as the healthy control group. Demographic characteristics of all infants and their parents were studied. Serum Zinc level was measured for all participants. Results: Zinc level had significant (p-value =0.000) differences between infants with acute diarrhea and the healthy control group. The mean serum zinc value ± SEM in children with acute diarrhea was 63.11 ± 1.7 which was significantly (p = 0.000) different from the mean serum zinc value ± SEM (78.6 ± 1.6) in healthy infants. A cut-off value 60.6μg/dl of total serum zinc level was significantly (p = 0.000) associated with a sensitivity of 100 % with the occurrence of acute diarrhea among exclusively breast-fed infants. Conclusions: Low serum zinc level is associated with the occurrence of acute diarrhea in exclusively breast-fed infants. A cutoff serum zinc value of 60.6 μg/dl has 100% sensitivity with the occurrence of acute diarrhea among breast-fed infants. Keywords: Zinc deficiency, diarrhea, infants, breastfeeding.

Zinc deficiency leads to reduced interleukin-2 production by active gene silencing due to enhanced CREMα expression in T cells

The micronutrient zinc is essential for proper immune function. Consequently, zinc deficiency leads to impaired immune function, as seen in decreased secretion of interleukin (IL)-2 by T cells. Although this association has been known since the late 1980s, the underlying molecular mechanisms are still unknown. Zinc deficiency and reduced IL-2 levels are especially found in the elderly, which in turn are prone to chronic diseases. Here, we describe a new molecular link between zinc deficiency and reduced IL-2 expression in T cells. The effects of zinc deficiency were first investigated invitro in the human T cell lines Jurkat and Hut-78 and complemented by invivo data from zinc-supplemented pigs. A short- and long-term model for zinc deficiency was established. Zinc levels were detected by flow cytometry and expression profiles were investigated on the mRNA and protein level. The expression of the transcription factor cAMP-responsive-element modulator α (CREMα) is increased during zinc deficiency invitro, due to increased protein phosphatase 2A (PP2A) activity, resulting in decreased IL-2 production. Additionally, zinc supplementation invivo reduced CREMα levels causing increased IL-2 expression. On epigenetic levels increased CREMα binding to the IL-2 promoter is mediated by histone deacetylase 1 (HDAC1). The HDAC1 activity is inhibited by zinc. Moreover, deacetylation of the activating histone mark H3K9 was increased under zinc deficiency, resulting in reduced IL-2 expression. With the transcription factor CREMα a molecular link was uncovered, connecting zinc deficiency with reduced IL-2 production due to enhanced PP2A and HDAC1 activity.

Effect of Zinc Deficiency on CKD Progression and Effect Modification by Hypoalbuminemia

Effect of Zinc Deficiency on CKD Progression and Effect Modification by Hypoalbuminemia

Role of Zinc in Mucosal Health and Disease: A Review of Physiological, Biochemical, and Molecular Processes.

Zinc is an essential trace element of all highly proliferating cells in the human body. It is essential to the development and growth of all organisms. Zinc plays a critical role in modulating resistance to infectious agents and reduces the duration, severity, and risk of diarrheal disease via improved regeneration of intestinal epithelium, improved absorption of water and electrolytes, increased levels of brush border enzymes, and, possibly, an enhancement in the immune response allowing better clearance of pathogens. On the cellular level, zinc finger motifs play various roles including diverse functions that involve specific gene expression for ion channels throughout the body. It maintains the function and the structure of the membrane barrier by contributing to host defense, which is particularly crucial in the intestines due to the continuous exposure to noxious agents and pathogens. Zinc deficiency is characterized by impaired immune function, loss of appetite, and growth retardation. More severe cases cause diarrhea, delayed sexual maturation, hair loss, eye and skin lesions, impotence and hypogonadism in males, as well as weight loss, taste abnormalities, delayed healing of wounds, and mental lethargy. The objective of this study is a critical review of the molecular and genetic regulation of zinc in various cellular processes and organs, the association between zinc and diarrheal disease, the recommended dietary zinc intake, and the effects of zinc deficiency on the human body.

Interleukin-4 Administration or Zinc Supplementation Is Effective in Preventing Zinc Deficiency-Induced Hemolytic Anemia and Splenomegaly.

Nutritional zinc deficiency aggravates inflammation, subsequently causing anemia and splenomegaly in rats; however, the mechanism underlying such splenomegaly remains poorly understood. Therefore, in this study, we aimed to elucidate the mechanisms underlying the splenomegaly and anemia occurring in zinc-deficient rats and investigate whether these effects of zinc deficiency could be reversed by interleukin (IL)-4 administration or zinc supplementation. Five-week-old male Sprague-Dawley rats were fed a standard diet; fed a zinc-deficient diet (n = 7 each) and injected with saline or IL-4; or fed a zinc-deficient diet for 6weeks followed by a standard diet for 4weeks thereafter. White blood cells, segmented neutrophils, platelets, CD4+ T cells, CD11b/c+ granulocytes, CINC/GRO+ cells, and myeloperoxidase-positive cells in the blood and spleen of the zinc-deficient rats were significantly higher than those in all the other groups. Conversely, red blood cells, hemoglobin, hematocrit, mean corpuscular volume, mean corpuscular hemoglobin, mean corpuscular hemoglobin concentration, lymphocytes, and CD8+ T cells in the blood of the zinc-deficient rats were significantly lower than those in the other groups. Furthermore, serum aspartate aminotransferase, lactate dehydrogenase, indirect bilirubin concentrations, and erythrocyte osmotic fragility in the zinc-deficient rats were significantly higher than those in the other groups. Moreover, zinc deficiency significantly decreased the GATA1 protein levels in the spleen. Collectively, these results indicate that zinc deficiency aggravates the inflammatory response and causes hemolytic anemia and splenomegaly. Importantly, IL-4 administration and zinc supplementation can reverse the zinc deficiency-induced hemolytic anemia and splenomegaly.

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.

Effect of Zinc deficiency on growth and biochemical characters of barnyard millet lines

Effect of Zinc deficiency on growth and biochemical characters of barnyard millet lines

Methylation‑associated silencing of miR‑128 promotes the development of esophageal cancer by targeting COX‑2 in areas with a high incidence of esophageal cancer.

Esophageal cancer is one of the most common cancer types in the world, with a widely varying incidence between different regions. Zinc deficiency(ZD) is very common in high‑risk areas for esophageal cancer. Dietary ZD is reported to be associated with esophageal squamous cell carcinoma(ESCC). In the current study, the effects of ZD on tumorigenesis and expression of inflammatory factors were investigated in mice. It was identified that a ZD diet advanced ESCC and increased the expression of cyclooxygenase‑2(COX‑2) prior to the occurrence of ESCC in mice. ZD significantly enhanced DNA methyltransferase(DNMT) activity and increased the expression of DNMT1 and DNMT3B. Furthermore, the expression of miR‑128 was downregulated by methylation, and COX‑2, a direct target of miR‑128, was upregulated with the reduction in miR‑128. Upregulation of miR‑128 inhibited the cell cycle, proliferation and metastasis, and the expression of COX‑2, cyclinD1 and retinoblastoma protein(Rb). Furthermore, the relative expression level of miR‑128 was negatively associated with COX‑2 in ESCC tissues. Collectively, these findings indicate that methylation‑associated silencing of miR‑128 promotes the development of esophageal cancer through upregulation of the expression of cyclinD1 and Rb by targeting COX‑2 in ZD regions with a high incidence of esophageal cancer.