Zinc-deficient Diet Research Articles

Proteomics analysis in rats reveals convergent mechanisms between major depressive disorder and dietary zinc deficiency

Abstract Background Preclinical and clinical studies have shown that dietary zinc deficiency can lead to symptoms similar to those observed in major depressive disorder (MDD). However, the underlying molecular mechanisms remain unclear. To investigate these mechanisms, we examined proteomic changes in the prefrontal cortex (PFC) and hippocampus (HP) of rats, two critical brain regions implicated in the pathophysiology of depression. Methods Rats were fed diets either adequate in zinc (ZnA, 50 mg Zn/kg) or deficient in zinc (ZnD, <3 mg/kg) for four weeks. High-throughput proteomic analysis was used to detect changes in protein expression, supplemented by enzyme activity assay for mitochondrial complexes I and IV, examining their functional impacts. Results ZnD led to significant alterations in protein expression related to zinc transport and mitochondrial function. Proteomic analysis revealed changes in zinc transporter family members such as Slc30a1 (6.64 log2FC), Slc30a3 (-2.32 log2FC), Slc30a4 (2.87 log2FC), Slc30a5 (5.90 log2FC), Slc30a6 (1.50 log2FC), and Slc30a7 (2.17 log2FC) in the PFC, and Slc30a3 (-1.02 log2FC), Slc30a5 (-1.04 log2FC), and Slc30a7 (1.08 log2FC) in the HP of rats subjected to ZnD. Furthermore, ZnD significantly affected essential mitochondrial activity proteins, including Atp5pb (3.25 log2FC), Cox2 (2.28 log2FC), Atp5me (2.04 log2FC), Cyc1 (2.30 log2FC), Cox4i1 (1.23 log2FC), Cox7c (1.63 log2FC), and Cisd1 (1.55 log2FC), with a pronounced decrease in complex I activity in the PFC. Conclusions Our study demonstrates that ZnD leads to significant proteomic changes in the PFC and HP of rats. Specifically, ZnD alters the expression of zinc transporter proteins and proteins critical for mitochondrial function. The significant decrease in complex I activity in the PFC further underscores the impact of ZnD on mitochondrial function. These results highlight the molecular mechanisms by which ZnD can influence brain function and contribute to symptoms similar to those observed in depression.

Dietary zinc deficiency promotes Acinetobacter baumannii lung infection via IL-13 in mice.

Dietary zinc deficiency is a major risk factor for pneumonia. Acinetobacter baumannii is a leading cause of ventilator-associated pneumonia and a critical public health threat due to increasing rates of multidrug resistance. Patient populations at increased risk for A. baumannii pneumonia are also at increased risk of zinc deficiency. Here we established a mouse model of dietary zinc deficiency and acute A. baumannii pneumonia to test the hypothesis that host zinc deficiency contributes to A. baumannii pathogenesis. We showed that zinc-deficient mice have significantly increased A. baumannii burdens in the lungs, dissemination to the spleen and higher mortality. During infection, zinc-deficient mice produce more pro-inflammatory cytokines, including IL-13. Administration of IL-13 promotes A. baumannii dissemination in zinc-sufficient mice, while antibody neutralization of IL-13 protects zinc-deficient mice from A. baumannii dissemination and mortality during infection. These data highlight the therapeutic potential of anti-IL-13 antibody treatments, which are well tolerated in humans, for the treatment of pneumonia.

Zinc Deficiency Leads to Reproductive Impairment in Male Mice Through Imbalance of Zinc Homeostasis and Inflammatory Response.

Zinc is an essential trace element crucial for growth and development and plays a significant role in male reproductive function. The aim of this study was explore the mechanism of male reproductive damage caused by different degrees of zinc deficiency. Thirty male ICR mice were randomly assigned to three groups: zinc-normal diet group (ZN, n = 10, Zn content = 30mg/kg), low zinc-deficiency diet group (LZD, n = 10, Zn content = 15mg/kg), and high zinc-deficiency diet group (HZD, n = 10, Zn content = 7.5mg/kg). The mice were maintained for 8weeks. At the end of the experiment, they were sacrificed, and their blood, testicular, and epididymal tissues were collected for further study. Zinc-deficient diet led to weight loss, testicular structural disorder, decreased semen quality, imbalance of zinc homeostasis, and inflammatory damage in mice. Semen quality, testosterone, serum Zn, testicular tissue Zn, testicular free Zn ions, Zrt-, Irt-like protein8 (ZIP8), Zrt-, Irt-like protein5 (ZIP5), and interleukin-10 (IL-10) were significantly decreased; zinc transporter 4(ZnT4), NF-κB p65, P-NF-κB p65, NLRP3, Caspase-8, and Caspase-3 were significantly increased in both LZD and HZD group mice. While compared with the LZD group, Zrt-, Irt-like protein13 (ZIP13), TNF-α, NF-κB p65, P-NF-κB p65, NLRP3, Caspase-1, and GSDMD were significantly increased in the HZD group. Both low and high zinc-deficiency diets can disrupt zinc homeostasis in mice, leading to heightened inflammatory responses, the activation of the NF-κB pathway, and increased apoptosis in testicular cells. Notably, a high zinc-deficiency diet led to an up-regulation of ZIP13 expression, exacerbated inflammation, and induced testicular pyroptosis, resulting in more severe reproductive damage in male mice.

Dietary zinc status is associated with ZnT3 (SLC30A3), IL-6 gene expressions and spinal cord tissue damage in spinal cord tissue in a cuprizone-induced rat Multiple Sclerosis model

The aim of this study was to investigate the effects of dietary zinc status on spinal cord tissue damage and ZnT3, IL-6 gene expressions in a cuprizone-induced rat Multiple Sclerosis (MS) model. The study was carried out on 46 adult male rats of the genus Wistar. The animals used in the study were divided into 5 groups (G) (Control 6, other groups 10). G1, Control. G2, Sham-MS: Carboxy-methyl-cellulose (KMS) solution in which Cuprizon was dissolved was given to rats by gavage daily for 8 weeks at the rate of 1 % of daily feed consumption. MS was formed by giving 1 % of the daily feed consumption cuprizon in KMS solution by gavage to the animals in G3, 4 and 5 for 8 weeks. G4 was fed with a zinc deficient (50 µg/kg zinc) diet. G5 was given intraperitoneal (ip) zinc sulfate (5 mg/kg/day) supplementation. MS formation in animals was determined by Rotarod tests and Myelin Basic Protein (MBP) gene expression analysis. ZNT3 and IL-6 gene expression levels in spinal cord tissue samples of animals by Real-Time-PCR method; MDA and GSH levels were determined by ELISA method. The highest spinal cord MDA and IL-6 levels were obtained in G3 and G4 (P<0.05). Zinc supplementation in G5 prevented the increase in the mentioned parameters and turned them into control values (P<0.05). The spinal cord GSH and ZnT3 levels of G3 and G4 were lower than all other groups (P<0.05). Zinc supplementation prevented suppression in the same parameters in G5 and reached the control values (P<0.05). The findings of the current study suggest that zinc supplementation in addition to treatment for MS may be beneficial in reducing the severity of the disease.

Rate of hydrolysis of the phosphate esters of B vitamins is reduced by zinc deficiency: Invitro and invivo.

Extracellular hydrolysis of the phosphate esters of B vitamins (B1, B2, and B6) is crucial for their cellular uptake and metabolism. Although a few zinc-dependent enzymes have been implicated in these processes, their exact mechanisms of action remain largely unknown. This study investigated the potential involvement of phosphate group hydrolyzing enzymes in the hydrolysis of B vitamin phosphate esters. We evaluated enzyme activity in membrane lysates prepared from cells transiently transfected with these enzymes or those endogenously expressing them. Specifically, we investigated how zinc deficiency affects the rate of hydrolysis of B vitamin phosphate esters in cellular lysates. Assessment of the activities of zinc-dependent ectoenzymes in the lysates prepared from cells cultured in zinc-deficient conditions and in the serum of rats fed zinc-deficient diets revealed that zinc deficiency reduced the extracellular hydrolysis activity of B vitamin phosphate esters. Furthermore, our findings explain the similarities between several symptoms of B vitamin and zinc deficiencies. Collectively, this study provides novel insights into the diverse symptoms of zinc deficiency and could guide the development of appropriate clinical strategies.

Zinc Deficiency Causes Glomerulosclerosis and Renal Interstitial Fibrosis Through Oxidative Stress and Increased Lactate Metabolism in Rats.

Chronic kidney disease (CKD) is a highly prevalent condition characterized by renal fibrosis as its ultimate manifestation. Zinc deficiency is closely associated with CKD, evidenced by its link to renal fibrosis.Recently, local lactic acidosis has beendemonstrated topromote renal fibrosis. Under zinc-deficient conditions,mitochondrial functioniscompromised and abnormal lactate metabolism might be inducedpotentially. However, it remains unclear whether zinc deficiency leads to renal fibrosisthrough local lactic acidosis. Zinc deficiency rat models were successfully established by feeding zinc-deficient diet. Western blot, qPCR, IHC, and other experiments were employed to investigate the key markers and molecular mechanisms of glomerulosclerosis and renal interstitial fibrosis. Our resultsindicate that zinc deficiency reduces specific markers of podocytes (podocalyxin, WT1, and nephrin) andactivates the Wnt3a/β-catenin pathway, a key pathway in podocyte injury. Concurrently, glomerulosclerosis is indicated by increased urinary microalbumin and serum creatinine levels along with histological alteration observed through PAS and Masson staining in zinc-deficient rats. Furthermore, various degrees of upregulation for several markers of interstitial fibrosis including α-SMA, FN1 and collagen III are also revealed. These findings were further confirmed by Masson staining and IHC. Additionally, alterations in four markers in the EMT process, N-cadherin, E-cadherin, Vimentin, and snail, were consistent with expectations. We then confirmed the activation of the non-canonical TGF-β1 pathway known as the PI3K/AKT/mTOR pathway. An elevation in renal ROS levels accompanied by increased mitochondrial marker cytochrome C expression as well as an elevated NADH/NAD + ratio is also observed within the kidneys. Furthermore, the activity of both MMP/TIMP system and fibrinolytic system was abnormally enhanced under zinc deficiency conditions. Finally, we find zinc supplementation could significantly ameliorate relevant pathological alterations induced by zinc deficiency. These results collectively point that zinc deficiency causes podocyte damage ultimately resulting in glomerulosclerosis via accumulation of ROS and induces interstitial fibrosis via lactic acidosis.

Intergenerational Impact of Parental Zinc Deficiency on Metabolic and Redox Outcomes in Drosophila melanogaster.

Zinc deficiency is a common nutritional disorder with detrimental health consequences. Whether parental zinc deficiency induces intergenerational effects remains largely unknown. We investigated the effects of a combined maternal and paternal zinc deficiency on offspring's metabolic outcomes and gene expression changes in Drosophila melanogaster. The parent flies were raised on zinc-deficient diets throughout development, and their progeny were assessed. Offspring from zinc-deprived parents exhibited a significant (p < 0.05) increase in body weight and whole-body zinc levels. They also displayed disrupted glucose metabolism, altered lipid homeostasis, and diminished activity of antioxidant enzymes. Gene expression analysis revealed significant (p < 0.05) alterations in zinc transport genes, with increases in mRNA levels of dZIP1 and dZnT1 for female and male offspring, respectively. Both sexes exhibited reduced dZnT35C mRNA levels and significant (p < 0.05) increases in the mRNA levels of DILP2 and proinflammatory markers, Eiger and UPD2. Overall, female offspring showed higher sensitivity to parental zinc deficiency. Our findings underscore zinc's crucial role in maintaining health and the gender-specific responses to zinc deficiency. There is the need for further exploration of the underlying mechanisms behind these intergenerational effects.

Zinc deficiency deteriorates ovarian follicle development and function by inhibiting mitochondrial function

Zinc (Zn) is a crucial trace element essential for human growth and development, particularly for reproductive health. Previous research has shown a decrease in serum zinc concentration with age and individuals with conditions such as polycystic ovary syndrome (PCOS) and diabetes mellitus. However, the specific effects of zinc deficiency on the female reproductive system, especially ovarian function, are not fully understood. In our study, we observed a significant reduction in the total number of follicles and mature follicles in the zinc deficiency group. This reduction correlated with decreased level of anti-Mullerian hormone (AMH) and abnormal gene expression affecting hormone secretion regulation. Furthermore, we found that zinc deficiency disrupted mitochondrial dynamics, leading to oxidative stress in the ovaries, which further inhibited autophagy and increased ovarian apoptosis. These changes ultimately resulted in the failure of germinal vesicle breakdown (GVBD) and reduced oocyte quality. Meanwhile, administration of zinc glycine effectively alleviated the oocyte meiotic arrest caused by dietary zinc deficiency. In conclusion, our findings demonstrated that dietary zinc deficiency can affect hormone secretion and follicle maturation by impairing mitochondrial function and autophagy.

Does zinc deficiency promote renal inflammation?

Background: Renal inflammation is implicated in the pathogenesis of CKD and plays a critical role in kidney damage. CKD-associated tubular damage stimulates the secretion of proinflammatory cytokines (e.g. IL-1β, IL-6, and TNF-α) which expedite CKD progression, further instigating kidney damage and inflammation. Studies have shown that zinc deficiency (ZnD) elevates oxidative stress and affects proinflammatory cytokine abundance. Based on these findings, we hypothesize that ZnD will promote renal inflammation. Experimental Design: To examine if ZnD promotes renal inflammation, wild-type adult mice (C57BL/6J) were placed on a zinc-adequate (ZnA) or zinc-deficient (ZnD) diet for 10 weeks. At week 8, a subset of the ZnD mice were placed back on a ZnA diet (ZnR) for 2 weeks. The kidneys were harvested, embedded in paraffn, and both immunohistochemistry and immunofluorescence were performed to assess morphological changes and proinflammatory cytokine abundance. Results: Compared to ZnA kidneys, morphological changes were observed in ZnD kidneys, such as loss of endothelial cells in the glomerulus and abnormalities in nuclei arrangement in tubular cells. However, these changes were mitigated with the replenishment of zinc. There were no significant changes in TNF-α expression between the ZnA and ZnD kidneys, but there was decreased expression in the ZnR kidney. Conclusions: Based on preliminary findings, we can conclude that ZnD (1) promotes abnormalities in glomerular and tubular morphology and (2) does not have a significant impact on TNF-α expression in the renal cortex. Zinc repletion was shown to mitigate the glomerular and tubular abnormalities instigated by zinc deficiency. Significance: These findings provide evidence for Zn’s influence on renal inflammation, and advocate for zinc supplementation as a plausible therapeutic strategy for CKD. Funding: R21 DK119879, R01 DK-133698. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Dietary zinc deficiency increases damage rate and copy number of mitochondrial DNA in the mouse liver

Zinc is an essential trace element involved in many physiological processes, ranging from cellular growth and immune functions to enzymatic activity and gene expression. Inadequate dietary zinc levels can disrupt the functioning of numerous organs, including the liver. Given the pivotal role played by the liver, in-depth understanding of the mechanisms driving disorders in this organ caused by zinc deficiency is of great importance. In the present study, the effects of a four-week low-zinc diet on the integrity and copy number of mitochondrial DNA (mtDNA) in the liver was assessed using a mouse model. The research revealed a significantly elevated damage rate and an increased copy number of mtDNA in the livers of mice subjected to a low-zinc diet when compared to control animals. These findings indicate that a zinc deficiency, by promoting DNA damage in mitochondrial genomes, increases a potential risk of harmful mutations that could compromise ATP production in the liver. The rise in the mtDNA copy number suggests an initial compensatory response to the detrimental effects of the zinc deficiency, which is likely to diminish with a chronic insufficiency of this element. The study confirmed the significant role of mitochondria in the processes leading to liver dysfunction induced by a zinc deficiency. It showed additionally that mtDNA is a very sensitive indicator of the liver's condition that is responsive to environmental changes such as a micronutrient deficiency in the diet.

Tolerability of Artemisia absinthium in anorexia: Targeting of neuronal appetite and satiety in zinc deficiency diet rat model

Anorexia is a neuronal metabolic disorders induced by factors such as malnutrition and brain metabolic abnormalities during crucial developmental stages. Anorexia nervosa is a complex condition that often requires a multidisciplinary approach, involving medical, nutritional, and psychological interventions. The available medications for specific symptoms for increasing feed intake, not applicable for children and pregnant and cancer patients such as Olanzapine, and Cyproheptadine. This study looked at how Artemisia absinthium (ART) affects brain metabolic syndrome brought on zinc deficiency diet (ZDD). The investigation examined the impact of a ZDD on a rat anorexia model. The second goal is to contrast how antihistamines and Artemisia absinthe extract affect the brain functions connected to appetite. For the studies, 40 mature male rats were divided into four groups. Four groups of forty rats each were used in the experiment. Each group consists of ten rats. The following groups are included in the study: the 1st group control group, the 2nd group treated with ZDD, the 3rd group treated with ZDD concurrent with Cyproheptadine (CH), the 4th group treated with ZDD concurrent with ART. CH and ART were taken orally for 30 days. Tests on biochemical markers were conducted after the examination. The findings showed that ZDD led to reduced levels of neurotransmitters in the brain. Lower concentrations of antioxidants, monoamine, and neuropeptide Y were also found. On the other hand, groups treated with CH and ART improved in comparison to ZDD and nearly recovered in comparison to the control group. Histopathological analysis was used to confirm biochemical data. Obtained data concluded that CH and ART reduce the effects of anorexia and oxidative stress, which function as neuromodulators and promote the release of monoamines.

Distribution of Zinc in Muscle, Adipose Tissue and Blood Serum of Rats Under Conditions of Zinc-Deficient, Iodine-Deficient, High-Carbohydrate and High-Fat Diets

The relevance of the study is due to the prevalence of hypothyroid dysfunction, type II diabetes mellitus, and metabolic syndrome. The study was carried out on sexually mature male rats that were on a standard vivarium diet (control group), zinc-deficient, iodine-deficient, high-carbohydrate and high-fat diets. Under the experimental conditions, the distribution of zinc in blood serum, adipose (visceral fat) and muscle (femoral and tibial muscles) tissues was studied. The study showed a decrease in serum zinc content by 13.79-30.89 % (p&lt;0.05) compared to the control group, regardless of diet. The concentration of the trace element in adipose tissue was significantly reduced relative to the control under conditions of zinc deprivation (by 18.37 %, p&lt;0.05), and especially high-fat feeding (by 74.74 %, p&lt;0.001). The increase in the content of the trace element in muscles under conditions of zinc deficiency (by 36.84 %, p&lt;0.001) compared to the same indicator in animals fed a standard diet) is noteworthy. Taking into account the role of the bioelement in the maintenance of thyroid homeostasis, carbohydrate metabolism, and antioxidant potential, the detected changes involving zinc may act as a trigger for changes in the hormonal profile, metabolic and oxidative disorders.

A Short-Term Zinc-Deficient Diet Maintains Serum Calcium Concentrations through Ca Absorption-Related Gene Expression in Rats.

We investigated the effects of short-term dietary zinc deficiency on zinc and calcium metabolism. Four-week-old male Wistar rats were divided into two pair-fed groups for a 1-wk treatment: zinc-deficient group (ZD, 1 ppm); control group (PF, 30 ppm). The mRNA expression of zinc transporters, such as Slc39a (Zip) 4, Zip5, Zip10, and Slc30a (ZnT) 1, in various tissues (liver, kidney, and duodenum) quickly responded to dietary zinc deficiency. Although there was no significant difference in serum calcium concentrations between the PF and ZD groups, serum 1,25-dihydroxycholecalciferol (1,25(OH)2D3) was higher in the ZD group than in the PF group. Moreover, short-term zinc deficiency significantly increased mRNA expression of transient receptor potential (TRP) cation channel subfamily vanilloid (V) member 6, S100 calcium binding protein G (S100g), and ATPase plasma membrane Ca2+ transporting 1 (Atp2b1) in the duodenum. Furthermore, short-term zinc deficiency increased vitamin D receptor (VDR) and cytochrome P450 family 24 subfamily A member 1 (Cyp24a1) mRNA expression in the kidney. These findings suggested that short-term zinc deficiency maintains serum calcium concentrations through Ca absorption-related gene expression in the duodenum, and that short-term zinc deficiency induced the expression of Cyp24a1 in kidney in response to an increase in the serum 1,25(OH)2D3 level.

Maternal Fed Zinc-Deficient Diet: Effects on Relaxin Family Peptides and Oxidant System in the Testis and Liver Tissue of Male Offspring

Today, the studies are limited on roles of insulin-like peptide 3 (INSL3), insulin-like peptide 7 (INSL7), and relaxin family peptide receptor 1 (RXFP1) which are synthesized by the testis. It is aimed to investigate the levels of the sex hormone as testosterone and the family of insulin-like proteins (relaxin family peptides), which are important in the puberty transition, in the testicular and liver tissues of male offspring born to female rats fed a zinc-deficient diet during the pregnancy, and in the changes in lipid peroxidation markers. The study was performed on 40 male offspring. In Group I: Control group, both male offspring and mothers were fed with standard rat chow. In Group II: Zinc deficient diet, both male offspring and mothers were fed a zinc-deficient diet (2.8 mg/kg zinc). In Group III: Normal diet, male offspring fed standard rat chow for 45 days (66th day) after being separated from their mothers with a maternal zinc-deficient diet. In Group IV: Zinc-supplemented diet, offspring fed with zinc supplemented (5 mg/kg/day intraperitoneal zinc sulfate, i.p.) in addition to standard rat chow after being separated from their mothers with maternal zinc deficiency until the termination of the study (66th day). Our study suggests that zinc-supplemented diets play an important role in the changes in INSL3, INSL7, RXFP1, and testosterone levels during spermatogenesis. INSL7, INSL3, and RXFP1 levels were higher in zinc-supplemented group than the zinc-deficient diet group. Liver levels of INSL3, INSL7, and MDA were significantly different in zinc-deficiency diet group than zinc-supplemented group.

Effects of dietary minerals deficiency and supplementation on different parts of muscle minerals content in grazing Mongolian sheep.

The objective of this study was to investigate the impact of dietary deficiency and supplementation of calcium, zinc, copper, cobalt, manganese or selenium on minerals content in the longissimus dorsi (LD), biceps femoris (BF) and triceps brachii (TB) of grazing Mongolian sheep. We randomly divided 98 sheep into 7 treatment groups and fed them specific diets for 60 days: a total mineral nutrition diet (LCG), a calcium deficiency diet (LCa), a zinc deficiency diet (LZn), a copper deficiency diet (LCu), a cobalt deficiency diet (LCo), a manganese deficiency diet (LMn) and a selenium deficiency diet (LSe). Then 7 sheep from each group were slaughtered and samples of LD, BF and TB were collected for mineral content analysis. The remaining sheep in each group were subsequently fed specific diets for an additional 41 days: a total mineral nutrition diet (SCG), a calcium supplementation diet (SCa), a zinc supplementation diet (SZn), a copper supplementation diet (SCu), a cobalt supplementation diet (SCo), a manganese supplementation diet (SMn) and a selenium supplementation diet (SSe). Afterward, all sheep were slaughtered, and muscle samples were collected and analyzed. Significant findings emerged that LCa decreased sulfur (S) content in BF and increased Ca content in LD and BF, while SCa increased S and Ca content in BF and TB, respectively (P < 0.05). LZn decreased Zn, S, and potassium (K) content in LD and BF, while SZn increased Zn and S content in LD and BF, respectively (P < 0.05). LCu decreased Cu and iron (Fe) content in LD and TB, while SCu increased Fe content in TB (P < 0.05). LCo decreased phosphorus, S, K, Ca, Mn, Fe, Cu, and Zn content in LD (P < 0.05). LMn decreased Mn content and increased K content in TB, while SMn decreased K content in BF and TB (P < 0.05). LSe and SSe decreased and increased Se content in LD, BF, and TB, respectively (P < 0.05). Dietary mineral levels have varying effects on lamb meat minerals content. It is important to ensure an adequate intake of minerals in the diet to enhance the mineral nutrition of lamb meat.

Effect of Zinc-Deficient Diet on Two Strains of Mice.

Zinc (Zn) deficiency is one of the most common nutritional deficiencies worldwide. It is associated with reduced nutritional status and has been reported in cases of growth retardation, alopecia, and decreased serum alkaline phosphatase (ALP). It has also been reported to occur during total parenteral nutrition (TPN) administration and is associated with various diseases, such as liver diseases, diabetes, and kidney disease. We used Zn-deficient mice of ICR and C57BL/6J strains to investigate the various effects of Zn deficiency on the body, assuming that a healthy person may also become deficient in Zn either due to an unbalanced diet or malabsorption. The results showed that a Zn-deficient diet suppressed body weight gain and increased the tissue weight of the kidneys and cecum in both strains of mice. Biochemical data showed no decrease in serum ALP activity in either strain. Furthermore, in C57BL/6J mice, a Zn-deficient diet caused alopecia, loss of villi in the small intestine, and eventually affected the intestinal mucosa, which could be a risk factor for poor nutritional status. Although previous reports have shown that serum ALP activity is decreased during Zn deficiency, this is the first study that used 4-wk-old mice of ICR and C57BL/6J strains to show that serum ALP activity, which is a Zn deficiency marker, did not decrease in the two strains of Zn-deficient mice; furthermore, a Zn-deficient diet causes various symptoms.

Effects of Dietary Zinc Deficiency and Supplementation on Prepubertal Rat Testes: Sulfhydryl and Antioxidant Status.

The study was designed to investigate the effects of dietary zinc deficiency and supplementation on antioxidant system viz. superoxide-dismutase, glutathione reductase, glutathione peroxidase, glutathione- S-transferase, catalase and sulfhydryls levels (GSH, TSH, NPSH and PBSH) in testes of Wistar rats. Pre-pubertal rats were divided into two groups with 6 sub-groups each viz. zinc control (ZC), pair fed (PF), zinc deficient (ZD), zinc control supplementation (ZCS), pair-fed supplementation (PFS) and zinc deficient supplementation (ZDS). Experiments were set for 2- and 4-weeks followed by 4weeks of zinc supplementation. The zinc deficient group animals exhibited significant decrease in gonado-somatic index (2- and 4- weeks), sulfhydryls levels, GSH, GPx, GR (2 and 4-weeks) and GST concentration (2-weeks). However, after zinc supplementation significant improvement in gonadosomatic index, SH, GSH, antioxidant enzyme levels (GR, GPx, and GST) in deficient groups has been observed. Zinc deficiency during pre-pubertal period affected growth and caused dysregulation of the glutathione antioxidant system. The significant alterations in the levels of antioxidant enzymes and non-enzymatic antioxidant system (GSH and SH) in zinc deficient groups could be due to alleviated generation of free radicals, causative factor for increased oxidative stress which may lead to infertility as oxidative stress is a common pathology seen during infertility. Altered antioxidant system and sulfhydryls levels in testes due to dietary zinc deficiency reflect the significance of optimum zinc for maintaining homeostatic balance in gonadal physiology. Supplementing zinc for 4weeks could reduce the redox imbalance which may help in alleviating oxidative stress induced alterations in testes.

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.

Chitosan zinc nanocomposite: A promising slow releasing zinc nano fertilizer

In the present era, zinc deficiency in agricultural soil is a globally widespread issue and it results in depressed plant growth and food grains with less nutrition. Consumption of such zinc-deficient diets may lead to many lifestyle diseases in humans. Sustained nutrient availability from conventional fertilizers is one of the challenges being faced in the agricultural sector. Nano fertilizers are a promising area for the fertilizer industry with a huge potential to improve nutrient retention for optimal growth. We herein report the synthesis of zinc nanocomposite utilizing chitosan, a nature-derived biopolymer as a nutrient carrier to sustain crop production. It was prepared by ionic gelation method using sodium tripolyphosphate as cross-linking agent. The morphology and the hybrid nature of the new nanocomposite were characterized by Field Emission Scanning Electron Microscopy(FE-SEM), EDAX, X-ray diffraction (XRD), and FT-IR spectroscopy. Results from the atomic absorption spectrum after soil percolation studies reveal the release of zinc nutrients in a controlled manner as compared to conventional zinc fertilizer. This indicates that a chitosan-based composite could be a viable alternative method to be used as a nanocarrier for nutrients in agronomic biofortification.

The therapeutic potential of “Crataegus azarolus” on zinc, lipid profile, and antioxidant status in streptozotocin-induced diabetic rats with zinc-deficient diet

The therapeutic potential of “Crataegus azarolus” on zinc, lipid profile, and antioxidant status in streptozotocin-induced diabetic rats with zinc-deficient diet