Zinc Oxide Nanoparticles Group Research Articles

Examining the Influence of Zinc Oxide Nanoparticles and Bulk Zinc Oxide on Rat Brain Functions: a Comprehensive Neurobehavioral, Antioxidant, Gene Expression, and Histopathological Investigation.

The study aimed to assess the impact of zinc oxide nanoparticles (ZnONPs) on rats' neurobehavior compared to bulk zinc oxide (BZnO). Thirty male Sprague-Dawley rats were randomly assigned to five groups. The control group received Tween 80 (10%), while the ZnONP groups were given ZnONPs at 5 and 10 mg/kg body weight dosages, and the bulk zinc oxide (BZnO) groups received BZnO at the same dosages. Behavioral observations, neurobehavioral examinations, and assessments of brain tissue oxidative markers, neurotransmitter levels, and histopathological changes were performed. The results indicated that ZnONP at a dosage of 5 mg/kg improved general behavior, locomotor activity, memory, and recognition and reduced fearfulness in rats. Conversely, the higher dosage of 10 mg/kg and the bulk form had adverse effects on general behavior, locomotor activity, and learning ability, with the bulk form demonstrating the most severe impact-znONP-5 treatment increased antioxidant enzyme levels and decreased inflammatory markers. BZnO-5 exhibited lower oxidative stress markers, although still higher than BZnO-10. Furthermore, ZnONP-5 and BZnO-5 increased neurotransmitter levels compared to higher dosages. ZnONP-5 upregulated the expression of brain-derived neurotrophic factor (BDNF) mRNA, while BZnO-5 showed increased BDNF mRNA expression and decreased expression of genes related to apoptosis and inflammation. In summary, ZnONPs at 5 mg/kg demonstrated positive effects on rat brain function and behavior, while higher dosages and the bulk form had detrimental effects. In conclusion, the studies emphasized the importance of further assessing various doses and forms of zinc oxide on brain health, highlighting the significance of dosage considerations when using nanomaterials.

Effect of Zinc Oxide Nanoparticles as Feed Additive on Blood Indices, Physiological, Immunological Responses, and Histological Changes in Broiler Chicks

A feeding trial of 5-week duration was performed to assess the response of broiler chicks to dietary supplementation with different doses of myco-fabricated zinc oxide nanoparticles (ZONPs) on blood indices, physiological, immunological response, antioxidant status, intestinal microbial count, and histological changes in immune organs. A total of 162 3-day-old Ross 308 broiler chicks were weighed individually and distributed equally into 3 dietary treatments with 6 replicate of 9 chicks in each in a completely randomized design. Chicks were fed ad libitum a basal ration prepared as starter, grower, and finisher supplemented with 0 (T1, control), 40 (T2), and 60 (T3) mg zinc oxide nanoparticles (ZONPs)/kg feed. Results showed that supplementing with ZONPs at both studied levels increased the relative weights of the spleen, bursa, thymus, and liver and decreased the relative weight of the kidney, gizzard, and intestine. A significant increase in the concentrations of hemoglobin (Hb), hematocrit (PCV%), red and white blood cell counts, total protein (TP), globulin (GLOB), aspartate transferase (AST), alanine transferase (ALT), alkaline phosphatase (ALP), superoxide dismutase (SOD), glutathione peroxidase (GPx), and total antioxidant capacity (TAC) and a significant decrease in malonaldehyde (MDA), uric acid, and creatinine concentration were observed. Furthermore, all immunological organs showed histological alteration and increased both types of immunity in ZONPs groups with more pronounced effects in the T2 group.

Insight into the responses of antibiotic resistance genes in microplastic biofilms to zinc oxide nanoparticles and zinc ions pressures in landfill leachate

Microplastic (MP) biofilms are hotspots of antibiotic resistance genes (ARGs) in landfill environment. MP biofilms in landfill leachate coexist with heavy metals and metallic nanoparticles (NPs) that considered to be the selective agents of ARGs. However, the effects of these selective pressures on ARGs in MP biofilms and their differences in MP-surrounding leachate have not been well understood. Herein, the changes of ARG abundances in MP biofilms and corresponding leachate under zinc oxide (ZnO) NPs and zinc ion (Zn2+) pressures were comparatively analyzed. The presence of ZnO NPs and Zn2+ promoted the enrichment of ARGs in MP biofilms, and the enrichment was more pronounced in ZnO NPs groups. ZnO NPs and especially Zn2+ mainly decreased the abundances of ARGs in leachate. The increase of integron abundances and reactive oxygen species production in MP biofilms implied the enhanced potential for horizontal transfer of ARGs under ZnO NPs and Zn2+ pressures. Meanwhile, the co-occurrence pattern between ARGs and bacterial genera in MP biofilms with more diverse potential ARG hosts was more complex than in leachate, and the enrichment of ARG-hosting bacteria in MP biofilms under ZnO NPs and Zn2+ pressures supported the enrichment of ARGs.

Bee venom (Apis mellifera L.) rescues zinc oxide nanoparticles induced neurobehavioral and neurotoxic impact via controlling neurofilament and GAP-43 in rat brain

This study investigated the possible beneficial role of the bee venom (BV, Apis mellifera L.) against zinc oxide nanoparticles (ZNPs)-induced neurobehavioral and neurotoxic impacts in rats. Fifty male Sprague Dawley rats were alienated into five groups. Three groups were intraperitoneally injected distilled water (C 28D group), ZNPs (100 mg/kg b.wt) (ZNPs group), or ZNPs (100 mg/kg.wt) and BV (1 mg/ kg.bwt) (ZNPs + BV group) for 28 days. One group was intraperitoneally injected with 1 mL of distilled water for 56 days (C 56D group). The last group was intraperitoneally injected with ZNPs for 28 days, then BV for another 28 days at the same earlier doses and duration (ZNPs/BV group). Depression, anxiety, locomotor activity, spatial learning, and memory were evaluated using the forced swimming test, elevated plus maze, open field test, and Morris water maze test, respectively. The brain contents of dopamine, serotonin, total antioxidant capacity (TAC), malondialdehyde (MDA), and Zn were estimated. The histopathological changes and immunoexpressions of neurofilament and GAP-43 protein in the brain tissues were followed. The results displayed that BV significantly decreased the ZNPs-induced depression, anxiety, memory impairment, and spatial learning disorders. Moreover, the ZNPs-induced increment in serotonin and dopamine levels and Zn content was significantly suppressed by BV. Besides, BV significantly restored the depleted TAC but minimized the augmented MDA brain content associated with ZNPs exposure. Likewise, the neurodegenerative changes induced by ZNPs were significantly abolished by BV. Also, the increased neurofilament and GAP-43 immunoexpression due to ZNPs exposure were alleviated with BV. Of note, BV achieved better results in the ZNPs + BV group than in the ZNPs/BV group. Conclusively, these results demonstrated that BV could be employed as a biologically effective therapy to mitigate the neurotoxic and neurobehavioral effects of ZNPs, particularly when used during ZNPs exposure.

Antioxidant effects of zinc-oxide nanoparticles on post-thaw quality and in vivo fertility of Beetal buck spermatozoa

Metallic nanoparticles are generally considered potential cryoprotectants during semen cryopreservation owing to their ability to improve the spermatozoa quality following cryopreservation when added in cryo-diluents. The present study aimed at investigating the effects of incorporating zinc oxide nanoparticles (ZnO-NPs) in the cryo-diluent on in vitro post-thaw sperm quality attributes, oxidant-antioxidant profile, and in vivo fertility rate in Beetal buck. After characterization, ZnO-NPs were added to the Tris-citric acid-fructose yolk extender. Semen samples, collected from five breeding bucks (5 ejaculates per buck) using an artificial vagina, were pooled. The pooled semen samples, distributed into five equal aliquots, were diluted in the Tris-citric acid cryo-diluent containing five different concentrations of ZnO-NPs (0.5 mg/ml, 1.0 mg/ml, 1.5 mg/ml, 2.0 mg/ml, and 0.0 mg/ml called control group), and were cryopreserved for 24 h. At post-thaw, various in vitro sperm quality parameters, and antioxidant enzyme profiles like superoxide dismutase (SOD), catalase (CAT), peroxidase (POD), and reduced glutathione (GSH) levels were determined. For the in vivo fertility experiment, breeding does (n = 152), aging from 1.5 to 4 years, were artificially inseminated with spermatozoa with intact acrosome containing the same five concentrations of ZnO-NPs. Results demonstrated that the 1.0 mg/ml ZnO-NPs (crystallite size of 19.73 nm) improved (p < 0.01) the activities of antioxidant enzymes (SOD, CAT, and POD) with concomitantly decreased levels (p < 0.001) of lipid peroxidation (LPO) and reactive oxygen species (ROS) when compared with the other groups. Total spermatozoa motility, rapid velocity, and average path velocity were higher (p < 0.05) with the 1.0 mg/ml ZnO-NPs when compared with the control group. Progressive motility and straight-line velocity were higher (p < 0.05) with the 0.5, 1.0, and 1.5 mg/ml of ZnO-NPs addition compared with the 2.0 mg/ml and control groups. The sperm kinematics parameters; the amplitude of the lateral head displacement, the beat cross frequency, the straightness, and the linearity were not influenced by the ZnO-NPs inclusion. Supra-vital plasma membrane integrity was higher (p < 0.001) with the 0.5 mg/ml and 1.0 mg/ml of ZnO-NPs added groups when compared with either 2.0 mg/ml ZnO-NPs or the control group. The viable sperm with intact acrosome was higher (p < 0.05) in the 1.0 mg/ml ZnO-NPs group compared with the other groups. Low supplementation rates improved (p < 0.05) the DNA integrity when compared with the higher dose (2.0 mg/ml ZnO-NPs). The pregnancy per AI was higher (59.3 %; P < 0.05) in the does inseminated with semen added with the 0.5 mg/ml ZnO-NPs followed by 1.0 mg/ml (58.8 %), 1.5 mg/ml (58.6 %), and 2.0 mg/ml (46.6 %) when compared with the control group (33.3 %). We concluded that the 1.0 mg/ml ZnO-NPs added in the citric acid-fructose yolk extender improved the post-thaw quality of Beetal buck spermatozoa in terms of elevated activities of endogenous antioxidant enzymes, improved structural and functional integrity along with higher fertility.

EVALUATION THE HEPATOPROTECTIVE EFFECT OF QUERCETIN AGAINST ZINC OXIDE NANOPARTICLES INDUCED TOXICITY IN MOUSE MODEL

Quercetin is a well-known flavonoid that resents in fruits and vegetables. Zinc oxide nanoparticles (ZnO-NPs) are widely used for packing and cosmetics. This study was conducted to determine the effect of Quercetin on the liver by ZnO-NPs toxicity in a mouse model. Thirty-six Swiss albino mice were divided into two groups, i.e. control group and the experimental group. The control group was administered saline for 28 days orally. The experimental group is further divided into three groups. To the first one, only ZnO-NPs (30 mg/kg, orally) were given for 28 days. To the second group, only quercetin (100 mg/kg, orally) was given for 28 consecutive days. To the third, a combination of quercetin and ZnO-NPs was given for alternate 28 days through the oral route. Animals were sacrificed after 14 and 28 days of dosing. Mouse liver was fixed in the 10% formalin to preserve organ integrity. Histopathological analysis was done to observe the structure of liver in treated mice. The ZnO-NPs group shows the central vein full of infiltrations, sinusoidal spaces congestions and some the necrosis of hepatocytes was observed. The quercetin group shows a normal central vein with no infiltrations. The animals that received both quercetin and ZnO-NPs showed infiltration in central vein and necrosis but less than that of only ZnO-NPs given group. Full recovery in the liver structure was observed in the quercetin+ZnO-NPs group after 28 days of treatment. This study showed the hepatoprotective effect of quercetin because it reduces the toxicity produced by ZnO-NPs.

The combined effect of zinc oxide nanoparticles and milrinone on acute renal ischemia/reperfusion injury in rats: Potential underlying mechanisms

AimTo investigate the efficacy of zinc oxide nanoparticles (ZnO-NPs) and/or milrinone (MIL) on renal ischemia/reperfusion injury (I/RI) in rats and their possible underlying mechanisms. Materials and methodsForty-eight adult male Sprague-Dawley albino rats were randomly assigned into six equal-sized groups (n = 8): normal control, sham-operated, I/R group (45 min/24 h), ZnO-NPs group (10 mg/kg i.p.), MIL group (0.5 mg/kg i.p.), and ZnO-NPs + MIL group in the same previous doses. Key findingsIn comparison to the I/R-operated group, administration of either ZnO-NPs or MIL significantly decreased serum creatinine and urea concentrations, and renal vascular permeability (p < 0.05). The oxidative stress was significantly declined, as evidenced by increased GPx, CAT, and SOD activities and decreased MDA and NO concentrations. Renal expressions of TNF-α, NF-κB, KIM-1, NGAL, and caspase-3 decreased significantly, while Nrf2 increased significantly. Histopathology investigation revealed improvement with minimal renal lesions and fibrosis after ZnO-NPs or MIL treatments. The combined treatments synergistically improved the studied parameters more than either treatment alone. These findings were validated by molecular modeling, which revealed that MIL inhibited TNF-α, NF-kB, caspase-3, KIM-1 and NGAL. SignificanceBoth ZnO-NPs and MIL exerted cytoprotective effects against acute renal I/RI, and a combination of both was found to be even more effective. This renoprotective effect is suggested to be mediated through activation of Nrf2 and the prevention of the NF-κB activation-induced oxidative stress and inflammation, which may strengthen the potential role of ZnO-NPs or MIL in renal I/RI protection during surgical procedures.

Ameliorative Effects of Vitamins A, C, and E on Sperm Parameters, Testis Histopathology, and Oxidative Stress Status in Zinc Oxide Nanoparticle-Treated Rats.

One of the most often utilized nanoparticles (NPs) in several technologies is zinc oxide (ZnO) NPs. However, these NPs are said to have harmful effects on the reproductive system. Thus, we designed this study to specify the potential preventive activity of vitamins (Vits) A, C, and E, as antioxidants, against toxicity of ZnO NPs in the testes of rats. A total of 54 Wistar rats were arranged in 9 groups of 6 and then orally received water (control 1), olive oil (control 2), Vit A (1000 IU/kg), Vit C (200 mg/kg), Vit E (100 IU/kg), ZnO (200 mg/kg), ZnO+Vit A, ZnO+Vit C, and ZnO+Vit E. To determine the amount of testicular injury, sperm analysis and histological evaluation were performed. In addition, oxidative stress status was examined using colorimetric and qRT-PCR methods. Our findings suggest that ZnO NPs cause adverse effects on sperm parameters and testicular histology. Furthermore, oxidative biomarkers (malondialdehyde and total oxidant capacity) were enhanced in the ZnO group. By contrast, the gene expression and activities of antioxidant enzymes (SOD, GPx, and CAT) noted a remarkable decrease in the ZnO group regarding control (p < 0.05). However, oxidative markers were remarkably mitigated after combined treatment of ZnO NPs and Vits A, C, or E compared to the rats given ZnO NPs (p < 0.05). Additionally, compared to the ZnO NP group, the rats receiving Vits+ZnO NPs exhibit increased antioxidant enzyme activity and mRNA expression (p < 0.05). The findings demonstrate the abovementioned Vits' ameliorative effects on toxicity incurred by ZnO NPs.

Neuroprotective effects of quercetin on the cerebellum of zinc oxide nanoparticles (ZnoNps)-exposed rats

ABSTRACT Engineered nanomaterials induce hazardous effects at the cellular and molecular levels. We investigated different mechanisms underlying the neurotoxic potential of zinc oxide nanoparticles (ZnONPs) on cerebellar tissue and clarified the ameliorative role of Quercetin supplementation. Forty adult male albino rats were divided into control group (I), ZnONPs-exposed group (II), and ZnONPs and Quercetin group (III). Oxidative stress biomarkers (MDA & TOS), antioxidant biomarkers (SOD, GSH, GR, and TAC), serum interleukins (IL-1β, IL-6, IL-8), and tumor necrosis factor alpha (TNF-α) were measured. Serum micro-RNA (miRNA): miRNA-21-5p, miRNA-122-5p, miRNA-125b-5p, and miRNA-155-3p expression levels were quantified by real-time quantitative polymerase-chain reaction (RT-QPCR). Cerebellar tissue sections were stained with Hematoxylin & Eosin and Silver stains and examined microscopically. Expression levels of Calbindin D28k, GFAP, and BAX proteins in cerebellar tissue were detected by immunohistochemistry. Quercetin supplementation lowered oxidative stress biomarkers levels and ameliorated the antioxidant parameters that were decreased by ZnONPs. No significant differences in GR activity were detected between the study groups. ZnONPs significantly increased serum IL-1β, IL-6, IL-8, and TNF-α which were improved with Quercetin. Serum miRNA-21-5p, miRNA-122-5p, miRNA-125b-5p, and miRNA-155-p expression levels showed significant increase in ZnONPs group, while no significant difference was observed between Quercetin-treated group and control group. ZnONPs markedly impaired cerebellar tissue structure with decreased levels of calbindin D28k, increased BAX and GFAP expression. Quercetin supplementation ameliorated cerebellar tissue apoptosis, gliosis and improved calbindin levels. In conclusion: Quercetin supplementation ameliorated cerebellar neurotoxicity induced by ZnONPs at cellular and molecular basis by different studied mechanisms.Abbreviations: NPs: Nanoparticles, ROS: reactive oxygen species, ZnONPs: Zinc oxide nanoparticles, AgNPs: silver nanoparticles, BBB: blood–brain barrier, ncRNAs: Non-coding RNAs, miRNA: Micro RNA, DMSO: Dimethyl sulfoxide, LPO: lipid peroxidation, MDA: malondialdehyde, TBA: thiobarbituric acid, TOS: total oxidative status, ELISA: enzyme-linked immunosorbent assay, H2O2: hydrogen peroxide, SOD: superoxide dismutase, GR: glutathione reductase, TAC: total antioxidant capacity, IL-1: interleukin-1, TNF: tumor necrosis factor alpha, cDNA: complementary DNA, RT-QPCR: Real-time quantitative polymerase-chain reaction, ABC: Avidin biotin complex technique, DAB: 3′, 3-diaminobenzidine, SPSS: Statistical Package for Social Sciences, ANOVA: One way analysis of variance, Tukey’s HSD: Tukey’s Honestly Significant Difference, GFAP: glial fiberillar acitic protein, iNOS: Inducible nitric oxide synthase, NO: nitric oxide, HO-1: heme oxygenase-1, Nrf2: nuclear factor erythroid 2-related factor 2, NF-B: nuclear factor-B, SCI: spinal cord injury, CB: Calbindin

Comparing different surface modifications of zinc oxide nanoparticles in the developmental toxicity of zebrafish embryos and larvae

Nanotechnology allows for a greater quality of life, but may also cause environmental and organismic harm. Zinc oxide nanoparticles (ZnONPs) are one of the most commonly used metal oxide nanoparticles for commercial and industrial products. Due to its extensive use in various fields, there has already been much concern raised about the environmental health risks of ZnONPs. Many studies have investigated the toxicological profile of ZnONPs in zebrafish embryonic development; however, the specific characteristics of ZnONPs in zebrafish embryonic/larval developmental damage and their molecular toxic mechanisms of liver development are yet to be fully elucidated. This study aimed to reveal the hazard ranking of different surface modifications of ZnONPs on developing zebrafish and the toxicological mechanisms of these modified ZnONPs in liver tissue. The ~30 nm ZnONPs with amino- (NH2- ZnONPs) or carboxyl- (COOH-ZnONPs) modification were incorporated during the embryonic/larval stage of zebrafish. Severe toxicity was observed in both ZnONP groups, especially NH2-ZnONPs, which presented a higher toxicity in the low concentration groups. After prolonging the exposure time, the long-term toxicity assay showed a greater retardation in body length of zebrafish in the NH2-ZnONP group. Response data from multiple toxicity studies was integrated for the calculation of the EC50 values of bulk ZnO and ZnONPs, and the hazard levels were found to be decreasing in the order of NH2-, COOH-ZnONPs and bulk ZnO. Notably, NH2-ZnONPs induced ROS burden in the developing liver tissue, which activated autophagy-related gene and protein expression and finally induced liver cell apoptosis to reduce liver size. In conclusion, our findings are conducive to understanding the hazard risks of different surface modifications of ZnONPs in aquatic environments and will also be helpful for choosing the type of ZnONPs in future industrial applications.

The therapeutic prospect of zinc oxide nanoparticles in experimentally induced diabetic nephropathy

ABSTRACT Diabetic nephropathy (DN) is the most frequent cause of end-stage renal failure. Zinc oxide nanoparticles (ZnO-NPs) are promising antidiabetic agents. Our aim was to evaluate the prospective efficacy of ZnO-NPs in treating DN in streptozotocin-induced diabetic rats. Rats were randomly dispersed into three sets: control group, DN group and DN + ZnO-NPs group. ZnO-NPs were given at a dose of 10 mg/kg/day by oral gavage for 4 weeks. Urine and blood samples were processed for biochemical analyses. Kidney samples were managed for light and electron microscopy studies. Immune histochemical staining of P53, aquaporin11 (AQP11) and mechanistic target of rapamycin (mTOR) were performed. Gene analyses of nephrin, podocin, beclin-1, LC3 and p62 were done. Administration of ZnO-NPs ameliorated the functional and histopathological alterations of the kidney in a rat model of diabetic nephropathy. ZnO-NPs retained the constancy of the glomerular filtration barrier and restored almost normal renal structure. This was confirmed by upregulation of mRNA expression of podocyte markers (nephrin and podocin) and AQP11 immune histochemical expression in the renal tubules. The beneficial outcomes of ZnO-NPs might be attributed to activation of autophagy through inhibiting mTOR signaling pathway. ZnO-NPs enhanced beclin-1 and LC3 mRNA expressions and reduced p62 mRNA expression. ZnO-NPs also exerted anti-apoptotic potential (evidenced by the decrease in p53 immune expression), anti-inflammatory and anti-oxidant effect [endorsed by suppression of serum cyclooxygenase-2 (COX-2) enzyme activity, tissue nuclear factor kappa beta (NF-κB) level and blood hypoxia-inducible factors (HIF-1α) level]. These results may point the way to an effective therapy of DN. Abbreviations: AQP11 Aquaporin11; BUN: Blood urea nitrogen; COX-2: Cyclooxygenase-2; DAB: 3, 3’-diaminobenzidine; DM: Diabetes mellitus; DN: Diabetic nephropathy; ELISA: Enzyme-linked immunosorbent assay; H&E: Hematoxylin & eosin; HIF-1α: Hypoxia-inducible factors; iNOS: inducible nitric oxide synthase; LC3: Microtubule-associated protein 1 light chain 3; mTOR: Mechanistic target of rapamycin; NF-κB: Nuclear factor kappa beta; NPs: Nanoparticles; PAS: Periodic acid Schiff; PCR: Polymerase chain reaction; PGE2: Prostaglandin E2; ROS: Reactive oxygen species; STZ: Streptozotocin; X ± SEM: Mean ± standard error of means; Zn: Zinc; ZnO-NPs: Zinc oxide nanoparticles.

Zinc oxide nanoparticles attenuate prepubertal exposure to cisplatin- induced testicular toxicity and spermatogenesis impairment in rats

Cisplatin exposure represents a significant fertility problem for childhood cancer. In this study we examined the possible therapeutic role of Zinc oxide nanoparticles (ZnO-NPs) on Cisplatin (Cis) induced impairment in the spermatogenesis initiation during puberty. Seventy-two male rats aged 30 days were distributed into four equal groups: Control group; ZnO-NPs group (intraperitoneal i.p. injected with 5 mg/kg ZnO-NPs once a week for eight weeks); Cis group (i.p. injected with a single dose of 5 mg/kg); ZnO-NPs + Cis group (ZnO-NPs injection 2 hrs before Cis). Each group was subdivided into three groups and was sacrificed 7, 30 and, 60 days after cisplatin induction, which considered prepubertal at 37-day-old, productive at 60-day-old, and completely adult at 90-day-old. Biochemical, molecular, immunohistochemical, and ultrastructural examinations were studied on the testicular tissues and sperm samples. Group treated with Cis showed a decrease in the antioxidant activity and an increase in the reactive oxygen species (ROS), which in turn caused disruption in blood-testis barrier (BTB) proteins in the three different rat ages, and sperm DNA damage in the adult rats compared to control group (p < 0.05). Moreover, alterations in the structural and the ultrastructural morphology of the testis were observed compared with the control at 37, 60 and 90 days old rats. ZnO-NPs administration to Cis group manifested a significant decrease in the ROS that restored the BTB proteins, enhanced the architecture of the testis in the three different rat ages, and increased sperm DNA integrity in the adult rats. Zinc oxide nanoparticles could restore the male reproductive capacity in the adult rats after induction of Cis in the prepubertal period by promoting spermatogenesis.

Effects of Zinc Oxide Nanoparticles on Neural Tube Development in Early Chicken Embryos.

In recent years, Zinc oxide nanoparticles (ZnO-NPs) have been widely used as a mineral filter in cosmetics. Therefore, the possible exposure of pregnant women to ZnO-NPs is gradually increasing. Thus, we aimed to investigate the effect of ZnO-NPs on neural tube development in early chicken embryos. Fifty pathogen-free fertilized eggs were initially incubated for thirty hours. The eggs were divided into 5 groups. In the control group (C) the egg's apex was opened and closed without any administration. In the distilled water group (DW), 10 microliters of distilled water were injected into the sub-blastodermic area. ZnO-NP suspensions were prepared in distilled water and injected sub-blastodermically into the low, medium and high dose ZnO-NP groups (10 mg/kg, 30 mg/kg, and 50 mg/kg, respectively). Incubation was completed in 72 hours, and embryological and neural tube development was evaluated histologically with a light microscope. Embryos in all groups were evaluated according to the Hamburger-Hamilton (HH) staging. It was observed that the staging progressed by the developmental process between 68-72 hours, which is equivalent to the 19-20th stage of HH. Differentiated otic vesicle, optic cup, lens vesicle, pharynx, and Rathke\'s pouch were all observed in embryo sections. Both forebrain and hindbrain vesicles were easily distinguished in the sections by cranial flexion. Neural tube closure defect was not detected in any of the groups. In our observations, ZnO-NPs did not affect neural tube development at the applied dose ranges. We believe that additional studies with higher doses using a higher number of subjects will help clarify the conflicting data in the literature.

The Effects of Pentoxifylline on Memory in Male Rats Treated with Zinc Oxide NPs

Background: Zinc oxide Nanoparticles (NPs) present irreversible effects on the nervous system, memory, and learning. Objective: The current study aimed to investigate the effects of pentoxifylline on memory impairments, CA1 hippocampal pyramidal cells, and blood serum antioxidant enzymes in male rats treated with zinc oxide NPs. Methods: Male Wistar rats were divided into the control, zinc oxide NPs (1.25 mg/kg), pentoxifylline (50 mg/kg), and pentoxifylline with zinc oxide NPs groups. In all study groups, saline, zinc oxide NPs, and pentoxifylline were intraperitoneally injected 30 minutes before training. In the co-treatment group, pentoxifylline was injected one hour before injecting Zno NPs. After performing the behavioral test, the tested animals’ brains were fixed and the number of healthy neurons in the CA1 region of the hippocampus was counted. In all research groups, malondialdehyde levels, total antioxidant power, superoxide dismutase levels, and glutathione peroxidase in blood serum were measured. Results: Zinc oxide nanoparticles decreased memory and the number of healthy neurons in the CA1 region of the hippocampus and increased oxidative stress in blood serum, compared to the controls. In the co-treatment group, using pentoxifylline improved the above-mentioned factors and reached the level of the control group. Pentoxifylline alone presented no significant effect on the aforementioned characteristics, compared to the control group. Conclusion: ZnO NPs may decrease memory retrieval and cause cell death in the pyramidal neurons of the CA1 region of the hippocampus by increasing oxidative stress. Pentoxifylline, as a potent antioxidant, can prevent the harmful effects of ZnO NPs.

Selenium and Zinc Oxide Multinutrient Supplementation Enhanced Growth Performance in Zebra Fish by Modulating Oxidative Stress and Growth-Related Gene Expression.

Selenium and zinc are important dietary micronutrients having antimicrobial and antioxidant roles, thereby assisting in normal development, and an enhanced immune system. Supplementation of selenium and zinc for enhancing the growth performance and reproductive capacity in fish was explored in this study. Selenium nanoparticles (SeNPs) and zinc oxide nanoparticles (ZnONPs) were synthesized by high-energy ball milling (HEBM) using a 10-h dry milling technique at a 10:1 ball-to-powder ratio (BPR) and were premixed with basal feed followed by the administration to adult zebra fish (D. rerio) (2 months old) for 30 days. Growth analysis revealed that zebra fish fed with SeNPs + ZnONPs (2 mg/ kg, equimolar mixture) had significantly higher length and weight than only SeNP (2 mg/ kg) or ZnONP (2 mg/ kg) groups and control zebra fish (p < 0.05). The average length–weight relationships were assessed by estimating the condition factor (C), which was highest in the SeNP + ZnONP group (1.96), followed by a downward trend in SeNP (C = 1.15) and ZnONP (1.11) (p < 0.05). Relative gene expression of growth hormone and insulin-like growth factor-1 was significantly high in the SeNP + ZnONP group compared to other groups (p < 0.05), which indicated that combined administration of both the nanoparticles in basal feed enhanced the growth performance of zebra fish. Intracellular ROS generation was low in the combined group, followed by control, SeNP, and ZnONP groups, indicating higher concentrations of both nanoparticles, in particular, ZnONPs induced oxidative stress. Fecundity and the development of fertilized embryos were significantly high in the SeNP + ZnONP–treated zebra fish compared to only the SeNP- or ZnONP-treated group or control (p < 0.05). These findings indicated that supplementation of SeNP + ZnONP in basal feed could considerably improve the growth performance and development of zebra fish which could be exploited for enhancing aquaculture production.

Zinc oxide nanoparticles improve gut health and reduce faecal zinc excretion in piglets

This study investigated the effects of zinc oxide nanoparticles (ZnON) on growth performance, gut health, and zinc and copper excretion in piglets. A total of 144 piglets (Duroc × Landrace × Large White, weaned at 21 days; mean initial weight 6.15 ± 0.01 kg) were assigned to six groups with six replicates of four pigs per pen for a 26-day feeding trial. The groups were: antibiotic group (basal diet + 75 mg/kg aureomycin), ZnO group (basal diet + 1,600 mg/kg zinc oxide), and four ZnON groups (basal diet + 200, 300, 400, or 500 mg/kg ZnON, respectively). No significant difference in growth performance was observed amongst the treatments. ZnON supplementation improved the activities of superoxide dismutase (linear or quadratic, p < 0.05), copper-zinc superoxide dismutase in the ileum (linear, p < 0.05), catalase in the jejunum and ileum (linear or quadratic, p < 0.05), total antioxidant capacity of duodenum and ileum (linear, p < 0.05), and glutathione peroxidase in the ileum (linear, p < 0.05), and reduced malondialdehyde content in the jejunum (linear, p < 0.05). As ZnON content was increased, the contents of jejunal IgA, interleukin (IL)-6, and IL-10 decreased (linear, p < 0.05), while IgM content increased (linear, p < 0.05). The contents of ileal IgA and IL-10 increased (linear and quadratic, p < 0.05), while the contents of IgM, IgG, and IL-6 decreased (linear or quadratic, p < 0.05). Villus height and the ratio of villus height to crypt depth in piglets fed with ZnON were higher than in the antibiotic group (p < 0.05). Pigs fed with 200–500 mg/kg ZnON showed lower contents of hepatic zinc and copper and faecal zinc than the ZnO group (p < 0.05). These results show that dietary ZnON enhanced intestinal antioxidant and immune capacity and intestinal morphology, particularly 500 mg/kg ZnON, and also that ZnON minimised zinc content in the liver and faeces.

Effects of Zinc Oxide Nanoparticles on Growth, Intestinal Barrier, Oxidative Status and Mineral Deposition in 21-Day-Old Broiler Chicks.

This experiment was to study the effects of zinc oxide nanoparticles (ZnO-NPs) on growth, intestinal barrier, oxidative status, and mineral deposition. In total, 256 one-day-old chicks were randomly allotted to 4 dietary groups and fed with basal diet plus 80mg/kg ZnSO4 (ZnSO4 group) or plus 40, 80, and 160mg/kg ZnO-NPs, respectively, for 21days. Compared with the ZnSO4 group, dietary 40, 80, and 160mg/kg ZnO-NPs did not alter growth (average daily gain, body weight, and gain to feed ratio), and serum activities of glutamic-pyruvic transaminase, alkaline phosphatase and glutamic oxalacetic transaminase (P > 0.05). However, dietary 80 and 160mg/kg ZnO-NPs linearly decreased serum D-lactate content and diamine oxidase activity (P < 0.01). Moreover, 80mg/kg ZnO-NPs enhanced zonula occludens-1 (ZO-1) mRNA expression in jejunal mucosa (P = 0.02). Dietary ZnO-NPs increased total antioxidant capacity activity (P = 0.01), and 80mg/kg ZnO-NPs decreased malondialdehyde content in jejunal mucosa as compared to the ZnSO4 group (P = 0.02). In contrast, dietary ZnO-NPs did not alter mRNA expressions of superoxide dismutase, catalase, glutathione peroxidase, glutathione S-transferase, heme oxygennase-1 (HO-1) and NAD (P)H: quinone oxidoreductase 1 (NQO1) (P > 0.05). No significant difference was found in selected mineral concentrations (Mn, Cu, Fe and Zn) in the liver among ZnSO4 and 3 ZnO-NP groups (P > 0.05). However, 160mg/kg ZnO-NPs increased fecal contents of Zn, Fe and Cu (P < 0.01), but did not affect fecal Mn level (P > 0.05). Therefore, results suggested that ZnO-NPs could be an additive to enhance the intestinal barrier and antioxidant capacity of broiler chicks, whereas the inclusion of 80mg/kg would be more efficient.

Effect of zinc oxide nanoparticles and ferulic acid on renal ischemia/reperfusion injury: possible underlying mechanisms

ObjectivesThe present study examined the effects of ferulic acid (FA) and Zinc oxide nanoparticles (ZnO-NPs) and a combination of both on renal ischemia/reperfusion injury (IRI) in rats and their possible underlying mechanisms. Methodstwo-hundreds male Sprague Dawley rats were randomly allocated into the 5 groups; i) sham group, ii) control (IRI) group (occlusion of the left renal pedicle for 45 min), iii) FA group as IRI group with FA (100 mg/Kg oral 24 hrs before ischemia), iv) ZnO-NPs group as IRI group with ZnO-NPs single 5 mg/Kg i.p. 2 hrs before ischemia and v) FA + ZnO-NPs group as IRI group with both FA and ZnO-NPs in the same previous doses. According to the reperfusion times, each group was further subdivided into 4 hr, 24 hr, 48 hr and 7 days reperfusion subgroups. Resultsadministration of either FA or ZnO-NPs caused significant improvement in the elevated serum creatinine and BUN and malondialdehyde (MDA) concentrations and expression of TNF-α, Bax, caspase-3 in kidney tissues with significant rise in the creatinine clearance, the activities of catalase (CAT) and superoxide dismutase (SOD) and the expression of HO-1, HIF-1α genes and proliferation marker (ki67) in kidney tissues compared to IRI group (p < 0.05). Moreover, a combination of both agents produced more significant improvement in the studied parameters than each agent did alone (p < 0.05). ConclusionsBoth FA and ZnO-NPs exerted cytoprotective effects against ischemic kidney injury and a combination of both exhibited more powerful renoprotective effect. This renoprotective effect might be due to suppression of oxidative stress, enhancement of cell proliferation (ki67), upregulation of antioxidant genes (Nrf2, HO-1 and HIF-1α) and downregulation of inflammatory cytokine (TNF-α) and apoptotic genes (caspase-3 and Bax).

Toxicopathological Effects of Zinc Oxide Nanoparticles on the Liver Function and Preventive Role of Silymarin In vivo

The zinc oxide nanoparticles (ZnONPs) are used in cosmetics and skincare products, and as drug deliverysystems. Because of their natural and therapeutic dangers, high attention was given to the toxicity ofnanoparticles. This experiment was designed to study the pathological influences of ZnONPs on the liverfunction parameters of rats, and to explore the protective action of Silymarin (SIL) against liver functiondisturbances of rats induced by ZnONPs. In our study, (24) albino rats were divided into (4) groups, (6)rats for each and used. The control animals included rats without treatment, while the ZnONPs group ratsreceived 50 mg/kg of ZnONPs for 28 days. In the ZnONPs+SIL group, rats were co-administered witha combination of ZnONPs at a 50mg/kg dose with SIL at a 100 mg/kg dose for 28 days. The SIL groupanimals were treated with 100 mg/kg of SIL for 28 days. All the animals were sacrificed and blood sampleswere obtained by cardiac puncture in the end of the experiments. The levels of biochemical parameters(hepatic enzymes) including alanine aminotransferase (ALT), aspartate aminotransferase (AST) and alkalinephosphatase (ALP) were measured to detect liver function disorders. The results revealed that ZnONPsinduced a significant increase in plasma enzyme activity in comparison to the control group (p&lt;0.05). Cotreatment of SIL significantly reduced levels of these enzyme activities. Based on these results, it can be saidthat Silymarin effectively protects against ZnONPs induced liver function disorders in rats.

Zinc oxide nanoparticles prevent multidrug resistant Staphylococcus-induced footpad dermatitis in broilers

ABSTRACT The current experiment was designed to evaluate the effects of dietary supplementations of zinc oxide nanoparticles (ZONPs) on some behavioural, performance, welfare and histopathological changes in broilers exposed to multidrug resistant Staphylococcus aureus (MRSA)-induced footpad dermatitis (FPD). Eighty-four male Indian River (IR) broilers were randomly allotted to six different dietary treatments as follows: C−ve, C+ve, 10, 20, 30 and 40 ppm ZONPs from 7 to 49d of age. At day 28, broilers (n = 70) were sub-cutaneously injected with 0.5 ml of saline containing 5.3 × 107 CFU/ml of S. aureus (MRSA) in each metatarsal foot pad. Control (non-infected) broilers were given 0.5 ml of saline (n = 14). Results clarified that non-infected birds and ZONPs-fed birds had significantly higher standing and feeding activities and lower resting activities in comparison with the infected group. Also, the S. aureus infected group had significantly lower body weight gain (BWG) and higher feed conversion ratio (FCR) than the non-infected group. In addition, the non-infected birds and ZONPs groups had significantly lower object crossing and tonic immobility times (TI) and gait scores (GS) in comparison with the S. aureus group. Only ZONPs 30, 40 ppm and non-infected groups had a significantly higher latency to lie time (LLT) and lower serum cortisol level in comparison with the S. aureus group. Moreover, there were significant changes in the gross lesion score and histopathological lesions between the different groups. In conclusion, the dietary supplementation of ZONPs can reduce S. aureus-induced negative effects of FPD in broilers.