Protective Effect Of Zinc Research Articles

Protective Effects of Zinc on 2.45GHz Electromagnetic Radiation-Induced Oxidative Stress and Apoptosis in HEK293 Cells.

Several epidemiological studies have shown that exposure to electromagnetic radiation (EMR) can be harmful to human health. The purpose of this study was to examine oxidative parameters and apoptosis induced by EMR in human kidney embryonic cells (HEK293) and to investigate whether zinc (Zn) has protective effect on EMR-induced apoptosis in HEK293 cells. For our experiment, HEK293 cells were divided into four main groups, control, EMR, 50μM Zn + EMR, and 100μM Zn + EMR. HEK293 cells of EMR groups were exposed to 2.45GHz EMR for 1h. In Zn groups, HEK293 cells were incubated with different concentrations of Zn for 48h before EMR exposure. Oxidative stress parameters were determined by spectrophotometric method; bcl-2 and caspase-3 were assessed immunohistochemically and TUNEL method was performed for apoptotic activity. EMR group had higher malondialdehyde (MDA) level and lower superoxide dismutase (SOD) activity compared with control group. In Zn-applied groups, MDA was decreased and SOD activity was increased compared with EMR group. The number of the apoptotic cells and caspase-3 immunopositive cells at EMR group was increased significantly compared with the control group, whereas bcl-2 was decreased. Besides, Zn-treated groups showed a significant reduction in the number of apoptotic cells and caspase-3 from that of EMR group, whereas there was an increase in bcl-2 immunopositivity. Our findings show that EMR caused oxidative stress and apoptotic activation in HEK293 cells. Zn seems to have protective effects on the EMR by increasing SOD activity and bcl-2 immunopositivity, decreasing lipid peroxidation and caspas-3 immunopositivity.

The protective effect of Zinc and Magnesium against subchronic Cadmium toxicity in Wistar rats (Biochemical and neurobehavioral effects)

Objective: The present study shows the beneficial effect of (zinc 10mg / kg + magnesium 10mg / kg) against cadmium poisoning at a dose of 15mg / kg on biochemical parameters and neurobehavioral functions in Wistar rats during a period of 45 days. Methods: The experiment was carried out on 20 Wistar rats, weighing 180 to 232g for an initial weight before starting treatment with cadmium. The rats are grouped in cages at a rate of 5 in groups:Group (1) control: was supplied only with waterGroup (2) contaminated with cadmium (Cd): water plus oral administration cadmium dose 15mg / Kg / l.Group (3) contaminated with (Cd) dose 15mg / Kg / l in water plus magnesium (Mg) dose 10mg / Kg / l oral administration.Group (4) contaminated with (Cd) dose 15mg / Kg / l in water plus zinc (Zn) dose 10mg / Kg / l oral administration.Results: The rats exposure to cadmium showed a very highly significant decrease in body weight of cadmium-contaminated rats (P <0.001) compared with the control group. Regarding the biochemical parameters, there was a very highly significant increase (P <0.001) in the cadmium group blood glucose level compared to the control group, a highly significant increase (P <0.01) in the group urea level. cadmium compared to the control, a very highly significant increase (P <0.001) in the creatinine level of the cadmium lot compared to the control, a very highly significant increase (P <0.001) of transaminases (GOT, GPT) of the group cadmium relative to the control, complete blood  count (CBC) demonstrated a very highly significant increase (P <0.001) in the white blood cell count, the hematocrit of the cadmium lot compared to the control, a very highly significant decrease (P <0.001). ) the red blood cell and hemoglobin levels of the cadmium group compared to the control. A significant improvement (P <0.001) (P <0.01) (P <0.05) of lots: zinc, magnesium, cadmium + zinc and cadmium + zinc compared to cadmium. However, the results obtained from the neurobehavioral tests reveal a significant elevation (P <0.001) (P <0.01) (P <0.05) in the number of cells crossed, the number of straightening in the test. Open field in the group exposed to cadmium resulting in locomotors hyperactivity compared to the control and it is minimal in other groups treated with zinc and magnesium. On the other hand, the plus maze (labyrinth test) revealed a very highly significant increase (P <0.001) (P <0.01) (P <0.05) of the time spent in the closed arms of the cadmium group compared to the control, a significant improvement (P <0.001) (P <0.01) (P <0.05) of the lots: zinc, magnesium, cadmium + zinc and cadmium + zinc compared with cadmium. Conclusion: Subchronic cadmium toxicity has harmful effects on the biochemical, hematological and neuro-behavioral parameters of  Wistar rats, with the installation of an anxiety that will lead to a depressive state, which will be reduced and improved by the antioxidant effect of zinc + magnesium. Keywords: Cadmium-zinc-magnesium-subchronic toxicity-Wistar-Open field-plus mazeÂ

Protective effects of zinc and N-acetyl-L-cysteine supplementation against cadmium induced erythrocyte cytotoxicity in Arbor Acres broiler chickens (Gallus gallus domesticus)

Cadmium (Cd) is one of the most toxic metals released into the environment. Here, we investigated the protective role of Zn2+ and/or N-acetyl-L-cysteine (NAC) against Cd cytotoxicity in the erythrocytes of Arbor Acres (AA) broiler chickens. Four hundred one-day-old AA chickens were divided into 12 groups for in vitro and in vivo studies. Zn2+ and/or NAC was given to the Cd exposed AA chickens to assess their protective roles. This was accomplished by investigating nuclear morphological abnormalities, oxidative stress (SOD, CAT, GPx, GSH and T-AOC), cell apoptosis, ROS accumulation and mitochondrial membrane potential (MMP). Results showed that Cd led to dose- and time-dependent cytotoxicity in the erythrocytes of AA chickens characterized by morphological abnormalities, nucleus damage, increased apoptosis rate and antioxidants depletion. Zn2+ or NAC significantly decreased the erythrocyte apoptosis, ROS production and mitochondrial membrane depolarization caused by Cd. SOD, CAT, GPx, GSH and T-AOC activities significantly decreased both in serum and erythrocytes of Cd exposed AA chickens. The supplementation with Zn2+ or NAC alleviated Cd induced oxidative stress through promoting SOD or GPx/GSH activities respectively. NAC presented a better role in reducing apoptosis, improving antioxidant activities more than Zn2+ in vitro. The combined use of Zn2+ and NAC enhanced cytoprotection in Cd exposed erythrocytes of AA chickens compared to Zn2+ or NAC alone. In conclusion, Zn2+ and NAC exerted remarkable protective roles in Cd exposed erythrocytes of AA chickens by inhibiting cell apoptosis and oxidative stress, and this provides a promising approach to antagonize Cd poisoning in poultry.

THE POSSIBLE PROTECTIVE EFFECT OF ZINC, QUERCETIN, OR THEIR COMBINATION ON LEAD-INDUCED NEPHROTOXICITY IN MALE ALBINO RATS: A LIGHT AND TRANSMISSION ELECTRON MICROSCOPIC STUDY

Lead (Pb)-induced nephrotoxicity has been recognized as a human major public health problem. The aim of the present study is to investigate the possible protective effects of zinc (Zn) or/and quercetin on Pb-induced histologic and ultrastructural changes in the rat kidney. For this purpose, 35 adult male albino rats (Rattus norvegicus) were divided equally into 5 groups, each of 7 rats. Group I (control group): rats received physiological saline intraperitoneally (i.p.) and distilled water orally for 14 consecutive days. Group II (Pb-treated group): rats were orally administered lead nitrate (20 mg/kg body weight/day) for 14 consecutive days. Groups III (Zn and Pb-treated group): rats were administered zinc chloride (2 mg/kg body weight/day, i.p.) 1 hour prior to Pb administration, for 14 consecutive days. Group IV (quercetin and Pb-treated group): rats were orally administered quercetin (50 mg/kg body weight/day), 1 hr prior to Pb administration, for 14 consecutive days. Group V (Zn-quercetin and Pb-treated group): rats received Zn, quercetin and Pb at the same doses, periods and ways of administration mentioned above. The kidney structure of Pb-treated rats revealed swollen, congested glomeruli, adhesion of the glomerular tufts to Bowman’s capsules and obliteration of the urinary spaces. Obliteration of the lumina of many glomerular capillary loops was also seen. Some of the renal tubules (mainly the proximal tubules) exhibited luminal dilatation with flattening of their lining epithelial cells, while the other tubules appeared swollen and necrotic with pyknotic or karyolytic nuclei. Exfoliated damaged epithelial cells were also observed within the tubules’ lumina. Interstitial inflammatory cell infiltration, intertubular haemorrhage and an increase in the number of fibroblasts were also detected in the degenerated tissue. Ultrastructurally, Malpighian corpuscles showed electron-dense nuclei of the parietal and endothelial cells, complete fusion and effacement of some foot processes of the podocytes, focal thickening of the glomerular basement membrane and an increase in the number of mesangial cells. Many proximal convoluted tubules revealed apoptotic cells with marginal condensed chromatin of their nuclei, fused distorted mitochondria, increased lysosomes, multiple cytoplasmic vacuoles, destructed microvilli of the brush border, and dilated basolateral invaginations. However, simultaneous administration of Zn or quercetin plus Pb partially protected the renal tissues against the toxic effects of lead. On the other side, the combination of Zn and quercetin offers additional protective effects against Pb-induced nephrotoxicity in rats. It is concluded from the present study that co-treatment with Zn and quercetin has a better renoprotective effect than that induced by Zn or quercetin alone.

The protective effects of zinc in lead-induced testicular and epididymal toxicity in Wistar rats.

The aim of this study was to investigate the beneficial effects of zinc (Zn) in preventing lead (Pb)-induced reproductive toxicity in Wistar rats. The rats were divided into four groups, namely, control group, Pb group, Zn group, and Pb + Zn group. Animals were exposed to Pb (819 mg of Pb/L) or Zn (71 mg of Zn/L) or both through drinking water for 65 days. Rats exposed to Pb showed decreased weights of testes and accessory sex organs. Significant decrease in the testicular daily sperm production, epididymal sperm count, motility, viability, and number of hypoosmotic tail coiled sperm was observed in Pb-exposed rats. Testicular 3β- and 17β-hydroxysteroid dehydrogenase activity levels and circulatory testosterone levels were also decreased significantly in Pb-exposed rats. A significant increase in the lipid peroxidation products with a significant decrease in the activities of catalase and superoxide dismutase were observed in the testes and epididymis of Pb-exposed rats. Moreover, the testicular architecture showed lumens devoid of sperm in Pb-exposed rats. Supplementation of Zn mitigated Pb-induced oxidative stress and restored the spermatogenesis and steroidogenesis in Pb-exposed rats. In conclusion, cotreatment of Zn is effective for recovering suppressed spermatogenesis, steroidogenesis, elevated oxidative status, and histological damage in the testis of rats treated with Pb.

In vitro effects of simultaneous exposure to platinum and cadmium on the activity of antioxidant enzymes and DNA damage and potential protective effects of selenium and zinc

Circulating platinum (Pt) is detectable in the blood of Pt-treated cancer patients for over a decade after the treatment. Prolonged exposure to Pt, in combination with adverse compounds from nutrition and lifestyle, such as cadmium (Cd), could increase the risk from second cancers. The aim of this study was to investigate the effects of simultaneous exposure to Cd- and Pt-compounds on oxidative and DNA damage and the possible protective effects of zinc (Zn) and selenium (Se). The aqueous solutions of PtCl4, CdCl2 × H2O, ZnCl2 and Na2SeO3 were added, alone or in combination, to whole blood and isolated erythrocytes to produce the final concentrations of 2000 μg/L of Pt, 8 μg/L of Cd, 100 μg/L of Se, and 1000 μg/L of Zn. The activity of copper, zinc-superoxide dismutase, glutathione peroxidase and glutathione in whole blood was determined after 1 h exposure in in vitro conditions. The induction of DNA strand-breaks in human peripheral blood leukocytes was determined with the alkaline comet assay after 24 h exposure. Exposure to Pt and/or Cd decreased the activities of antioxidant enzymes and elevated DNA damage compared to control. A statistically significant change in the activity of both enzymes and in the induction of DNA strand-breaks was observed in the cells treated with Pt + Cd combination, while the addition of Se and/or Zn resulted in partial recovery of these effects. The results indicate that combined exposure to Pt and Cd could disrupt antioxidant protection of the organism and increase DNA damage, whereas Se and Zn could partially ameliorate these harmful effects.

Zinc and autophagy

Autophagy refers to a catabolic process,in which the damaged organelles or biological macromolecules, such as protein aggregates, are degraded via lysosome. The completion of autophagy depends on a series of autophagy-related genes (Atgs) and many upstream regulatory molecules. Zinc is an essential trace element, and plays an important role in the process of autophagy as a component of enzymes and structural proteins like zinc transporters or zinc finger protein. The regulation of autophagy is closely associated with the zinc ion homeostasis. In addition, many studies suggest that the protective effects of zinc on cells are likely to be done by autophagy. This review aims to summarize the current research progress and discuss the reciprocal regulation mechanism between zinc and autophagy, which may provide insights into the intricate roles of autophagy in diseases and find novel strategies for treatment and prevention of human diseases.

Protective effect of selenium and zinc against cadmium toxicity in SHSY-5Y neurons

Cadmium is a widespread heavy metal environmental toxicant and pollutant. Cadmium toxicity affects many tissues and organs including the central nervous system and cadmium exposure has been related to many neurodegenerative diseases (1). Cadmium-induced toxic effects include oxidative damage, apoptosis, interference with calcium/zinc-dependent mechanisms, inhibition of cellular respiratory processes and others, but the underlying mechanisms of cadmium neurotoxicity are not completely understood (2). On the other hand heavy metal toxicity can be counteracted by bioelements such as zinc, selenium and others mainly through the induction of metallothionein expression levels and other antioxidant pro-teins (3). Human neuroblastoma SHSY-5Y cell line, in both the undifferentiated and neuronal-like differentiated state, were used in this study to better elucidate the mechanisms un-derlying the protective effect of zinc and selenium against the cadmium neurotoxicity. Toxic effects of cadmium chloride (10 mM, 24h) observed by cell viability assay, western blot anal-ysis of Bax and Gap-43, and immunostaining of b3 tubulin and cytochrome c proteins, were reverted to control values by a 24h-pretreatment with zinc chloride (50 mM) both in undiffer-entiated and differentiated neurons. Interestingly, the reverting effect of a 24h-pretreatment with sodium selenite (100 nM) against cadmium toxicity, was observed only in undifferentiat-ed neurons. In conclusion we can hypothesize that in undifferentiated and differentiated SHSY-5Y neurons, the protective effects of zinc and selenium compounds against cadmium toxicity depend on the activation of partially common signalling pathways. Moreover sodium selenite dont exert a significant protective effect in differentiated SHSY-5Y demonstrating that the differentiated and undifferentiated phenotypes show different responses.

Protective Effect of Zinc against Postnatal Lead-Induced Alterations in the Neurobehavioral Development of Normally-Fed and Protein Malnourished Rats

Background: The most critical effects of lead (Pb) toxicity occur among children exposed during fetal development, postnatal development or both. Malnutrition is a common problem worldwide and occurs in both developing and developed countries. Zinc is an essential mineral and a fundamental component of the endogenous enzymatic antioxidant system. Objective: To evaluate the possible protective effects of zinc against postnatal Pb-induced alterations in the physical and neurobehavioral development in both normally-fed (NF) and protein malnourished (PM) rats. Methods: Protein sufficient diet (20% casein) for NF groups and protein deficient one (8% casein) for PM groups were utilized. Both NF and PM groups were subdivided to 3 groups 6 dams/each and received daily from parturition until weaning (together with diet); saline for control, 1 ml lead acetate (12 mg/ml) and zinc sulphate (32 mg/kg) with Pb. Pups were evaluated for physical and neurobehavioral development as well as for performance in Neonatal T-maze and Open-field test (OFT). Results: Postnatal Pb exposure inhibited most physical and neurobehavioral development of both NF and PM pups. It also reduced number of correct choices as well as ambulation and rearing frequencies in both pups, the effect was more pronounced in PM pups. However, Zinc increased these parameters in NF and PM pups but increased body weight, ambulation and rearing frequencies while decreased time of appearance of eye opening and grooming time in NF pups only. Conclusion: Postnatal Pb exposure caused alteration in some aspect of physical and neurobehavioral development as well as in some behavioral functions as learning, emotionality as well as locomotor and exploratory activities. The alterations were much greater under the condition of protein malnutrition. Zinc was shown to protect against these lead-induced alterations in both NF and PM rat pups. However the protective effect of Zinc sometimes declined under concomitant protein malnutrition.

Protective Effects of Zinc Against Acute Arsenic Toxicity by Regulating Antioxidant Defense System and Cumulative Metallothionein Expression.

Arsenic (As), a toxic metalloid, is one of the major global concerns. The toxicity resulting from As exposure is linked to the generation of reactive oxygen intermediates during their redox cycling and metabolic activation processes that cause lipid peroxidation (LPO). Zinc (Zn), a redox-inactive metal, helps to maintain cellular functions because of its prominent role in antioxidant network through multiple mechanisms. The present study, therefore, explores the effectiveness of administered Zn to combat against acute As toxicity by analysis of antioxidant defense status, alkaline phosphatase (ALP) activity, histological profile, MT expression, and elemental status in rat liver. To achieve this goal, four experimental groups, one control and three receiving different metal supplementations, were chosen (group 1, control; group 2, Zn supplemented; group 3, As substituted; group 4, Zn + As supplemented). The levels of reduced glutathione (GSH) and activities of glutathione reductase (GR) and ALP were lowered, whereas LPO levels and activity of superoxide dismutase (SOD) were elevated with no significant change in catalase (CAT) activity. Histopathological changes were also observed in the As substituted group in comparison to the control. Particle-induced X-ray emission (PIXE) analysis showed decrease in Fe and S concentration in rat liver after As intoxication, whereas As was below detection limit, i.e., <1ppm. Zn administration almost restored the antioxidants, ALP activity, histopathological changes, and elemental status. A cumulative increase in MT expression was found with the combined treatment of Zn and As. Also, Zn alone caused no significant change in the antioxidant defense system. It can be concluded that restoration of antioxidant activity and increased MT expression are the two independent protective mechanisms of Zn to reduce acute As toxicity.

Cortisol 유발 세포독성에 대한 아연 관련 항산화 유전자 발현 증가에 의한 세포보호 효과

The protective effect of zinc against cortisol-induced cell injury was examined in rainbow trout gill epithelial cells. Cells exposed to cortisol for 24 h showed increased leakage of lactate dehydrogenase (LDH) as well as decreased cell viability in a dose-dependent manner. Treatment with zinc (100 μM ZnSO₄) reduced the severity of both LDH release and cell death as well as protected cells against cortisol-induced caspase-3 activation, indicating reduction of apoptosis. Cortisol-induced cell death, leakage of LDH, and caspase-3 activation were blocked by the glucocorticoid receptor antagonist Mifepristone (RU-486), suggesting that cell injury was cortisol-dependent. In addition, we studied the effect of zinc on the expression of antioxidant genes such as metallothionein A (MTA), metallothionein B (MTB), glutathione-S-transferase (GST), and glucose-6-phosphate dehydrogenase (G6PD) during cortisol-induced cell injury. MTA, MTB, GST, and G6PD mRNA levels increased after treatment with zinc or cortisol, separately or in combination. Higher mRNA levels of MTA, MTB, GST, and G6PD were detected when cells were treated with 100 μM ZnSO₄ and 1 μM cortisol in combination at the same time compared to treatment with zinc or cortisol separately. Cells treated with zinc showed increased intracellular free zinc concentrations, and this response was significantly enhanced in cells treated with cortisol and zinc. In conclusion, zinc treatment inhibited cortisol-induced cytotoxicity and apoptosis through indirect antioxidant action.

Induction of autophagy by zinc during acute ethanol intoxication in mice

Recently, autophagy has emerged as an important player in the defense against ethanol toxicity. The potential role of zinc in the modulation of autophagy during ethanol stress in humans and animal models has not been examined previously. In this study, the effect of zinc deficiency, adequacy and excess on hepatic autophagic flux, liver injury, lipids accumulation and metallothionein expression was examined in C57BL/6 mice acutely exposed to ethanol. Mice were fed diets containing three different levels of zinc: low, adequate and excess for 30 days. After this, mice were given ethanol or water at a total accumulative dosage of 4.5‐g/kg body weight. Mice were sacrificed at 24h after the first gavage. Hepatic autophagic flux was estimated by measuring LC3II/LC3I ratio and Beclin1, p62/ SQSTM1 and Lamp2 levels. The dietary treatments did not affect food intake and body weight. Low zinc intake caused inhibition of autophagic flux in mice exposed or not to ethanol. In addition, zinc deficient mice exhibited increased liver injury and accumulation of lipids in liver. Conversely, high zinc intake was associated with increased autophagic flux and decreased accumulation of lipids in liver in mice exposed to ethanol. Lastly, ethanol consumption increased the expression of metallothionein mRNA in liver. The results of this study suggest that adequate zinc intake is critical to maintain autophagy. The protective effects of zinc against ethanol toxicity could be mediated by autophagy.Supported by NIH 1R03AA022451‐01

Histopathological and Histochemical Assessment of the Protective Effects of Zinc on Ethanol-Induced Acute Hepatotoxicity in Adult Albino Rats

Alcoholic hepatotoxicity is a worldwide major cause of death. The objectives of the present study are to evaluate qualitatively as well as to a less extent quantitatively the protective effects of zinc on acute alcoholic hepatotoxicity. Forty five adult male albino rats were equally divided into three groups. Group I, the ‘control’ one while group II, ‘ethanol-treated’ was received ethanol with a total accumulative dosage of 15 g/kg/36 hours (10 g/kg/day) by three equally divided gavages of 5 g/kg/12 hours each, to simulate acute alcohol intoxication or quadruple bingedrinking among humans. Group III, ‘zinc/ethanol-treated’ was received an intraperitoneal injection of zinc sulfate as 5 mg/kg/day for three days before ethanol administration. Qualitative histological and histochemical parameters were undertaken by using hematoxylin and eosin, iron hematoxylin, periodic acid-Schiff and detectors for the activity of succinic dehydrogenase and ATPase. Also some quantitative morphometric parameters were utilized. Ethanol-treated animals showed loss of normal architecture of hepatic lobules, high cellular degeneration and fatty changes, increased apoptosis, marked mitochondrial affection, inflammatory infiltration in portal space and sinusoids, depletion of glycogen content and decrease in the activity of succinic dehydrogenase and ATPase. Zinctreated animals showed ameliorative changes as mild cellular degeneration, proportionally less apoptosis, mild mitochondrial affection, almost no inflammatory infiltration, mild decrease of glycogen content and mild decrease of succinic dehydrogenase activity while ATPase activity was rendered normal. These results conclude that Zinc is an essential hepatoprotective agent against alcoholic hepatotoxicity. Zinc is qualified to be the first essential and the modest trace element in the map of prophylaxis and management of liver diseases. Finally, the classical histological, histochemical and morphometric techniques are fair enough to explore the big picture of these effects.

Effect of zinc treatments on lead exposed periparturient bovine lymphocytes in vitro on their proliferation and superoxide dismutase (SOD) expression

The study was conducted to observe adverse effects of lead (Pb) treatments and protective effect of zinc on lymphocyte proliferation and to quantify the expression levels of superoxide dismutase (Cu/ZnSOD) genes involved in antioxidant’s defenses in periparturient Karan Fries (Tharparker × Holstein-Friesian) cow. Blood samples were collected from peripartum Karan Fries cow at 30 and 15 days prepartum, at day of calving (0 day) and 15 and 30 days postpartum for estimation of lymphocytes proliferation and SOD expression. A fixed number of cells (2×106) were grown in culture for 72 h with different levels of Pb (10–4, 10–5, 10-6 M) and their adverse effects were counteracted by Zn (50, 55, 60 μM) and analysed for the lymphocyte proliferation (MTT assay) and for the expression level of Cu/ZnSOD using the realtime PCR technique with light upon extension (LUX) fluorogenic primers. Pb dosage had no adverse effect and the overall mean proliferation values indicated that 60μM Zn may be optimum for maximizing lymphocyte proliferation. The Cu/ZnSOD mRNA expression in lymphocytes was higher at higher dosage of Pb in comparison to lower dosage in all the 3 (50, 55, 60 μM) Zn treatments. There was no significant difference at different levels of Zn on SOD expression. Cu/ZnSOD mRNA expression decreased from –30 days to 0 days but increased from 0 to 30 days after calving. The results suggested that the zinc may have an ameliorative effect on lead exposed oxidative stress on lymphocytes proliferation and Cu/ZnSOD mRNA expression through modulation of superoxide dismutase expression

The effects of heavy metals and pesticides on survival of miracidia stage of Fasciola hepatica

Abstract The effect of heavy metals and pesticides on viability of miracidia stage of Fasciola hepatica was investigated. The experimental groups with chemicals were compared with the untreated control group. After 16 days of exposure, the groups contained Cr, Zn, CdZn, exhibited decreased motility of miracidia inside the egg shells. In the groups which contain AGCr, GCdZn, CdCrZn and AGCdCrZn no effect on movement of emerged miracidia were observed. In the rest of the groups immobile or dead miracidia inside the egg shells have been identified. The possible protective effect of zinc on miracidia of Fasciola hepatica is discussed.

Effects of Different Sources and Levels of Zinc on H2O2-Induced Apoptosis in IEC-6 Cells

Zinc has been shown to be an inhibitor of apoptosis for many years. The present study was designed to investigate effects of three zinc chemical forms on H2O2-induced cell apoptosis in IEC-6 cells via analysis of cell vitality, LDH activity, apoptosis percentage, caspase-3 activity, and Bcl-2, Bax, and caspase-3, -8, and -9 gene expression. Cells were divided into H2O2 and zinc sources+H2O2 groups, and there are three different zinc sources [zinc oxide nanoparticle (nano-ZnO), zinc oxide (ZnO), and zinc sulfate (ZnSO4)] and three concentrations (normal = 25 μM, medium = 50 μM, and high = 100 μM) used in this article. In the present study, we found the striking cytotoxicity of H2O2 higher than 200 μM on cell vitality, LDH activity, and apoptosis percentage in the cells using five different concentrations (50, 100, 200, 400, and 800 μM) of H2O2 for 4 h. Moreover, we observed that cell vitality was increased, LDH activity and apoptotic percentage were decreased, and gene expression level of Bax and caspase-3 and -9 was markedly reduced, while gene expression level of Bcl-2 and ratio of Bcl-2/Bax were increased in normal concentration groups of nano-ZnO and ZnSO4 compared with H2O2 group, but no significant difference was observed in caspase-8 gene expression. Furthermore, medium or, more intensely, high concentrations of nano-ZnO and ZnSO4 enhanced H2O2-induced cell apoptosis. Compared with nano-ZnO and ZnSO4, ZnO showed weakest protective effect on H2O2-induced apoptosis at normal concentration and was less toxic to cells at high level. Taken together, we proposed that preventive and protective effects of zinc on H2O2-induced cell apoptosis varied in IEC-6 cells with its chemical forms and concentrations, and maybe for the first time, we suggested that nano-ZnO have a protective effect on H2O2-induced cell apoptosis in IEC-6 cells.

Protective effect of Zinc and Salvia on the immune system caused by noise in rats

Objective To observe the protective effect of the zinc gluconate combined with Salvia injection on noise induced serum immunoglobulin(IgG,IgM,IgA) and immune molecules (IL-2,IL-4) in rats.Methods 50 female SD rats were randomly divided into control group,noise group,zinc gluconate noise group(plus zinc group),Salvia injection noise group (plus Salvia group) and Zinc gluconate oral liquid and Salvia injection noise group(combined group),10 rats in each group.Except the control group,rats in the other groups were continuously exposed to high frequency steady noise for two weeks.The concentrations of serum immunoglobulin (IgG,IgM,IgA) and immune molecules (IL-2,IL-4) after the intervention of noise were compared.Results Serum levels of IgG,IgM,IL-2,IL-4of the control group were significantly higher than the noise group (all P ＜ 0.05),plus zinc group (all P ＜ 0.05),plus Salvia group(all P ＜0.05),the differences were statistically significant.Serum level of IgA of each group was not statistically different compared with control group (all P ＞ 0.05).Serum levels of IgG,IgM,IL-2,IL-4 in the noise group were significantly lower than those in the control group (all P ＜ 0.05),combined group (all P ＜ 0.05),the differences were statistically significant.Serum levels of IgG,IgM,IL-2 in plus zinc group were significantly higher than the noise group(all P ＜ 0.05).Serum IgA concentration of each group showed no significant difference compared with noise group(all P ＞ 0.05).Conclusion Zinc gluconate oral solution and Salvia injection have protective effect on immune system affected by noise in rats,the protective effect of combination of zinc gluconate oral solution and Salvia injection is stronger than the individual. Key words: Noise; Zinc gluconate; Salvia injection; Immunoglobulin ; Immune molecules

Protective effect of zinc-N-acetylcysteine on the rat kidney during cold storage

Cold storage of kidneys before transplantation is problematic because of the limited survival time of the allografts. In this study, zinc-N-acetylcysteine (ZnNAC) was shown to be a potent endonuclease inhibitor and antioxidant, and it was tested as a potential additive to a cold storage solution for kidney preservation. Exposure of normal rat kidney NRK-52E cells to ZnNAC resulted in zinc delivery to the cells as determined by TFL-Zn fluorophore and partial protection of the cells against injury by cold storage in University of Wisconsin solution (UWS) as measured by propidium iodide assay. Ex vivo, rat kidneys demonstrated time- and temperature-dependent DNA fragmentation as assessed by TUNEL assay, indicating irreversible cell death. DNA fragmentation was faster in the medulla than in the cortex, and tubules were affected more than glomeruli. Perfusion of rat kidneys with cold ZnNAC solution in UWS significantly inhibited cell death both in the cortex and medulla at concentrations of 0.3-30 mM compared with UWS alone, with a maximum effect at 1-10 mM ZnNAC. Cold storage of the kidney significantly increased quantities of cleaved caspase-3 and endonuclease G (EndoG) in the tissue, which were abolished by 10 mM ZnNAC, indicating its ability to suppress both caspase-dependent and -independent cell death. Therefore, supplementation of UWS with ZnNAC can decrease DNA fragmentation and protect kidney allografts from cell death due to cold storage.

Assessment of cadmium-induced hepatotoxicity and protective effects of zinc against it using an improved cell-based biosensor

Cadmium (Cd) is a toxic environmental pollutant which creates risks to human health. Liver is one of the major sites of Cd accumulation in the organism and target organs under chronic and acute exposure of Cd. It was estimated that Zn2+ supplementation can prevent apoptosis induced by a variety of agents such as Cd2+. In this paper, an improved electric cell-substrate impedance sensing (ECIS) assay was developed to investigate the Cd2+-induced hepatotoxicity and the effects of Zn2+ at different concentrations on it in vitro. Normal liver L-02 cells were cultured onto interdigitated electrodes. With ECIS technology the dynamic responses of L-02 cells were monitored in a non-invasive and label-free manner. The results showed a clear dose- and time-depending toxic effect of Cd2+ on L-02 cells. The half-inhibition concentration of Cd2+ was 20μM after 24h of exposure. The results also revealed that enhanced Zn2+ consumption (10–20μM) may be beneficial for preventing Cd2+-induced hepatotoxicity. However, its excessive intake (40μM) may intensify the hepatotoxicity. Furthermore, for improving the detection sensitivity of the system, a cell immobilization approach using self-assembly techniques was applied to bind cells on electrodes for improving the detection sensitivity of the system. This study demonstrated that the ECIS system holds promise as a utility platform for real-time studying cell status and evaluating chemical effect with high detection sensitivity.

Protective effect of zinc on cadmium embryotoxicity and antioxidant status of blood plasma in newly hatched chicks

Among the multiple mechanisms of cadmium toxicity proposed, the most common is the disruption of the cellular antioxidant system, which may be limited by pre- or co-treatment with zinc. The aim of this study was to determine if simultaneous zinc supplementation of hen's egg could reduce embryotoxic effect of cadmium. Egg albumen was injected on day 4 of incubation with cadmium alone (50 nmol per egg) or in combination with zinc (100 and 500 nmol). Hatching results and antioxidant activity in plasma of newly hatched chicks were determined by photochemiluminescence (PCL) and FRAP methods. Administration of cadmium markedly reduced hatchabilty (30.2 %), while both zinc doses used were embryotoxic (43.2 and 48.9 %) as compared to the control group (61.9 %). This adverse effect was reduced by simultaneous zinc administration (completely at 10-fold higher molar concentration). This observation was confirmed by examination of the antioxidant capacity in plasma of Cd-treated chicks. A slight decrease in the hydrophilic and lipophilic antioxidant capacity induced by cadmium was compensated by a co-treatment with higher zinc dose administration, whereas the exposure of hen embryos to zinc caused an increase in antioxidant potential in the plasma of chicks. It is concluded that Zn supply in conditions of exposure to Cd can protect against Cd-induced oxidative stress in chicken embryos.