Zinc Pretreatment Research Articles

Zinc Supplementation Reduces ROS Production and Prevents MDMA-Induced Apoptosis in TM3 Leydig Cells via the Inhibition of Pro-Apoptotic Proteins.

MDMA can cause serious adverse effects on vital organs such as the heart, brain, and liver. Additionally, MDMA consumption can also potentially cause various endocrine system dysfunctions. The previous study has shown that pre-treatment of zinc can reduce the cytotoxicity of MDMA on the Leydig cell line (TM3). In this study, we investigated the mechanisms involved in the treatment with MDMA on the apoptosis of TM3 cells and the effects of zinc pre-treatment on reducing the apoptotic effects of MDMA. TM3 cells were incubated with MDMA (5 mM), zinc (8 µM), and zinc (8 µM) prior to MDMA (5 mM) for 48 h. The cells were pre-treated with zinc for 24 h prior to the administration of MDMA, and the total culture time was 48h. The effect of different treatment groups in causing oxidative stress and apoptosis in TM3 cells was measured by DCF, TUNNEL, and western blot tests, respectively. Our results revealed that the number of DCF and tunnel-positive cells increases as a result of MDMA treatment. In addition, the treatment with MDMA increased the expression of pro-apoptotic proteins caspase 3, Bax, and p53. Conversely, the expression of anti-apoptotic protein Bcl-2 decreased. Zinc pre-treatment significantly decreased the expression of pro-apoptotic proteins and the number of tunnels and DCF-positive cells compared to the MDMA-only group. It is concluded that MDMA has a toxic effect and causes apoptosis on TM3 cells, and also, pre-treatment with zinc mitigates the ROS production and toxic effect of MDMA and MDMA-induced apoptosis in TM3 cells.

In vitro Pretreatment with Zinc Alleviates the Adverse Effects of Tetrahydrocannabinol on Cultured Mouse Sertoli Cells: Role of Anti-apoptotic and Antioxidant Activities.

Global rise in cannabis abuse during reproductive years has placed a large number of men at risk for the adverse consequences of δ-9-tetrahydrocannabinol (THC), the primary active component of cannabis. It has been reported that THC affects male fertility and causes testicular cell dysfunction and apoptosis. This study aimed to investigate the possible protective role of zinc pretreatment against the toxic effects of THC in cultured mouse Sertoli cells and the underlying mechanism. The Mus Musculus Sertoli cell line (TM4) was cultured, exposed to THC alone (470 μM, 24 h), co-administered with zinc (8 μM, 48 h), and investigated in three groups: control, THC, and THC + zinc. The MTT was performed to evaluate cell viability. TUNEL assay was also applied for the detection of cell apoptosis and a western blot was performed for measuring protein expression levels of Caspase3, Pro-caspase3, SOD, and PDGF-A. THC significantly decreased cell viability (p < 0.001) and expression levels of SOD, PDGF-A, and pro-caspase3 proteins (p < 0.05 for all), whereas increased Sertoli cells apoptosis (p < 0.001) and expression level of cleaved caspase3 protein (p < 0.001). Pretreatment with zinc reversed THC-induced apoptotic and oxidative effects and reduced cleaved caspase3/pro-caspase3 ratio but could not reverse THC-induced reduction of PDGF-A expression level in TM4 cells. The present data suggest that THC induces Sertoli cell damage through a multitarget mechanism. Zinc was reported to protect against THC-induced Sertoli cell damage due to its antiapoptotic and antioxidant activities, indicating its clinical importance against THC-induced testicular toxicity among addicted men.

Effect of zinc supplementation on immunotoxicity induced by subchronic oral exposure to glyphosate-based herbicide (GOBARA®) in Wistar rats

To evaluate the effect of zinc supplementation on immunotoxicity induced by subchronic oral exposure to glyphosate-based herbicide (GBH). Sixty adult male Wistar rats randomly divided equally into six groups were exposed to GBH by gavage daily for 16 weeks with or without zinc pretreatment. Group DW rats received distilled water (2 mL/kg), group Z rats received zinc (50 mg/kg), and group G1 and G2 rats received 187.5 and 375 mg/kg GBH, respectively. Group ZG1 and ZG2 rats were pretreated with 50 mg/kg zinc before exposure to 187.5 and 375 mg/kg GBH, respectively. Tumor necrosis factor alpha (TNF-α) and immunoglobulin (IgG, IgM, IgE) levels were measured by enzyme-linked immunosorbent assay. Spleen, submandibular lymph node, and thymus samples were processed for histopathology. Exposure to GBH (G1 and G2) significantly increased serum TNF-α concentrations and significantly decreased serum IgG and IgM concentrations compared with the control levels. Moderate-to-severe lymphocyte depletion occurred in the spleen, lymph nodes, and thymus in the GBH-exposed groups. Zinc supplementation mitigated the immunotoxic effects of GBH exposure. GBH exposure increased pro-inflammatory cytokine responses, decreased immunoglobulin production, and depleted lymphocytes in lymphoid organs in rats, but zinc supplementation mitigated this immunotoxicity.

Immunotoxic Effects of Cypermethrin in Male Wistar Rats: Attenuation by Co-Administration of Zinc and Alpha-Lipoic Acid

Aim The present study investigated the effects of cypermethrin exposure on humoral and cellular immune response in rat and its attenuation by zinc and alpha-lipoic acid. Methods Cypermethrin at the dose levels of 40 mg and 80 mg/kg body weight were orally administered and pre-treatment of zinc (227 mg/L in drinking water) and alpha-lipoic acid (35 mg/kg body wt.) were done. Total leukocyte and differential leukocyte counts (DLC), phagocytic index, serum nitric oxide (NO) activity, total immunoglobulin concentration, quantitative hemolysis, proliferation assay of blood mononuclear cells were estimated and histological examination of spleen was accomplished. Results Total white blood cell (WBC) count and percentage of lymphocyte, serum nitric oxide activity (p&lt;0.001) and quantitative hemolysis were increased significantly increased whereas neutrophil %, total serum immunoglobulin, and blood mononuclear cell proliferation (p&lt;0.001) and the phagocytic function of peritoneal macrophages were significantly reduced in cypermethrin treated rats compared to control group rats at a dose-dependent manner. Zinc and alpha-lipoic acid pre-treatment reversed the results. Conclusion From the findings it can be concluded that the co-administration of zinc and alpha-lipoic acid significantly attenuated the immunotoxic effects in cypermethrin exposed rat.

Effect of zinc application on water content and photosynthetic pigments of mungbean (Vigna radiata L.) under water stress

A field experiment was conducted during rabi season of 2017-18 at agricultural college farm, Bapatla to investigate the effect of seed pretreatment and foliar application of zinc on relative water content (RWC) and photosynthetic pigments in mungbean under moisture stress, in a split plot design with three replications. The treatments comprised of two main treatments viz., no stress i.e. control (M0) and stress from flowering stage (i.e. from 30 DAS) up to harvest (M1) and seven sub-treatments viz., no zinc application (S0), seed treatment with 0.05% and 0.075% ZnSO4 solutions for 5 hrs before sowing (S1 and S2), foliar spray of 300, 400 and 500 ppm ZnSO4 at 30 DAS (S3, S4 and S5) and water spray at 30 DAS (S6). The results of the study revealed that plants that were subjected to water stress from flowering stage decreased the RWC, total chlorophyll and carotenoid contents by 10.0, 7.5 and 12.6 per cent, respectively, over control plants. Among zinc treatments, Zinc foliar spray @ 500 ppm at 30 DAS increased the RWC, total chlorophyll and carotenoid contents by 8.1, 10.2 and 6.1 per cent respectively, over untreated plants. It can be concluded that the use of zinc spray @ 500 ppm at 30 DAS counteracted the negative effects of water stress on mungbean by maintaining high water potential and by actively synthesizing the photosynthetic pigments.

Effect of zinc application on water content and photosynthetic pigments of mungbean (Vigna radiata L.) under water stress

A field experiment was conducted during rabi season of 2017-18 at agricultural college farm, Bapatla to investigate the effect of seed pretreatment and foliar application of zinc on relative water content (RWC) and photosynthetic pigments in mungbean under moisture stress, in a split plot design with three replications. The treatments comprised of two main treatments viz., no stress i.e. control (M0) and stress from flowering stage (i.e. from 30 DAS) up to harvest (M1) and seven sub-treatments viz., no zinc application (S0), seed treatment with 0.05% and 0.075% ZnSO4 solutions for 5 hrs before sowing (S1 and S2), foliar spray of 300, 400 and 500 ppm ZnSO4 at 30 DAS (S3, S4 and S5) and water spray at 30 DAS (S6). The results of the study revealed that plants that were subjected to water stress from flowering stage decreased the RWC, total chlorophyll and carotenoid contents by 10.0, 7.5 and 12.6 per cent, respectively, over control plants. Among zinc treatments, Zinc foliar spray @ 500 ppm at 30 DAS increased the RWC, total chlorophyll and carotenoid contents by 8.1, 10.2 and 6.1 per cent respectively, over untreated plants. It can be concluded that the use of zinc spray @ 500 ppm at 30 DAS counteracted the negative effects of water stress on mungbean by maintaining high water potential and by actively synthesizing the photosynthetic pigments.

Insulin Secretion by β-Cell-Like Cells Derived from Pulp Stem Cells Depends on Augmented Cytosolic Zinc Levels than GABA Levels

Background: Stem cells harvested from human exfoliated deciduous teeth (SHED) are pluripotent and can be differentiated into insulin-secreting β-cells, i.e., SHED β-cells. Previously, we showed that zinc upregulates insulin secretion from SHED β-cells, potentially providing an extra source for insulin. Rationale: In this study, we determined the role of ionotropic γ-aminobutyric acid A (GABAA) receptor in zinc-enhanced insulin secretion from SHED β-cells. Autocrine/paracrine activation of GABAA receptors by GABA elevates calcium influx in pancreatic β-cells, in which intracellular chloride is maintained at high levels. Method and Findings: Differentiating SHED into SHED β-cells resulted in an increase in the expression of GABAA receptor subunits and Zrt-/irt-like protein3 (ZIP3), a zinc uptake transporter. Zinc pretreatment elevated the insulin gene transcription, whereas knockdown of ZIP3 reduced levels of intracellular zinc, and concomitantly reduced insulin secretion by SHED β-cells. Zinc-pretreated SHED β-cells exhibited a GABA-induced increase in Ca2+ influx, detected with a ratiometric calcium-sensitive dye, suggesting zinc-mediated regulation of GABAA receptors. Conclusion: Our results indicate that elevated levels of zinc and GABAA receptors are indispensable for efficient insulin secretion by SHED β-cells. These findings suggest an opportunity for using SHED β-cells for treating diabetes.

Effect of zinc supplementation on chronic hepatorenal toxicity following oral exposure to glyphosate-based herbicide (Bushfire®) in rats.

ObjectivesTo assess the effects of zinc pretreatment on hepatorenal toxicity following chronic exposure to glyphosate-based herbicides in male rats.MethodsFollowing zinc pretreatment (50 mg/kg and 100 mg/kg), 14.4 to 750 mg/kg of oral glyphosate (Bushfire® herbicide) was administered daily for 36 weeks. Thereafter, serum samples were obtained following jugular venipuncture. Liver and kidney samples were processed for histopathological examination.ResultsSerum aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase activity as well as levels of bicarbonate, calcium, creatinine were significantly increased following chronic exposure to Bushfire®. Serum levels of sodium, potassium, chloride, total protein, albumin, globulin and urea were unchanged. Moderate to severe coagulative necrosis of hepatocytes as well as glomerular and renal tubular necrosis were observed in herbicide-treated rats. Zinc pretreatment reduced the elevation of serum enzymes associated with hepatobiliary lesions, abrogated hypercalcemia and metabolic alkalosis, and mitigated serum accumulation of creatinine following Bushfire® exposure, but was ineffective in completely preventing histological lesions.ConclusionChronic Bushfire® exposure in rats caused hepatorenal toxicity. The effects of exposure on serum parameters were ameliorated by zinc pretreatment, but the histopathological changes associated with toxicity persisted in milder forms in zinc-pretreated animals.

Pretreatment with zinc protects Kupffer cells following administration of microbial products

BackgroundSystemic inflammation and severe fibrosis can reduce serum zinc levels, while zinc supplementation is reported to improve the prognosis of patients with chronic liver disease (CLD). ObjectivesWe aimed to investigate the clinical application of serum zinc in patients with CLD and the anti-infective mechanism of zinc supplementation. MethodsBased on the serum zinc level, 149 CLD patients were divided into 3 groups and their clinical parameters were compared. In in-vitro experiments, microbial isolates derived from patients were used to stimulate human liver non-parenchymal cells, and the zinc sulfate solution was added in certain experiments. The effect of zinc was compared by LDH and thromboxane A2 levels in the cell supernatant. ResultCompared with other groups, patients with low serum zinc levels had significantly higher C-reactive protein (CRP), total bilirubin, INR, creatinine, and MELD scores, while albumin and GOT levels were reduced. Only CRP and albumin were significantly correlated with serum zinc in both low and normal-zinc groups. Bacterial isolates significantly increased LDH levels in Kupffer cells (KCs) and stellate cells but had no effect on sinusoidal endothelial cells, whereas zinc pretreatment protected KCs but not stellate cells. Thromboxane A2 secreted by KCs can also be induced by bacterial stimulation, accompanied by increased gene expression of Myd88, MAPK and NF-kB, while zinc pretreatment can attenuate that. ConclusionSerum zinc levels can be used to estimate infection and liver fibrosis in CLD patients. As a new antibacterial weapon, zinc supplementation acts on KCs through Myd88-MAPK related pathways.

Zinc-aggravated M1 microglia regulate astrocytic engulfment via P2×7 receptors

BackgroundGlial cells such as astrocytes and microglia play an important role in the central nervous system via communication between these glial cells. Activated microglia can exhibit either the inflammatory M1 phenotype or the anti-inflammatory M2 phenotype, which influences astrocytic neuroprotective functions, including engulfment of cell debris. Recently, extracellular zinc has been shown to promote the inflammatory M1 phenotype in microglia through intracellular zinc accumulation and reactive oxygen species (ROS) generation. PurposeHere, we investigated whether the zinc-enhanced inflammatory M1 phenotype of microglia affects the astrocytic engulfing activity. MethodsEngulfing activity was assessed in astrocytes treated with microglial-conditioned medium (MCM) from lipopolysaccharide (LPS)-activated or from ZnCl2-pretreated LPS-activated M1 microglia. The effect of zinc on microglia phenotype was also validated using the zinc chelator N,N,N’,N’-tetrakis(2-pyridylmethyl)ethylenediamine (TPEN) and the ROS scavenger Trolox. ResultsAlthough treatment of astrocytes with LPS showed no significant effect on the engulfing activity, MCM from LPS-induced M1 microglia increased the beads uptake by astrocytes. This increased uptake activity was suppressed when MCM from LPS-induced M1 microglia pretreated with ZnCl2 was applied to astrocytes, which was further abolished by the intracellular zinc chelator TPEN and the ROS scavenger Trolox. In addition, expression of P2×7 receptors (P2×7R) was increased in astrocytes treated with MCM derived from M1 microglia but not in the M1 microglia pretreated with ZnCl2. ConclusionThese findings suggest that zinc pre-treatment abolishes the ability of LPS-induced M1 microglia to increase the engulfing activity in astrocytes via alteration of astrocytic P2×7R.

Zinc-induced protective effect for testicular ischemia-reperfusion injury by promoting antioxidation via microRNA-101-3p/Nrf2 pathway.

The present study was performed to determine the protective effect of Zinc on the rat testicular ischemia-reperfusion (I/R) injury and its mechanism. In vivo, the pathological changes and the apoptosis index were significantly relieved in the rats with Low-dose Zinc pretreatment, compared to the I/R group. After Low-dose Zinc treatment, the levels of tissue Malondialdehyde (MDA) were significantly decreased, while tissue antioxidant indices were significantly increased. Meanwhile, the level of NF-κB was significantly lower compared to I/R group, while the levels of Nrf2-dependent antioxidant enzymes were significantly higher in Low-dose Zinc+I/R group. In vitro, Low-dose Zinc markedly increased Leydig cell (TM3) cell viability, and relieved testicular oxidative damage via down-regulating ROS. A total of 22 differently expressed microRNAs were screened out using microRNA microarray in rat testicular tissue caused by I/R injury, especially showing that miR-101-3p was selected as the target miRNA. Furthermore, the levels of Nrf2 and NF-κB were apparently increased/decreased in TM3 cells treated with Hypoxic/Reoxygenation (H/R) after miR-101-3p mimics/inhibitor. In addition, H/R-induced testicular oxidative damage was recovered in TM3 administrated with miR-101-3p inhibitor and si-Nrf2. Therefore, this study provided a novel insight for investigating protective effect of Zinc on testicular I/R injury by promoting antioxidation via miR-101-3p/Nrf2.

Effect of zinc on erythrocyte osmotic fragility and hemogram following chronic exposure to glyphosate-based herbicide in Wistar rats

The study was conducted to assess the effect of zinc on erythrocyte osmotic fragility and hemogram of rats following chronic oral exposure to glyphosate-based herbicide (BUSHFIRE®) at daily doses of 14.4–750 mg/kg of glyphosate. The erythrocyte osmotic fragility, estimated as percentage hemolysis in hypotonic saline, was significantly (p < 0.05) increased in glyphosate-exposed groups at 0.5–0.9% NaCl concentrations, and the fragility was ameliorated in the groups with zinc pretreatments only at 0.5% NaCl. The toxicity did not have any significant effect on the packed cell volume and other erythrocyte parameters. There was significant (p < 0.05) decrease in total white blood cell and lymphocyte counts in glyphosate-exposed groups, which was absent in zinc-pretreated groups. In conclusion, increased erythrocyte osmotic fragility induced by glyphosate could be prevented following zinc pretreatment, but the altered leukogram caused by the toxic action was not fully ameliorated in the pretreated group.

Suitable Pre-Treatment of Hot-Dip Zinc to Increase the Adhesion of Organic Coatings

The article describes the possibilities of pre-treatment of hot-dip galvanized parts and their influence on the adhesion of organic coating. The main objective of this work was to compare the current possibilities of pre-treatment of hot-dip galvanized parts, this means phosphating, chromating and mechanical pre-treatment by light blasting and compare these technologies with today's alternative pre-treatment technologies based on chemical substances containing fluorozirconates. The basic function of these pre-treatments is to increase the adhesion of the organic coatings and to increase the lifetime of the entire corrosion protection. Another objective is to reduce the environmental impact of these pre-treatments, reduce energy for the technological process of pre-treatment and many other aspects. Last but no least to compare the different types of organic coating systems with using these pre-treatments on the hot-dip galvanized surface.

Influence of extracellular zinc on M1 microglial activation

Extracellular zinc, which is released from hippocampal neurons in response to brain ischaemia, triggers morphological changes in microglia. Under ischaemic conditions, microglia exhibit two opposite activation states (M1 and M2 activation), which may be further regulated by the microenvironment. We examined the role of extracellular zinc on M1 activation of microglia. Pre-treatment of microglia with 30–60 μM ZnCl2 resulted in dose-dependent increases in interleukin-1 beta (IL-1β), interleukin-6 (IL-6), and tumour necrosis factor-alpha (TNFα) secretion when M1 activation was induced by lipopolysaccharide administration. In contrast, the cell-permeable zinc chelator TPEN, the radical scavenger Trolox, and the P2X7 receptor antagonist A438079 suppressed the effects of zinc pre-treatment on microglia. Furthermore, endogenous zinc release was induced by cerebral ischaemia–reperfusion, resulting in increased expression of IL-1β, IL-6, TNFα, and the microglial M1 surface marker CD16/32, without hippocampal neuronal cell loss, in addition to impairments in object recognition memory. However, these effects were suppressed by the zinc chelator CaEDTA. These findings suggest that extracellular zinc may prime microglia to enhance production of pro-inflammatory cytokines via P2X7 receptor activation followed by reactive oxygen species generation in response to stimuli that trigger M1 activation, and that these inflammatory processes may result in deficits in object recognition memory.

Ameliorative role of zinc on cypermethrin-induced changes in haematological parameters and oxidative stress biomarkers in rat erythrocytes

Cypermethrin is an active pesticide that has been used for more than three decades which controls a wide variety of pests in agriculture. The present study designed to evaluate the protective role of zinc in attenuating cypermethrin induced haematological toxicity and oxidative stress in erythrocytes of male rat. Wistar male rats received oral cypermethrin at two dose levels and zinc alone or zinc pre-treatment with cypermethrin for consecutive 14 days. The toxic effects of cypermethrin were observed on various haematological parameters. Administration of cypermethrin resulted in enhanced malondialdehyde level, depletion of reduced glutathione content and antioxidant enzymes of rat erythrocytes. However pre-treatment of zinc in combination with cypermethrin improved haematological status and restored the oxidative markers to their normal levels. Based upon these data, the present study reveals that zinc treatment attenuates cypermethrin exposed haematotoxicity.

Effects of zinc against mercury toxicity in female rats 12 and 48 hours after HgCl2 exposure.

This work investigated the toxicity of inorganic mercury and zinc preventive effects in female rats sacrificed 12 or 48 h after HgCl2 exposure. Female Wistar rats were subcutaneously injected with ZnCl2 (27 mg/kg) or saline (0.9 %), and 24 h later they were exposed to HgCl2 (5 mg/kg) or saline (0.9 %). Rats sacrificed 12 hours after Hg administration presented an increase in kidney weight and a decrease in renal ascorbic acid levels. Zinc pretreatment prevented the renal weight increase. Rats sacrificed 48 h after Hg exposure presented a decrease in body weight gain, an increase in renal weight, a decrease in renal δ-aminolevulinic acid dehydratase activity, an increase in serum creatinine and urea levels, and a decrease in kidney total thiol levels. Zinc pretreatment partly prevented the decrease in body weight gain and increase in creatinine levels, in addition to totally preventing renal δ-aminolevulinic acid dehydratase inhibition. Mercury accumulation in the kidney and liver in both periods was observed after Hg administration. These results show the different Hg effects along the time of intoxication, and a considerably preventive effect of zinc against Hg toxicity.

Zinc supplementation prolongs the latency of hyperthermia-induced febrile seizures in rats.

Some studies have shown a relationship between febrile seizures and zinc levels. The lowest dose zinc supplementation in pentylenetetrazole seizure model has a protective effect. But, zinc pretreatment has no effect in maximal electroshock model. However, it is unclear how zinc supplementation affects hyperthermia-induced febrile seizures. The aim of the present study was to investigate the effects of zinc supplementation on febrile seizures in male Sprague-Dawley rats. The rats were randomly assigned to four groups. Zinc supplementation was commenced 5 days prior to febrile seizure induction by placing the animals in a water bath at 45°C. We measured the rectal temperature and determined the febrile seizure latency, duration, and stage. In the zinc-supplemented group, both the seizure latency and the rectal temperature triggering seizure initiation were significantly higher than in the other groups. We suggest that zinc supplementation can positively modulate febrile seizure pathogenesis in rats.

Low dose zinc supplementation beneficially affects seizure development in experimental seizure models in rats.

The role of zinc in seizure models and with antiepileptic drugs sodium valproate (SV) and phenytoin (PHT) was studied using experimental models of seizures in rats. Male Wistar rats, 150-250g were administered zinc 2, 20, and 200mg/kg, orally for 14days. Sixty minutes after the last dose of zinc, rats were challenged with pentylenetetrazole (PTZ, 60mg/kg, ip) or maximal electroshock (MES, 70mA, 0.2s duration). In another group, SV (150/300mg/kg, ip) or PHT (40mg/kg, ip) was administered after 30min of zinc administration followed by seizure challenge. Zinc pretreatment at all doses had no effect on MES seizures. In PTZ seizures, with the lowest dose used, i.e., 2mg/kg, a protective effect was observed. Neither the protection offered by the 100% anticonvulsant dose of SV (300mg/kg) in PTZ seizures was affected by pre-treatment with zinc nor a combination of subanticonvulsant dose of SV (150mg/kg) and zinc offer any statistically significant advantage over either drug alone. The combination of phenytoin with zinc had no effect on any of the parameters tested. Apart from this, chronic zinc administration hampered development of chemically (PTZ)-kindled seizures in rats. Zinc supplementation is unlikely to have any undesirable effect when used in epileptics rather it may offer advantage in epileptic and seizure prone patients.

Protective effect of zinc on mouse renal ischemia-reperfusion injury by anti-apoptosis and antioxidation.

The paper discussed the protective effect of zinc pretreatment on renal ischemia-reperfusion injury (RIRI) and its mechanism. 50 male ICR mice were randomly divided into five groups: sham-operated group, model group, high-dose group with zinc sulfate pretreatment (60mg/kg body weight), medium-dose group with zinc sulfate pretreatment (30mg/kg body weight) and low-dose group with zinc sulfate pretreatment (15mg/kg body weight). The mice were administrated with zinc sulfate once a day for two weeks, subsequently the RIRI animal models were prepared by ligation of the left renal pedicle 30 minutes. 24h after reperfusion, the kidney tissue was removed and pathological results by HE staining showed that in the model group, kidney surface covered with a large number of red exudates, renal tubular dilatated, disorganized, renal tubular epithelial cell vacuolar degenerated, nuclear pyknosis and necrosis appeared; congestive and necrosis were visible in medullary junction. The pathological changes of renal ischemia- reperfusion were obviously relieved in the animals with medium and low-dose zinc pretreatment. The superoxide dismutase (SOD) activity in the lowdose zinc sulfate pretreatment group was significantly higher than that in the model and high-dose groups (P <0.05). The malondialdehyde (MDA) content of renal tissue, the apoptotic cells percentage in the medium and low dose groups were significantly lower than those in the model group (P <0.05), and MDA content in the low-dose group was significantly lower than that in the medium dose group (P <0.05). The ratio of BCL-2/BAX protein expression in the medium and low dose groups was significantly higher than that in the model group (P<0.05), the ratio in the low groups was significantly higher than that in the medium dose and high dose group by double immunofluorescence staining (P <0.05). In conclusion, zinc has a protective effect on the renal ischemia-reperfusion injury by antioxidant capacity and inhibition of apoptosis in the kidney.

Lactating and non-lactating rats differ in sensitivity to HgCl2: Protective effect of ZnCl2

This work investigated zinc (Zn) and mercury (Hg) effects on oxidative parameters, markers of toxicity and metal levels in different tissues from non-lactating rats (NLR) and lactating rats (LR). Adult NLR and LR received ZnCl2 (27mg/kg) or saline (0.9%) subcutaneously and after 24h they received HgCl2 (5mg/kg) or saline (0.9%). Twenty four hours later, they were sacrificed and the preparation of biological material and biochemical analyses were performed. With respect to oxidative parameters, Hg exposure decreased kidney total SH levels from NLR and LR and hepatic catalase activity (not statistically significant) in NLR. Zinc pre-treatment partly prevented the decrease of kidney total SH levels in LR. Zinc per se increased hepatic non-protein SH levels of NLR and LR. Regarding toxicity markers, Hg exposure inhibited the δ-aminolevulinic acid dehydratase (δ-ALA-D) activity from kidney and liver of NLR, inhibited serum alanine aminotransferase (ALT) activity of LR and increased serum creatinine and urea levels of NLR and LR. Zinc pre-exposure prevented the enzymatic alterations caused by Hg. NLR and LR Hg exposed presented accumulation of mercury in the kidney, liver, blood and urine. Zinc pre-treatment prevented this accumulation partly in NLR liver and blood and completely in LR kidney and liver. These results show that NLR and LR are differently sensitive to HgCl2 and that ZnCl2 showed a promising effect against Hg toxicity.