前列腺癌患者血清中铜、锌与铜/锌比值的变化及意义

目的探讨血清铜、锌含量与前列腺癌之间的关系，并将其与血清前列腺特异性抗原（PSA）比较，探讨其在前列腺癌诊断中价值比较。方法采用原子吸收分光光度法测定76例前列腺癌患者、125例前列腺增生患者和191例健康男性的血清铜、锌含量。结果前列腺癌组血清锌明显低于健康对照组，血清铜和铜/锌比值明显高于健康对照组（P〈0.05）。前列腺癌组血清铜及铜/锌比值与前列腺增生组比较未见显著性差异;前列腺癌组血清锌低于前列腺增生组（P〈0.05）。前列腺增生组血清锌与健康对照组比较未见显著性差异;前列腺增生组血清铜和铜/锌比值高于健康对照组（P〈0.05）。PSA在4.0-10.0ng/ml灰色区域的前列腺癌组，血清锌ROC-AUC（receiver operator characteristic curve-area under curve）为66%，高于PSA的ROC-AUC。结论血清铜、铜/锌比值升高及血清锌降低可能是前列腺癌发生的危险因素，血清锌在PSA（4.0～10.0）ng/ml灰色区域的前列腺癌诊断效率高于PSA，其可能为前列腺癌的诊断提供有价值的指标。     

葡萄糖酸锌泡腾片的制备及质量控制

目的介绍葡萄糖酸锌泡腾片的制备及质量控制方法。方法选用碳酸氢钠为碱源;枸橼酸为酸源;甘露醇为填充剂;羧甲基淀粉钠为崩解剂;阿斯帕坦为矫味剂;薄荷油为芳香剂;微粉硅胶为助流剂;硬脂酸镁为润滑剂。用酸、碱分开制法制备葡萄糖酸锌泡腾片,并对其性状、鉴别、装量差异、发泡量、崩解时限、含量测定、稳定性等进行了检测。采用络合滴定法测定其含量。结果制得的葡萄糖酸锌泡腾片口感好、表面光滑美观、色泽均匀、硬度适中、服用方便。葡萄糖酸锌的平均回收率为100.05%,RSD为0.19%(n=9)。本品在5min内可完全崩解。结论本品处方合理,制备工艺简单,可进行推广开发。     

Spreading depression and related events are significant sources of neuronal Zn2+ release and accumulation

Spreading depression (SD) involves coordinated depolarizations of neurons and glia that propagate through the brain tissue. Repetitive SD-like events are common following human ischemic strokes, and are believed to contribute to the enlargement of infarct volume. Accumulation of Zn²⁺ is also implicated in ischemic neuronal injury. Synaptic glutamate release contributes to SD propagation, and because Zn²⁺ is costored with glutamate in some synaptic vesicles, we examined whether Zn²⁺ is released by SD and may therefore provide a significant source of Zn²⁺ in the postischemic period. Spreading depression-like events were generated in acutely prepared murine hippocampal slices by deprivation of oxygen and glucose (OGD), and Zn²⁺ release was detected extracellularly by a Zn²⁺-selective indicator FluoZin-3. Deprivation of oxygen and glucose-SD produced large FluoZin-3 increases that propagated with the event, and signals were abolished in tissues from ZnT3 knockout animals lacking synaptic Zn²⁺. Synaptic Zn²⁺ release was also maintained with repetitive SDs generated by microinjections of KCl under normoxic conditions. Intracellular Zn²⁺ accumulation in CA1 neurons, assessed using microinjection of FluoZin-3, showed significant increases following SD that was attributed to synaptic Zn²⁺ release. These results suggest that Zn²⁺ is released during SDs and could provide a significant source of Zn²⁺ that contributes to neurodegeneration in the postischemic period.     

Intracellular Zn2+ signaling in the dentate gyrus is required for object recognition memory

The role of perforant pathway‐dentate granule cell synapses in cognitive behavior was examined focusing on synaptic Zn²⁺ signaling in the dentate gyrus. Object recognition memory was transiently impaired when extracellular Zn²⁺ levels were decreased by injection of clioquinol and N,N,N′,N′ ‐t etrakis‐(2‐pyridylmethyl) ethylendediamine. To pursue the effect of the loss and/or blockade of Zn²⁺ signaling in dentate granule cells, ZnAF‐2DA (100 pmol, 0.1 mM/1 µl), an intracellular Zn²⁺ chelator, was locally injected into the dentate molecular layer of rats. ZnAF‐2DA injection, which was estimated to chelate intracellular Zn²⁺ signaling only in the dentate gyrus, affected object recognition memory 1 h after training without affecting intracellular Ca²⁺ signaling in the dentate molecular layer. In vivo dentate gyrus long‐term potentiation (LTP) was affected under the local perfusion of the recording region (the dentate granule cell layer) with 0.1 mM ZnAF‐2DA, but not with 1 – 10 mM CaEDTA, an extracellular Zn²⁺ chelator, suggesting that the blockade of intracellular Zn²⁺ signaling in dentate granule cells affects dentate gyrus LTP. The present study demonstrates that intracellular Zn²⁺ signaling in the dentate gyrus is required for object recognition memory, probably via dentate gyrus LTP expression. © 2014 Wiley Periodicals, Inc.     

Zinc Incorporation Improves Biological Activity of Beta-tricalcium Silicate Resin–based Cement

Introduction

Matrix metalloproteinase (MMP) inhibition may improve endodontic treatment prognosis. The purpose of this study was to determine if zinc incorporation into experimental resin cements containing bioactive fillers may modulate MMP-mediated collagen degradation of dentin.

Methods

Human dentin samples untreated and demineralized using 10% phosphoric acid or 0.5 mol/L EDTA were infiltrated with the following experimental resins: (1) unfilled resin, (2) resin with Bioglass 45S5 particles (OSspray, London, UK), (3) resin with beta-tricalcium silicate particles (βTCS), (4) resin with zinc-doped Bioglass 45S5, and (5) resin with zinc-doped βTCS particles. The specimens were stored in artificial saliva (for 24 hours, 1 week, and 4 weeks) and submitted to radioimmunoassay to quantify C-terminal telopeptide. Scanning electron microscopy analysis was also undertaken on dentin samples after 4 weeks of storage.

Results

Collagen degradation was prominent both in phosphoric acid and EDTA-treated dentin. Resin infiltration strongly reduced MMP activity in demineralized dentin. Resin containing Bioglass 45S5 particles exerted higher and stable protection of collagen. The presence of zinc in βTCS particles increases MMP inhibition. Different mineral precipitation was attained in dentin infiltrated with the resin cements containing bioactive fillers.

Conclusions

MMP degradation of dentin collagen is strongly reduced after resin infiltration of dentin. Zinc incorporation in βTCS particles exerted an additional protection against MMP-mediated collagen degradation. However, it did not occur in resin containing Bioglass 45S5 particles, probably because of the formation of phosphate-zinc compounds.     

VC、VE和Zn协同脂肪提高大鼠耐寒力的研究

目的观察饲料中增加脂肪和VC、VE、Zn的含量对提高大鼠耐寒力的效果.方法实验I为间歇冷暴露,36只大鼠按照饲料脂肪生热比分为3组,为20%脂肪组(按照脂肪生热比)、35%脂肪组和45%脂肪组.每日在0±1℃冷室暴露8h,室温饲养16h,观察冷习服建立时间.实验Ⅱ中156只动物饲以高脂和VC、VE或Zn 4周后再冷暴露观察耐寒效果.设①7%脂肪普食对照组(作为-15℃2 h冷暴露对照),②20%脂肪组,③35%脂肪组,④45%脂肪组,⑤35%脂肪加vC组,⑥35%脂肪加VE组和⑦35%脂肪加Zn组.②③④每组皆有室温对照.室温高脂饲养4周后,于-15℃冷暴露2 h观察肛温下降幅度.②③④组部分处死测生化指标,其余复温后室温饲养1周,再于0±1℃冷暴露3周观察冷习服状况,检测脂代谢和酶学指标.结果实验I中,①、②组5周冷习服优于③组.实验Ⅱ中,冷暴露前先食高脂饲料4周可提高大鼠耐寒力并加速冷习服,在35%脂肪饲料中加vc、VE或Zn,效果优于单纯高脂饲料组.结论高脂饲料可提高大鼠耐寒力,加速冷习服,VC、VE、Zn可协同脂肪提高耐寒力;冷环境下短期食高脂不影响脂代谢,甘油三酯低于室温对照组;心肌线粒体细胞色素C氧化酶和肝脏脂蛋白脂酶活性明显提高.     

Studies on the mechanisms of arsenic-induced self tolerance developed in liver epithelial cells through continuous low-level arsenite exposure.

Arsenic (As) is a human carcinogen. Our prior work showed that chronic (>18 weeks) low level (500 nM) arsenite (As3+) exposure induced malignant transformation in a rat liver epithelial cell line (TRL 1215). In these cells, metallothionein (MT) is hyper-expressible, a trait often linked to metal tolerance. Thus, this study examined whether the adverse effects of arsenicals and other metals were altered in these chronic arsenite-exposed (CAsE) cells. CAsE cells, which had been continuously exposed to 500 nM arsenite for 18 to 20 weeks, and control cells, were exposed to As3+, arsenate (As5+), dimethylarsinic acid (DMA), monomethylarsonic acid (MMA), antimony (Sb3+), cadmium (Cd2+), cisplatin (cis-Pt), and nickel (Ni2+) for 24 h and cell viability was determined by metabolic integrity. The lethal concentration for 50% of exposed cells (LC50) for As3+ was 140 microM in CAsE cells as compared to 26 microM in control cells, a 5.4-fold increase in tolerance. CAsE cells were also very tolerant to the acute toxic effects of As5+ (LC50 > 4000 microM) compared to control (LC50 = 180 microM). The LC50 for DMA was 4.4-fold higher in CAsE cells than in control cells, but the LC50 for MMA was unchanged. There was a modest cross-tolerance to Sb3+, Cd2+, and cis-Pt in CAsE cells (LC50 1.5-2.0-fold higher) as compared to control. CAsE cells were very tolerant to Ni2+ (LC50 > 8-fold higher). Culturing CAsE cells in As(3+)-free medium for 5 weeks did not alter As3+ tolerance, implicating an irreversible phenotypic change. Cellular accumulation of As was 87% less in CAsE cells than control and the accumulated As was more readily eliminated. Although accumulating much less As, a greater portion was converted to DMA in CAsE cells. Altered glutathione (GSH) levels were not linked with As tolerance. A maximal induction of MT by Zn produced only a 2.5-fold increase in tolerance to As3+ in control cells. Cell lines derived from MT normal mice (MT+/+) were only slightly more resistant (1.6-fold) to As3+ than cells from MT null mice (MT-/-). These results show that CAsE cells acquire tolerance to As3+, As5+, and DMA. It appears that this self-tolerance is based primarily on reduced cellular disposition of the metalloid and is not accounted for by changes in GSH or MT.     

茶及茶加锌对小鼠耐缺氧及脂质过氧化作用的影响

目的：探讨茶及茶加锌对小鼠的耐缺氧和脂质过氧化的影响。方法：小鼠１００只随机分为８组，（１）灌胃自来水组，（２）灌茶水组，（３）灌锌水组，（４）灌茶加锌水组。（５￣８）且与（１￣４）同样处理，１５ｄ后测小鼠的游泳时间、耐缺氧时间及血清、肝脏的脂质过氧化指标。结果：锌和茶加锌组小鼠的游泳时间分别为（４１±３１）ｍｉｎ，（４６±３１）ｍｉｎ，明显高于灌胃自来水组（２６±２１）ｍｉｎ，Ｐ〈０．０１），茶     

THE EFFECTS OF LOW CONCENTRATIONS OF ZINC ON ETOPOSIDE INDUCED HL-60 CELLS APOPTOSIS

ffeStlln Mif Etudier leS effets du zinc d faible concntration (20 -- 4W/L, tw d lacoeatration Phwtque) sur I' ewbe des celluleS ffe60 induite per I' e~. bo Cytcrndtris au fias, extractthe et dlect-- de l' ADN, fortha mOWque por mimp d fiuons-ceme. Wlfots II eSt theontrd que le zinc d concentration faible peut infiuencer l' awrbe nd celIules.Si le zinc est ajoutd tris t6t, W une concentratthe de W/L, arrve d inhiler comPlebet en 4 heuresl'M des celluleS ffe60 induite per Who. Miis d c…     

葡萄糖酸锌抗石英溶血作用的剂量反应关系研究

采用体外溶血试验方法,观察了葡萄糖酸锌(ZnG)对溶血作用的影响。结果显示,ZnG与红细胞共孵后能抑制石英的溶血作用,且存在剂量反应关系,这说明ZnG具有保护细胞膜的作用。本研究为寻找最佳给锌剂量及其作用机制提供了科学依据。