母体铅暴露对仔鼠海马中一氧化氮/环鸟苷酸的影响

目的：通过研究母体铅暴露对发育期仔鼠海马组织NO／cGMP水平变化，分析母体铅暴露对子鼠海马NO／CGMP途径的影响。方法：将母鼠从孕期第1天至仔鼠出生第20天分别饮用双蒸水、200、100、50mg/L醋酸铅溶液，检测20日龄和60日龄仔鼠物血铅、脑铅水平及海马组织nNOS神经原细胞、NO、NOS、cGMP浓度。结果：20日龄染毒组仔鼠的血铅、脑铅浓度与对照组相比有显著性增高，60日龄仔鼠的血铅与对照组相比，差异无显著性，但脑铅仍比对照组高；20日龄和60日龄染毒组仔鼠海马组织nNOS阳性神经元强度值、吸光度（A）、一氧化氮、NOS、cGMP浓度与对照组相比有显著降低，一氧化氮、NOS、cGMP三者相关性较好。结论：母体铅暴露可损伤仔鼠海马组织NO／cGMP途径，这种损伤在停止铅接触一段时间后仍持续存在。     

钙、锌对铅致大鼠记忆障碍的保护机制探讨

目的　主要探讨饲料钙、锌干预对脑发育期低水平铅暴露致大鼠仔鼠学习记忆障碍保护作用的可能机制。方法　大鼠孕 14d至仔鼠出生 40d饮 10 0mg L含铅水 ,进食加钙 (1 2 5 % )和加锌 (10 0mg kg)配方饲料组 ,观察仔鼠生长发育情况 ,仔鼠 40d取股动脉血分析全血铅含量 ;取右半侧大脑分析脑铅含量 ;取左侧海马和小脑分析NO含量 ,右侧海马分析蛋白激酶C(PKC)活性。结果　两干预组仔鼠脑铅平均值分别为 3 0 5和 0 62 μg g ,明显低于进食普通配方饲料组 ,而加钙组血铅平均值为 0 2 9μmol L,明显低于加锌和普通配方组 ;两干预组海马和小脑一氧化氮 (NO)平均值分别为 2 7 68和 13 82 μmol g组织蛋白 ,均高于普通配方组 ,而海马细胞胞浆蛋白激酶C活性平均值分别为 0 3 3和 0 3 8pmol (min .μg组织蛋白 ) ,均低于普通配方组。结论　饲料中钙、锌干预对低水平铅暴露致大鼠学习记忆障碍的保护作用可能与降低其体内血、脑中铅蓄积水平 ,升高海马和小脑NO含量以及降低海马细胞胞浆内PKC活性有关     

低水平铅暴露对仔鼠白细胞78kd糖调蛋白表达的影响

目的 通过建立低水平铅暴露模型,研究宫内和哺乳期低水平铅暴露对仔鼠白细胞葡萄糖调节蛋白78(glucose regulated protein 78,GRP78)蛋白表达量的影响,从内质网应激的角度探讨铅的发育免疫毒性.方法 将母鼠孕0天至仔鼠出生21天分成不同时期对仔鼠进行低水平铅暴露,用原子吸收分光光度法测定血铅含量,用Western印迹法检测白细胞内质网GRP78蛋白表达量.结果 3个染铅组血铅含量均明显高于对照组,哺乳组的白细胞中GRP78蛋白表达量明显高于对照组,有显著性差异.结论 哺乳期低水平铅暴露可使仔鼠白细胞内质网上的GRP78蛋白应激性表达增加而表现出发育免疫毒性,内质网上的GRP78是铅的重要蓄积库.     

补充胡麻籽油对子代小鼠学习记忆能力的影响

目的探讨富含α-亚麻酸(α-LNA)的胡麻籽油(亚麻油)对子代小鼠脑发育及功能的影响。方法取性成熟小鼠45只,雌雄为2∶1,将怀孕雌鼠随机分为4组,分别给予胡麻籽油2g(A组)、5g(B组)、10g(C组)/kg体重和对照组(0组),连续给孕鼠经口灌胃至仔鼠断乳,母鼠处死,将仔鼠雌雄分笼,雄鼠立即处死进行脑体重量测定并计算脑体比;再将雌鼠C组分为C组和D组,A、B、C组雌鼠继续按母鼠剂量补充胡麻籽油,每天1次,D组不补充胡麻油继续喂养;5周后进行小鼠避暗和水迷宫实验,测定后取脑进行蛋白质(TPRO)、乙酰胆碱脂酶(AChE)及一氧化氮(NO)指标测定。结果①子鼠体重随剂量的增加而下降,C组下降明显,与对照组比较差异有统计学意义(P<0.05),脑体比各组之间差异无统计学意义(P>0.05)。②水迷宫实验结果显示:B组、D组与对照组比较游泳时间缩短,错误次数减少(P<0.05);小鼠避暗实验结果显示各剂量组的潜伏期较对照组延长,而错误次数减少,但差异无统计学意义。③TPRO随剂量的增加而增高,D组较0组和A组明显增高,差异有统计学意义(P<0.05);AchE各组之间差异无统计学意义;NO含量A组较C组有明显增高(P<0.05),较B、D组差异有统计学意义(P<0.01)。结论在小鼠胚胎期及婴幼期补充胡麻籽油可提高脑内蛋白质含量,促进小鼠学习记忆能力,可引起脑内NO含量的变化。     

纳米铅和醋酸铅暴露对仔鼠海马和皮质中铁调素表达的影响

目的探讨纳米铅和醋酸铅暴露后对仔鼠海马和皮质中铁调素表达的影响。方法 SPF级SD大鼠60只,雌雄各半,将大鼠按雌∶雄=1∶1合笼饲养。发现阴栓为受孕第1天。将孕鼠随机分为3组,即对照组、纳米铅组和醋酸铅组,纳米铅组孕鼠经口给入10 mg/kg纳米硫化铅,醋酸铅组经口给入100 mg/kg的醋酸铅,对照组经口给入等量的生理盐水。仔鼠出生后21 d(post-natal day 21,PND21)断乳,继续给予相应的处理直到出生后42 d(PND42)。应用电感耦合等离子体质谱(ICP-MS)法检测仔鼠皮质及海马中铅和铁的含量。应用实时PCR和ELISA方法检测铁调素的mRNA和蛋白的含量。应用Perl's染色法观察仔鼠皮质及海马中铁分布情况。结果纳米铅和醋酸铅染毒后,PND1、PND21及PND42仔鼠皮质、海马中铅含量均高于对照组,差异有统计学意义(P0.05);且海马中铅含量均高于皮质。同样,纳米铅及醋酸铅暴露后,PND1、PND21和PND42仔鼠皮质及海马中铁含量均高于对照组,差异有统计学意义(P0.05);纳米铅组仔鼠海马中铁含量高于醋酸铅组(P0.05)。醋酸铅暴露PND1、PND21和PND42仔鼠皮质中铁调素含量分别为对照组的1.40、1.56和2.00倍,海马中铁调素含量分别为对照组的1.42、1.22和140倍;纳米铅暴露PND1、PND21、PND42仔鼠皮质中铁调素含量分别为对照组的1.57、2.05和2.34倍,海马中铁调素含量分别为对照组的1.54、1.45和1.60倍;纳米铅暴露组PND21及PND42仔鼠皮质及海马中铁调素含量均高于醋酸铅组。与对照组比较,纳米铅及醋酸铅暴露后仔鼠皮质及海马中铁调素mRNA表达均增高,且纳米铅暴露后仔鼠皮质及海马中铁调素mRNA表达高于醋酸铅组,差异有统计学意义。结论母鼠孕期纳米铅及醋酸铅暴露后可导致仔鼠铁调素表达增加,这可能是纳米铅及醋酸铅暴露致仔鼠皮质及海马氧化损伤的机制之一。     

孕期暴露壬基酚对母鼠雌、孕激素及生产和哺乳的影响

目的探讨母鼠(SD大鼠)孕期暴露壬基酚(NP)对孕中期及产后雌激素(E_2)、孕激素(P)以及血清NP水平和生产的影响。方法试验分为NP 50、100和200 mg/kg·d和玉米油对照4组。母鼠受孕第6~20 d灌胃染毒NP,分别在孕12 d,分娩后1 d处死母鼠,取血清,化学发光法检测E_2、P水平,液相色谱法检测NP含量,并观察母鼠生产及产后哺乳的相关指标。结果孕12 d,与对照组比较,低、中、高剂量组大鼠血清中NP、E_2、P及E_2/P差异有统计学意义(P0.01)。孕12 d,低、中和高剂量组大鼠血清中NP和E_2高于对照组、P低于对照组(P0.01)。分娩后1 d,与对照组比较,低、中、高剂量组母鼠血清中NP、E_2差异有统计学意义(分娩后1 d,低、中、高剂量组母鼠血清中NP、E_2均高于对照组,P0.01)。各染毒组母鼠未能正常生产和产后不哺乳数量均高于对照组,低剂量组和中剂量组仔鼠窝重均小于对照组(P0.05),与对照组比较,中剂量组和高剂量组的雌雄比例较大(P0.05)。结论孕期暴露NP,可降低孕鼠的体质量,血清NP的含量随暴露剂量增高而升高,干扰孕鼠体内E_2、P水平,导致孕鼠不能正常生产和产后不哺乳,增加F1代仔鼠雌雄比例。     

维生素E对高脂血症小鼠血管内皮细胞凋亡相关蛋白基因表达的影响

目的研究维生素E对高脂血症小鼠血管内皮细胞凋亡相关蛋白基因表达的影响。方法选择性成熟雄性ICR小鼠50只,随机分为A、B、C、D、E组,每组10只,A、B、C、D组高脂饲料喂养,其中B、C、D组同时灌胃不同浓度维生素E,E组普通饲料喂养,连续喂养4周后处死小鼠,取主动脉内皮细胞测定凋亡相关蛋白基因的表达及静脉血脂的浓度。结果 B、C、D组中动脉血管内皮细胞中Bax蛋白基因mRNA水平的表达量明显低于A组（P〈0.05）,但高于E组（P〈0.05）;B、C、D组中Bcl-2蛋白基因mRNA水平的表达量明显高于A组（P〈0.05）,但低于E组（P〈0.05）;Bax与Bcl-2基因mRNA水平的表达量之间为负相关;B、C、D组中静脉血清总胆固醇（TC）、甘油三酯（TG）明显低于A组（P〈0.05）,除D组TC外均高于E组（P〈0.05）。结论维生素E能抑制高脂血症所导致的血管内皮细胞凋亡相关基因的表达并升高抗凋亡基因的表达,同时降低血脂。     

氯沙坦对兔实验性动脉粥样硬化血管内皮的保护作用

目的　评估氯沙坦对高脂血症兔血管内皮的影响。方法　 5 0只日本♂长耳大白兔随机分为 5组 ,每组 10只。A组喂以含 1%胆固醇的兔饲料 ,B、C、D组在喂以含 1%胆固醇兔饲料的同时分别喂以 10mg·kg-1·d-1和 2 5mg·kg-1·d-1的氯沙坦以及 10mg·kg-1·d-1的开搏通 ,E组为正常对照组 ,喂以标准普通兔饲料 ,共 12wk。实验结束时 ,抽血对血脂水平进行测定。麻醉后处死动物 ,分离从主动脉根部至髂动脉分叉处的血管段 ,取主动脉弓处的组织行组织学检查 ;将胸主动脉切成 4mm长的血管环置浮槽中做离体实验 ,观察对乙酰胆碱、硝酸甘油、去甲肾上腺素的剂量反应曲线 ;剩余的血管制成组织匀浆 ,用放射免疫的方法对组织中的AngⅡ和ET 1进行测定。 结果　①A、B、C、D组的血脂和AngⅡ水平均明显高于E组 ,差异有显著性 (P <0 0 1) ;A、D组血管组织中ET 1水平明显高于B、C、E组 ,组间相比差异有显著性 (P <0 0 1) ;②A组的血管环对乙酰胆碱、硝酸甘油的舒张反应明显减弱 ,与E组相比差异有显著性 (P<0 0 1) ;B、C、D组与E组相比差异无显著性 (P >0 0 5 )。对去甲肾上腺素的缩血管效应在A、B组明显增强 (P <0 0 1) ,C、D组与E组相比差异无显著性 ;③各组的血管中膜面积相似 ;A、B、C、D组的血管横截面积明显增加 ,?     

妊娠中期可卡因对小鼠的发育毒性

目的:探讨可卡因对小鼠妊娠中期的发育毒性,尤其是对脑发育的影响.方法:建立妊娠中期给药的小鼠动物模型,体重相近的妊娠母鼠被分为三组:(1)可卡因注射自由饮食组(COC);(2)盐水注射伴有饮食对照组(SPF),饮食参考体重相近、妊娠时间相同的COC组母鼠;(3)盐水注射自由饮食组(SAL).从妊娠第8天(E8)至第12天(E12)给药,记录母鼠、胎鼠和仔鼠的各项生理指标,并用HPLC分析各组胎鼠纹状体中多巴胺、5-HT含量的变化.结果:尽管COC和 SPF组母鼠与 SAL组母鼠相比摄食量少,体重增加量少,但E17 天取材时,仅COC组胎鼠表现为脑和纹状体重量低;COC组仔鼠生后第 1天(P1)双顶径(BPD)也小于其它两组仔鼠.此外,COC组胎鼠表现出脑/体重比的降低,说明宫内暴露可卡因引起的胎鼠的发育迟缓是一个不平衡过程,脑组织的受累比其它组织严重.神经递质分析和组织学分析表明 COC组胎鼠脑内多巴胺和5-羟色胺的水平增高,肝脏呈现出形态学改变.结论:妊娠中期暴露可卡因可引起胎鼠宫内发育迟缓,尤其是脑发育迟缓.单纯母体营养不良在宫内暴露可卡因引起的后代发育迟缓过程中不能起决定性作用,而可能是药物直接作用的结果.     

预防使用氟康唑对头孢哌酮引起的大鼠肠道真菌增殖和易位的影响

目的：探讨预防性使用氟康唑不同的时间对肠道真菌增殖及易位的影响。方法 Wistar大鼠30只、雌雄不限，随机分为三组，每组大鼠每天均按体质量比例使用头孢哌酮舒巴坦钠直至取实验动物标本，每组动物均在第7天始分别加用生理盐水或氟康唑行腹腔注射，生理盐水使用3d（A组），氟康唑使用3d（B组），氟康唑使用5d （C组）后各组取血液、肠系膜、胰腺、肺组织及肠内容物行真菌培养，同时检测血浆1‐3‐β‐D葡聚糖水平。结果与A组比较，B组和C组肠道真菌数量明显减少（P＜0．05）、血浆1‐3‐β‐D葡聚糖水平相应明显下降（P＜0．05）；与B组比较，C组肠道真菌数量显著减少（P＜0．05）、血浆1‐3‐β‐D葡聚糖水平也明显下降（P＜0．05），与A组、B组比较， C组真菌易位至肠外组织器官总数均明显减少（P＜0．05）。肠道真菌增殖分别与血浆1‐3‐β‐D葡聚糖水平和真菌易位至肠外组织器官总数呈正相关（ r＝0．943和0．923），真菌易位至肠外组织器官总数与血浆1‐3‐β‐D葡聚糖水平呈正相关（ r＝0．998）。结论预防性使用氟康唑可以明显减少肠道真菌增殖及易位，预防用药5天比较合适，血浆1‐3‐β‐D葡聚糖检测有助于深部真菌感染早期诊断。     

硫酸锌对小鼠半数致死量测定的可行性分析

目的探讨硫酸锌对小鼠半数致死量(LD50)测定的可行性。方法将60只小鼠随机分成6组,每组10只,分别按0.2437g/kg、0.3482g/kg、0.4973g/kg、0.7106g/kg、1.0150g/kg、1.4500g/kg质量浓度受试值以体质量(0.2m l/kg)给小鼠灌服不同浓度的硫酸锌溶液。观察小鼠的中毒症状及死亡情况。采用B liss法计算硫酸锌的LD50值及其95%的可信范围。结果给药后不同时间内小鼠出现活动受抑制,自由活动减少;濒死时出现呼吸困难、紫绀等症状;剖开腹腔可见胃肠道呈松弛膨胀,肝、肺充血等状态。硫酸锌的LD50为583.2mg/kg,LD50的95%平均可信限为(583.2±0.1528)mg/kg。结论明确了硫酸锌对小鼠LD50适宜剂量范围,为后续的实验研究工作提供了参考依据。     

硫酸锌对高脂喂养载脂蛋白E基因敲除小鼠主动脉基质金属蛋白酶-9和CD40表达的影响

目的探讨硫酸锌对高脂喂养载脂蛋白E（ApoE）基因敲除小鼠血脂和氧化低密度脂蛋白（oxLDL）水平,及主动脉中基质金属蛋白酶9（MMP-9）和细胞分化抗原40（CD40）mRNA表达的影响。方法 AopE基因敲除小鼠连续14周喂饲高脂饲料,同时分别给予小鼠浓度为2.5、25 mmol/L硫酸锌水溶液作为低剂量组和高剂量组。测定小鼠血脂和oxLDL水平,并测定主动脉中MMP-9和CD40 mRNA表达水平。结果低剂量组和高剂量组小鼠血清中甘油三酯和oxLDL水平明显低于动脉粥样硬化（AS）模型组（P〈0.01）。低剂量组和高剂量组小鼠主动脉MMP-9 mRNA和CD40 mRNA水平与AS模型组没有差异。结论补充硫酸锌降低了AS模型动物的甘油三酯和oxLDL水平,具有潜在的抗AS作用,但对主动脉MMP-9和CD40 mRNA表达无影响。     

Antidotes for zinc intoxication in mice

Sixteen chelating agents were examined to determine their relative efficacy as antidotes in acute zinc acetate intoxication in mice after i.p. administration. For a i. p. dose of 0.49 mmol/kg (LD₅₀) of zinc acetate, the i. p. administration of chelating agents at a 21 and 51 mole ratio resulted in a significant antidotal action for EDTA, DTPA, CDTA, d-penicillamine (d-PA), DMPS and DMSA. EGTA, l-cysteine, triethylentetraamine (TTHA), N-acetylcysteine (NAC), 4,5-dihydroxi-1,3-benzenedisulfonic acid (Tiron), sodium salicylate, glutathione, sodium diethyldithiocarbamate (DDC), 6-mercaptopurine and N-acetyl-d, l-penicillamine (NAPA) were not effective for acute zinc acetate poisoning. The therapeutic indices and therapeutic effectiveness of the most effective chelators were, respectively: EDTA (5.0, 7.0), DTPA (7.3, 13.7), CDTA (8.6, 6.3), d-PA (4.6, 1.9), DMPS (1.3, 1.0), DMSA (3.2, 5.4). DTPA, CDTA, and EDTA appear to be the most effective agents of those tested in offsetting acute zinc intoxication in mice.     

Dietary zinc deficiency predisposes mice to the development of preneoplastic lesions in chemically-induced hepatocarcinogenesis

Although there is a concomitance of zinc deficiency and high incidence/mortality for hepatocellular carcinoma in certain human populations, there are no experimental studies investigating the modifying effects of zinc on hepatocarcinogenesis. Thus, we evaluated whether dietary zinc deficiency or supplementation alter the development of hepatocellular preneoplastic lesions (PNL). Therefore, neonatal male Balb/C mice were submitted to a diethylnitrosamine/2-acetylaminefluorene-induced hepatocarcinogenesis model. Moreover, mice were fed adequate (35 mg/kg diet), deficient (3 mg/kg) or supplemented (180 mg/kg) zinc diets. Mice were euthanized at 12 (early time-point) or 24 weeks (late time-point) after introducing the diets. At the early time-point, zinc deficiency decreased Nrf2 protein expression and GSH levels while increased p65 and p53 protein expression and the number of PNL/area. At the late time-point, zinc deficiency also decreased GSH levels while increased liver genotoxicity, cell proliferation into PNL and PNL size. In contrast, zinc supplementation increased antioxidant defense at both time-points but not altered PNL development. Our findings are the first to suggest that zinc deficiency predisposes mice to the PNL development in chemically-induced hepatocarcinogenesis. The decrease of Nrf2/GSH pathway and increase of liver genotoxicity, as well as the increase of p65/cell proliferation, are potential mechanisms to this zinc deficiency-mediated effect.     

Antibacterial effect of intraprostatic zinc injection in a rat model of chronic bacterial prostatitis

High levels of prostatic zinc are associated with prostatic antimicrobial activities and are depressed in patients with chronic prostatitis. We investigated the inhibition of bacterial growth in the rat prostate with chronic prostatitis after intraprostatic injection of zinc and compared two different types of zinc delivery. Ninety male Wistar rats were used in the study. Experimental chronic bacterial prostatitis was induced by instillation of bacterial suspension (Escherichia coli 10⁸ per ml) into the prostatic urethra. Animals were followed for 4 weeks and then injected intraprostatically with either 0.2 ml of zinc liposome (ZL) or zinc solution (ZS) (0.04 M zinc sulphate) or 0.2 ml of phosphate-buffered saline (PBS) for the controls. Ten rats in each group were sacrificed 4, 6 and 8 weeks after injection. The inhibition of inflammation and its consequences were analyzed microbiologically and histologically. Prostatic zinc concentrations were measured by inductively coupled plasma atomic emission spectrometry. Microbiological culture of the prostates demonstrated bacterial growth inhibition by the intraprostatic injection of zinc. The average infection rates and mean log₁₀ cfu/g of the zinc-treated groups were significantly lower than those of the controls. The histopathology showed resolving prostatitis in zinc-treated groups compared with the controls. Prostatic zinc levels were higher in the zinc-treated groups than in the controls 4 and 6 weeks after zinc injection (P<0.05). However, the ZL and ZS groups were found to be effectively identical in terms of prostatic zinc levels, bacterial cfu, and histological findings throughout the experiment period. The intraprostatic injection of zinc inhibited bacterial growth by increasing zinc levels in the rat prostatitis model. Our results suggest that the local application of zinc to the prostate may be a new treatment for chronic bacterial prostatitis at the point of its pathogenesis.     

The anti-diabetic effects of ethanol extract from two variants of Artemisia princeps Pampanini in C57BL/KsJ-db/db mice.

The anti-diabetic effects of two variants of Artemisia princeps Pampanini, sajabalssuk (SB) and sajuarissuk (SS), were investigated in type 2 diabetic animal using their ethanol extracts. Male C57BL/KsJ-db/db (db/db) mice were divided into control, SB ethanol extract (SBE), SS ethanol extract (SSE), or rosiglitazone (RG) groups and their age-matched littermates (db/+) were used. Supplementation of the SBE (0.171 g/100g diet), SSE (0.154 g/100g diet), and RG (0.005 g/100g diet) improved glucose and insulin tolerance and significantly lowered blood glycosylated hemoglobin levels, as compared to the control group. Plasma insulin, C-peptide and glucagon levels in db/db mice were higher in the db/+ mice, however these values were significantly lowered by SBE, SSE or RG-supplement. Hepatic GK activity was significantly lower in the db/db mice than in the db/+ mice, while hepatic G6Pase activity was vice versa. Supplementation of SBE, SSE and RG reversed these hepatic glucose-regulating enzyme activities. In addition, SBE and SSE markedly increased the hepatic glycogen content and muscle ratio as compared to the control group, but they did not alter the food intake, body weight and plasma leptin level. The RG group, however, showed a significant increase in the food intake, body weight and plasma leptin. These results suggest that SBE and SSE exert an anti-diabetic effect in type 2 diabetic mice.     

Aluminum exposure through the diet: metal levels in AbetaPP transgenic mice, a model for Alzheimer's disease

Aluminum (Al), iron (Fe), copper (Cu), and zinc (Zn) cause have been implicated in the etiology of certain neurodegenerative disorders. Moreover, these elements cause the conformational changes of Alzheimer's amyloid beta protein. In this study, we determined the concentrations of Al, Cu, Zn, Fe, and Mn in various tissues of Tg 2576 (AbetaPP transgenic) Al-treated mice. Female Tg 2576 mice and wild-type littermates were exposed through the diet to 1mg Al/g for 6 months. At 11 months of age, metal concentrations were measured in various tissues. In brain, Al levels were higher in hippocampus than in cortex and cerebellum. In hippocampus, Cu concentrations decreased in non-treated Tg 2576 mice, while Zn levels were higher in Al-treated mice. Copper, Zn, Mn and Fe concentrations in liver, kidney and bone were not affected by Al exposure. The current results show that Al exposure of Tg 2576 and wild-type mice did not produce important metal changes related with the genotype, responding similarly both groups of animals. As Tg 2576 mice have been considered as a potential model for Alzheimer's disease (AD), the present results would not support the hypothetical role of Al in the etiology of AD.     

Acute toxicity of nano- and micro-scale zinc powder in healthy adult mice

The purpose of this study is to evaluate the acute toxicity of oral exposure to nanoscale zinc powder in mice. The healthy adult male and female mice were gastro-intestinally administered at a dose of 5 g/kg body weight with two size particles, nanoscale zinc (N-Zn) and microscale zinc (M-Zn) powder, while one group mice treated with sodium carboxy methyl cellulose was used as the control. The symptoms and mortality after zinc powder treatment were recorded. The effects of particles on the blood-element, the serum biochemical level and the blood coagulation were studied after 2 weeks of administration. The organs were collected for histopathological examination. The N-Zn treated mice showed more severe symptoms of lethargy, vomiting and diarrhea in the beginning days than the M-Zn mice. Deaths of two mice occurred in the N-Zn group after the first week of treatment. The mortalities were confirmed by intestinal obstruction of the nanoscale zinc aggregation. The biochemical liver function tests of serum showed significantly elevated ALT, AST, ALP, and LDH in the M-Zn mice and ALT, ALP, and LDH in the N-Zn mice compared with the controls (P<0.05), which indicated that the liver damage was probably induced by both micro- and nano-scale zinc powders. The clinical changes were observed in the two treated group mice as well. The levels of the above enzymes were generally higher in the M-Zn mice than in the N-Zn mice, which implied that M-Zn powder could induce more severe liver damage than N-Zn. The biochemical renal function tests of serum BUN and CR in the M-Zn mice markedly increased either compared with the N-Zn mice or with the controls (P<0.05), but no significant difference was found between the N-Zn and the control mice. However, severe renal lesions were found by the renal histopathological examination in the N-Zn exposed mice. Therefore, we concluded that severe renal damage could occur in the N-Zn treated mice, though no significant change of blood biochemical levels occurred. Blood-element test showed that in the N-Zn mice, PLT and RDW-CV significantly increased, and HGB and HCT significantly decreased compared to the controls, which indicated that N-Zn powder could cause severe anemia. Besides the pathological lesions in the liver, renal, and heart tissue, only slight stomach and intestinal inflammation was found in all the zinc treated mice, without significant pathological changes in other organs.