小鼠不同锌营养状态对胸腺(九)肽的影响

目的观察小鼠不同锌营养状态对胸腺(九)肽的影响。方法在锌耗竭期,分低锌组(DC)(饲料含锌5.2mgkg)、对饲组(PZ)和正常锌组(饲料含锌25.6mgkg)。继后的锌补充期,分低锌组(DC)、低锌正常组(DZNZ)和对饲自由组(PZNZ)。动态观察血锌含量和胸腺(九)肽的含量。结果在血锌未发生明显变化时,胸腺(九)肽含量即随锌的耗竭而迅速下降,又伴随锌的补充而快速上升。结论胸腺(九)肽是锌营养状态变化的敏感指标。     

锌对老年小鼠自然杀伤细胞活性的影响

<正> 大量研究表明,微量元素锌是维护机体正常免疫功能及保持宿主防御机制完整性所必需的物质,特别是在调节淋巴细胞功能方面发挥重要作用。缺锌可引起机体广泛的免疫功能损害,这些损害可通过膳食等途径适量补锌获得完全纠正。但迄今为止,研究锌对老年机体免疫功能的影响,国内外报道甚少。因此,我们以老年小鼠为动物模型,饲以缺锌或补锌饲料,观察其对老年小鼠自然杀伤(NK)细胞活性的影响。现将结果报     

不同剂量锌缺乏对小鼠及其胚胎发育的影响

目的 :　用昆明种雌性小鼠建立成不同程度缺锌动物模型 ,研究不同程度锌缺乏和孕早期补锌对小鼠及其胚胎发育的影响 ,并探求其发育毒性作用的阈剂量。方法 :　实验分两阶段进行。实验一用 36只初断乳 1 4～ 1 8g小鼠 ,分为低锌 (ZD)、中锌 (ZM)、常锌 (ZN)三组 ,喂饲含锌分别为 3.0± 0 .5、1 5、30 mg/kg的饲料 ,经 50 d喂养平均体重达 30 g后交配。实验二选用 80只 ,2 5～ 30 g成熟小鼠 ,随机分为低锌组 [ZD,饲料含锌 (3.0± 0 .5) mg/kg];低锌补锌组 (ZS,于孕第 7d将低锌饲料换为含锌 30 mg/kg的常锌饲料 ) ;边缘缺锌组 (MD,饲料含锌 9mg/kg) ;常锌组(ZN,饲料含锌 30 mg/kg)。 2 5d锌耗竭性喂养后交配。所有孕鼠于妊第 1 8d活杀。结果 :　实验一 :低锌组小鼠锌水平显著低于常锌组 (P<0 .0 5) ,有典型缺锌症状 ,几乎全部出现生长抑制 ,58.33%的小鼠衰竭死亡 ,存活小鼠亦不能正常交配妊娠。 1 5mg/kg剂量组小鼠则生长发育良好 ,各项指标与常锌组间无异 (P>0 .0 5)。实验二 :ZD组小鼠血清碱性磷酸酶 (AKP)活性 ,股骨锌含量显著低于 ZN组 (P<0 .0 1 ) ;该组小鼠胚胎有明显发育不良 ,畸胎及死胎出现率显著高于 ZN组 (P<0 .0 1 )。ZS组小鼠在孕第 7d补锌后活胎仔大小已趋正常 (P>0 .0 5) ,畸胎出现率与 ZD?     

锌对D-半乳糖诱导的衰老小鼠学习和记忆行为的影响

目的: 研究缺锌和补锌对衰老小鼠的学习和记忆能力的影响及其机制。方法: 取雄性小鼠70只,随机分组,按剂量100 mg/kg bw给予D-半乳糖注射液,颈背部皮下注射,青龄对照组给予等剂量的生理盐水,连续30 d。衰老缺锌组和补锌组开始均给予缺锌饲料(含锌1.61 mg/kg),其他组给予正常饲料(含锌50 mg/kg)。补锌组在实验最后2w给予补锌饲料(100 mg/kg)。在实验的最后1 w进行有关行为学试验,期满后断颈处死小鼠后取样检测。结果: 与衰老模型组相比,衰老缺锌组血清锌水平下降,老年小鼠自主活动度降低,学习和记忆能力下降。彗星试验显示缺锌使得老龄小鼠脑细胞DNA损伤程度加重,彗星细胞尾长/总长比值显著增加。补锌后上述指标均有显著改善。结论: 缺锌可以降低DNA的损伤修复功能,进而影响小鼠的学习和记忆能力。而补锌则有助于改善这一现象。     

缺锌和补锌对烫伤大鼠血清和组织锌含量,含锌酶、激素、蛋白质的影响

目的 观察缺锌和补锌对烫伤大鼠体内锌、含锌酶、激素和蛋白质含量的影响。方法 雄性Sprague-Dawley大鼠112只，56只用含锌量正常（40μg/g）的饲料喂养，其余56只用含锌4μg/g的低锌饲料喂养，1周后各取8只大鼠，40μg/g锌喂养大鼠为正常对照组（NC组），4μg/g锌喂养的为缺锌对照组（DC组），处死后留取标本。其余大鼠15％深Ⅱ度烫伤，40μg/g锌喂养大鼠随机分为正常烫伤组（NB组，继续用含锌40μg/g饲料喂养）和烫伤补锌组（NH组，改用含锌80μg/g饲料喂养）；4μg/g锌喂养大鼠随机分成缺锌烫伤组（DB组，改用含锌10μg/g饲料喂养）和缺锌烫伤补锌组（DH组，改用含锌80μg/g的饲料喂养），各组24只大鼠。分别于烫伤后第1、3、7天，各组处死大鼠8只，留取标本检测血清、肝脏、骨骼和皮肤锌含量以及血清碱性磷酸酶（ALP）、生长激素（GH）和肝脏金属硫蛋白（MT）水平。结果 烫伤前缺锌大鼠血清、肝脏、骨骼和皮肤锌含量以及ALP、GH和肝脏MT水平均低于正常大鼠。烫伤后缺锌和正常大鼠的血清、骨骼锌含量及ALP下降，肝脏、烫伤皮肤锌、GH和肝MT呈上升趋势；补锌后血清、组织锌、ALP、GH、MT均明显上升，但缺锌大鼠的变化幅度小于正常大鼠。结论 机体缺锌不仅使血清、组织中锌含量下降，还影响含锌酶ALP、GH和肝脏MT的活性及功能。口饲补锌可以纠正缺锌状态，烫伤后应注意锌的补充。     

缺锌及不同补锌方式仔鼠海马超微结构的改变

【目的】研究孕期和哺乳期母鼠缺锌及不同补锌方式,对仔鼠海马神经元及血脑屏障超微结构的影响。【方法】怀孕1 d的孕鼠随机分为2组,每组3只:对照组,缺锌组,口服补锌组,注射补锌组。对照组自由食用正常饲料(含锌25 mg/kg);其它3组自由食用缺锌饲料(含锌5 mg/kg)。产后每窝各保留体重相近的3只。至21 d断乳仔鼠:对照组继续饲以正常饲料;缺锌组继续饲以缺锌饲料;口服补锌组改饲以正常饲料;注射补锌组继续饲以缺锌饲料并腹腔注射硫酸锌溶液。实验期至仔鼠35 d龄。海马CA3区组织切片及透射电镜观察超微结构的改变。【结果】缺锌组:电镜下神经元明显皱缩,核不规则形、异染色质散在分布。胞质中线粒体肿胀、嵴脱失,粗面内质网有扩张;毛细血管管腔充盈,内皮细胞线粒体肿胀,周围原浆型星形胶质细胞的胞体明显空泡样改变。口服补锌组神经元细胞及血脑屏障超微结构基本同对照组。注射补锌组海马神经元细胞及血脑屏障超微结构基本同缺锌组。【结论】生命早期缺锌可使大鼠海马神经元及血脑屏障发生病理改变,合适的补锌方式可逆地修复仔鼠海马超微结构的改变。     

高锌对小鼠睾丸生精细胞作用的观察

锌是人体必需的微量元素。人体300多种酶的是含锌酶，缺锌可引起多种疾病。为了解高锌对机体产生的影响，本实验利用不同剂量的高锌饲料饲养小鼠，观察高锌对雄性小鼠生殖功能的影响，为科学合理地补锌提供指导。     

补锌对缺锌大鼠烫伤后肠粘膜上皮细胞增殖的影响

目的 探讨补锌对缺锌大鼠烫伤后肠粘膜上皮细胞增殖的影响。方法 1个月龄大鼠饲予低锌饲料（含锌量：1.6μg/g）1周造成缺锌模型。20%深Ⅱ度烫伤后改饲3种不同含锌饲料（含锌量分别为：16,24.7,286.9644g/g)1周,同时设1组大鼠烫伤前后均饲予正常含锌饲料（含锌量：24.7μg/g）作为对照组,烫伤后第8天处死大鼠,留取标本,在动物处死前6h腹腔注射长春新碱（1mg/kg),诗数肠腺细胞增殖率（CCRP）与标记指数（LI）用以反映肠粘膜增殖情况。结果 各补锌组空肠CCPR,LI均高于缺锌组,回肠也存在类似的趋势,结论 改善锌营养状态有利于烧伤后肠粘膜损伤的修复。     

锌营养状态对烧伤创面修复的实验研究

目的研究烧伤动物缺锌状况,通过不同剂量、不同途径补锌观察对创面愈合的影响.方法 Wistar大鼠80只,以沸水烫伤8秒致15%深Ⅱ度烫伤,设正常对照组(C组),通过经口和创面补锌者3组,分别以正常含锌饲料(40 mg/kg,N组)、高锌饲料(80 mg/kg,H组)喂养,正常含锌饲料加创面涂银锌霜(含锌761 mg/kg,W组),于伤后1、3、7天活杀动物取血,检查血清锌含量和生长激素(GH)水平,取烫伤皮肤检测组织中的锌含量和羟脯氨酸(OHP)水平.另设2组大鼠,对比外用银锌霜或碘伏后创面愈合过程. 结果伤后第1天血锌、皮肤锌及OHP即明显降低,血GH略有升高,饲以高锌饲料可以尽快提高血锌、皮肤锌和血GH水平,经创面补锌可以提高皮肤锌、皮肤OHP含量,有助于加速创面修复.在创面愈合过程的对比中发现,应用银锌霜的深Ⅱ度创面(12.3±2.1)d即愈合,而对照组至21 d只有66.7%的创面愈合. 结论烧伤后血锌、皮肤锌及皮肤OHP水平都降低,经口饲和创面补锌可提高上述水平,口饲补锌侧重于提高血锌和GH水平,创面补锌有助于增加皮肤中锌和OHP含量,且能促进创面愈合.     

重组人胸腺素α原对衰老和缺锌时免疫功能的影响

观察重组人胸腺素α原对衰老和缺锌所致的免疫功能低下的调节作用,并初步了解胸腺素α原在神经内分泌免疫网络中的作用和地位。方法：以自然衰老至１５月龄昆明小鼠为模型,随机分为两组,实验组每只鼠日腹腔注射胸腺素α原３００ｎｇ,对照组注射等量生理盐水,连续３周。取血测定溶血素和甲状腺激素水平,取胸腺和脾脏称重计算相应指数。另选４８只８０～９０ｇＷｉｓｔａｒ大鼠,随机分为：正常对喂、缺锌、缺锌补锌、缺锌补锌补α原四组。缺锌组饲以缺锌饲料,三周后,补锌组换饲正常对喂组饲料,两周后,取血测定血浆锌和皮质醇含量,取胸腺和脾脏称重,并制备脾脏细胞,测定ＣＤ４＋和ＣＤ８＋的比率。结果：胸腺素α原可以明显提高衰老小鼠胸腺的重量和指数,也可提高脾脏的重量和指数。同时显著升高特异性抗体溶血素的水平。胸腺素α原可明显提高血浆甲状腺激素Ｔ３和Ｔ４的水平。缺锌大鼠,食欲减退,生长发育迟缓。胸腺明显萎缩,同时血浆皮质醇的水平明显升高。缺锌后补充锌,与缺锌对照比较,胸腺重量和指数明显增加,但仍明显低于正常对喂组;锌补充不能降低血皮质醇水平。腹腔注射胸腺素α原后,不仅明显升高胸腺重量和指数,降低脾脏细胞中ＣＤ８＋的比例,而且也可调节因缺锌而升高的?     

应激对缺锌大鼠免疫功能的影响

目的 观察应激和缺锌双重因素作用下机体免疫功能的变化，并初步了解机体在不同锌水平下的应激反应能力。方法 将Wistar大鼠胺体重随机分为缺锌组（ZD），缺锌应激组（SZD）；对喂组（PF），对喂应激组（SPF）；常锌组（CT），常锌应激组（SCT）。缺锌组以缺锌饲料9锌含量2.0mg/kg），对喂组和常锌组饲以正常饲料（锌含量38.5mg/kg）。喂养1周后，各应激组大鼠接爱光－电刺激，连续15d。然后，取血测定血清皮质醇，取胸腺和脾脏称重，并制备脾脏细胞以测定T细胞增列反应。结果 缺锌或应激时皮质醇含量均明显上升，以缺锌应激组最为明显。缺锌级大鼠食欲减退，生长发育迟缓，出现缺锌体征。应激和非应激条件下，缺锌均可以使胸`腺脾脏萎缩，脏体指数明显下降；各应激组珉春对应的非应激组比较，上述免疫器官的重量和指数均有不同程度的下降，其中，SZD组的胸腺重量和指数、脾脏指数，SPF组的胸腺指数均明显低于对应的非应激组。应激时T细胞增殖能力下降，以缺锌组最为明显。结论 应激和缺锌均可使机体的免疫功能下降；机体锌营养不良使得应激对其免疫功能的损害更为严重。     

锌对免疫器官的影响

通过建立大鼠缺锌（ＺＤ）、高锌（ＺＥ）模型，研究锌对免疫器官——骨髓、胸腺、脾脏的影响。结果表明：（１）ＺＤ、ＺＥ组体重、体重增长值、饲料效价均非常显著地低于配对（ＰＦ）组和自由喂养（ＡＬ）组，缺锌补锌（ＺＤ＋ＡＬ）组达正常水平。（２）ＺＤ组血清、毛发、股骨、肝脏锌均非常显著地低于ＰＦ、ＡＬ组，而ＺＥ组则相反，ＺＤ＋ＡＬ组达正常水平。（３）ＺＤ、ＺＥ组的胸腺重量、胸腺指数、胸腺肽量和胸腺活性均非常显著地低于ＰＦ、ＡＬ组，ＺＤ＋ＡＬ组达正常水平。（４）ＺＤ、ＺＥ组脾脏重量、脾脏指数均非常显著地低于ＰＦ、ＡＬ组，ＺＤ＋ＡＬ组达正常水平。（５）ＺＤ、ＺＥ组骨髓细胞３Ｈ一ＴｄＲ掺入率和外周血白细胞总数显著下降，其中尤以淋巴细胞减少为着。（６）骨髓细胞、脾脏淋巴细胞周期显示ＺＤ、ＺＥ组静止期细胞明显增高，而增殖期细胞下降，与ＰＦ、ＡＬ组间差别非常显著。以上结果提示，适量锌有促进免疫器官——骨髓、胸腺、脾脏发育和功能活动的作用。而缺锌和高锌则抑制免疫器官的发育和免疫细胞的功能。     

缺锌对0～2月龄大鼠免疫功能影响的研究

目的 观察缺锌对0～2月龄大鼠免疫器官及细胞因子分泌的影响,为进一步阐明缺锌影响免疫系统的机制及对婴幼儿期、青少年期合理补锌提供参考依据.方法 将9只Wistar孕鼠产仔后随机分为足锌(ZA)、对喂(PF)和缺锌(ZD)3组,每组3只母鼠.ZA组和PF组喂饲足锌饲料(30mg/kg),ZD组喂饲缺锌饲料(1.Omg/k...     

Immune functions are maintained in healthy men with low zinc intake

Although immunity is impaired during severe zinc deficiency, there is limited information about the effects of mild zinc depletion on immune response in humans. We evaluated the effects of a zinc-restricted diet (4.6 mg/d) on several indices of immunity in 8 healthy men. The subjects consumed zinc supplements with 9.1 mg/d during the 5-wk baseline (BL) and 5-wk repletion (RP) periods, and placebos during the 10-wk zinc-restriction (ZR) period. Leukocyte numbers and functions were studied at the end of each metabolic period. After ZR, there were reductions in the proliferation of peripheral blood mononuclear cells (PBMNC) stimulated with phytohemagglutinin (PHA, 1.2, 2.5, 5.0, 10.0 [corrected] and 20.0 mg/L; P < 0.01) and in the in vitro secretion of interleukin-2 receptor (IL-2R) (PHA, 2.5 mg/L; P = 0.058). These variables remained reduced (P < 0.05) even after 5 wk of zinc repletion. The amount of zinc consumed did not alter the numbers of circulating neutrophils, monocytes and lymphocytes, the in vitro PBMNC secretion of interferon-gamma and tumor necrosis factor-alpha or neutrophil superoxide production. The results suggest that changes in lymphocyte proliferation and IL-2R expression may be early markers of mild zinc deficiency.     

锌缺乏对生长期大鼠免疫细胞凋亡的影响

目的: 观察饲料锌缺乏对生长期大鼠免疫细胞凋亡的影响,并探讨其分子机制。方法: 通过喂食锌含量不同的饲料,构建生长期缺锌大鼠模型;TUNEL方法原位检测胸腺、脾脏组织淋巴细胞凋亡,半定量RT-PCR方法检测一对凋亡调控基因bcl-2/bax mRNA的表达。结果: 与锌充足组(ZA)和配饲组(PF)相比,缺锌组(ZD)大鼠胸腺、脾脏淋巴细胞凋亡增多,促凋亡基因bax mRNA表达增高,补锌后上述改变可得到恢复。结论: 饲料锌缺乏导致发育中和成熟的淋巴细胞凋亡增多,凋亡调控基因bcl-2/bax表达失衡是重要机制之一。     

Reevaluation of zinc deficiency on concanavalin-A-induced rat spleen lymphocyte proliferation

Zinc concentrations of serum, nonlymphoid and lymphoid tissues, and the responsiveness of concanavalin-A (Con-A)-stimulated spleen lymphocytes (SL) and cervical lymph node cells ( CLNC ) from ad libitum-fed zinc-deficient (ZD), pair-fed (PF) and ad libitum-fed zinc-adequate rats (AL) were determined. In vitro effects of serum from ZD, PF and AL rats on responsiveness of Con-A-stimulated SL and CLNC were determined. Weanling male Long-Evans rats were fed ad libitum zinc-deficient (less than 1.0 microgram Zn/g diet) and zinc-adequate (20 micrograms Zn/g diet) diets for 7-42 days. Effects of undernutrition on test parameters were determined on PF rats, which received a restricted zinc-adequate diet (restricted in amount to that consumed by ZD rats). Growth, food intake and zinc concentrations in serum, liver and pancreas were significantly depressed in ZD and PF rats. Zinc per gram of thymus tissue and per number of SL was elevated in ZD and PF rats. Spleen lymphocytes from ZD and PF rats displayed equivalent to significantly increased levels of proliferation following stimulation with Con-A. [3H]Thymidine incorporation by Con-A-stimulated SL and CLNC from ZD, PF and AL rats was not significantly different when cultured in medium containing serum from ZD, PF and AL rats. The present study shows that zinc deficiency causes major changes in total-body and organ growth but minor changes in zinc content and mitogen-induced proliferation of lymphocytes.     

Effect of zinc deficiency and food restriction in rats on erythrocyte membrane zinc, phospholipid and protein content

Zinc deficiency in rats increases the osmotic fragility of erythrocytes, suggesting a structural defect in the plasma membrane. The purpose of this study was to determine the effect of zinc deficiency on membrane components that might be responsible for the increased fragility. Immature male rats were fed for 3 wk a zinc-deficient (0.5 mg Zn/kg) or a control (100 mg Zn/kg) diet either ad libitum or pair-fed. Red blood cell membranes were analyzed for zinc after wet ashing in nitric-perchloric acid. The fatty acid composition of membrane phosphatidylcholine and phosphatidylethanolamine was determined by gas-liquid chromatography, and the protein composition was determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The membrane zinc concentration was decreased by zinc deficiency, but returned to control levels upon repletion with a zinc-adequate diet for 3 d. The increased osmotic fragility was also restored to the control level during the same repletion period, suggesting that zinc is an important determinant of membrane stability. The phospholipid fatty acid composition was altered by zinc deficiency, but these changes were not rapidly reversed by repletion. The membrane cholesterol:phospholipid ratio was also increased by zinc deficiency. Zinc status had no influence on the membrane protein profiles of the components visualized by staining. Only the concentration of membrane zinc correlated with osmotic fragility during zinc depletion and repletion.     

Zinc-deficient rats have fewer recent thymic emigrant (CD90+) T lymphocytes in spleen and blood

It has been hypothesized that increased expression of the signaling protein p56(lck) disrupts maturation of T lymphocytes, leading to the lymphopenia associated with dietary zinc deficiency and malnutrition. Our objective was to examine p56(lck) protein levels, flow cytometric markers of T cell development (CD4, CD8, TCRalphabeta, TCRgammadelta and CD90) and absolute cell numbers in thymus, spleen and blood of zinc-deficient (ZD), diet-restricted (DR) and control (CTL) rats. Recent thymic emigrant (CD90+) T lymphocytes were also investigated after dietary repletion. P56(lck) protein levels were one- to twofold greater in thymocytes than splenocytes, and ZD rats had more thymocyte p56(lck) protein than CTL rats. In the thymus and blood, the proportions of T lymphocyte subpopulations (CD4-CD8-, CD4+CD8+ and CD4+CD- or CD4-CD8+) were unchanged, except for a higher percentage of TCRalphabeta+CD-CD8+ thymocytes in ZD rats. The 15-29% fewer CD90+ T cells in the blood and spleen of ZD rats were reversed after dietary repletion for 7 and 23 d, respectively. In summary, T-cell numbers were proportional to thymus and spleen weights and unaltered per unit blood volume, despite elevated thymocyte p56(lck) protein in ZD rats. In zinc deficiency, the decreased percentages of CD90+ cells in the blood and spleen could adversely affect the T-cell repertoire.     

Resting energy expenditure in cancer patients.

In this review, we provide evidence based on our studies, for zinc deficiency and cell mediated immune disorders, and the effects of protein and zinc status on clinical morbidities in patients with head and neck cancer. We investigated subjects with newly diagnosed squamous cell carcinoma of the oral cavity, oropharynx, larynx, and hypopharynx. Patients with metastatic disease and with severe co-morbidity were excluded. Nutritional assessment included dietary history, body composition, and prognostic nutritional index (PNI) determination. Zinc status was determined by zinc assay in plasma, lymphocytes, and granulocytes. Pretreatment zinc status and nutritional status were correlated with clinical outcomes in 47 patients. Assessment of immune functions included production of TH1 and TH2 cytokines, T cell subpopulations and cutaneous delayed hypersensitivity reaction to common antigens.

At baseline approximately 50% of our subjects were zinc-deficient based on cellular zinc criteria and had decreased production of TH1 cytokines but not TH2 cytokines, decreased NK cell lytic activity and decreased proportion of CD4+ CD45RA+ cells in the peripheral blood. The tumor size and overall stage of the disease correlated with baseline zinc status but not with PNI, alcohol intake, or smoking. Zinc deficiency was associated with increased unplanned hospitalizations. The disease-free interval was highest for the group which had both zinc sufficient and nutrition sufficient status.

Zinc deficiency and cell mediated immune dysfunctions were frequently present in patients with head and neck cancer when seen initially. Zinc deficiency resulted in an imbalance of TH1 and TH2 functions. Zinc deficiency was associated with increased tumor size, overall stage of the cancer and increased unplanned hospitalizations. These observations have broad implications in the management of patients with head and neck cancer.