缺锌对大鼠复合型叶酸吸收的影响及其机理的探讨

方法：将２４只大鼠随机分成三组：缺锌组（ＺＤ）、锌正常对照组（ＺＮ）和对饲组（ＰＦ）。分别喂以缺锌（３．０８ｍｇ锌／ｋｇ饲料）、锌正常饲料（５６．２０ｍｇ锌／ｋｇ饲料），２４天后测定大鼠血清锌浓度、叶酸浓度、胰脏蛋白质含量及胰脏结合酶活性。结果：与对照组相比缺锌组上述指标均显著降低。大鼠血清叶酸水平、胰脏结合酶活性、血清锌水平成正相关；胰脏蛋白质含量和血清锌水平成正相关。结论：缺锌可降低结合酶的活性，还可能通过减少结合酶的量降低对叶酸的吸收     

不同钙、铁、锌水平对大鼠营养状况及生殖机能影响的研究

目的：研究喂养边缘缺乏水平和充裕水平钙、铁、锌含量的饲料对大鼠生长发育，营养状况及生殖机能的影响，并探讨三种营养素间的相互作用。方法：采用三因素两水平的正交设计，将四周龄Ｗｉｓｔａｒ雌性大鼠按体重随机分成８组，分别饲以不同钙、铁、锌含量的饲料，１６周后与正常雄鼠合笼交配。以发现阴栓日计为妊娠第０天，妊娠第２０天时处死孕鼠并剥离胎盘和胎鼠，测定各项指标。结果：饲料中不同钙、铁、锌水平对大鼠营养状况有显著影响。大鼠血清铁水平分别受饲料钙、铁水平独立作用的影响，血清锌水平分别受饲料铁、锌水平独立作用的影响，饲料中铁、锌水平及钙与铁的交互作用对大鼠血清碱性磷酸酶的活性有显著影响，红细胞游离原卟啉（ＦＥＰ）含量受饲料铁水平及钙与铁交互作用的影响，饲料中不同钙、铁、锌水平对大鼠血红蛋白含量无显著影响。饲料中不同钙、铁、锌水平对母鼠生殖机能未见显著影响。结论：边缘缺乏水平的钙、铁、锌对大鼠的生殖机能无显著影响，但对大鼠营养状况有直接影响，导致体内营养素储备降低，尤其是处于边缘缺乏水平的铁和锌更容易受到饲料中其它元素的影响而加剧营养缺乏。     

硒和锌对人食管癌细胞株Eca109生长增殖影响的血清生理学研究

目的观察不同剂量硒、锌灌胃大鼠血清对人食管癌细胞株Eca109生长增殖的影响。方法将SD大鼠随机分为7组(基础饲料组、低硒组、高硒组、低锌组、高锌组、低硒低锌组、高硒高锌组),每组8只。喂养30天后取大鼠血清培养人食管癌细胞株Eca109和人正常肝上皮细胞株HL7702。用AAS法分别测定各组大鼠血清硒、锌;采用MTT法、3H-TDR掺入实验研究不同浓度硒、锌灌胃大鼠血清对两株细胞生长增殖的影响。结果 (1)基础饲料组血清硒、锌水平最低,高锌组血清锌最高;高硒高锌灌胃组大鼠血清硒水平最高,低硒低锌灌胃组血清硒水平次之,均明显高于基础饲料组;而此两组大鼠血清锌与基础饲料喂饲组大鼠血清锌水平差异无统计学意义(P>0.05);(2)与小牛血清对照组相比,只有高硒高锌灌胃组大鼠血清从第72h起抑制癌细胞生长(P<0.05),其余各组均促进食管癌细胞的生长;且该组大鼠血清也抑制肝细胞生长(P<0.05);(3)高硒高锌灌胃组大鼠血清明显抑制食管癌细胞DNA合成(P<0.05),其余各组与对照组作用相近,但该组对肝细胞DNA合成的抑制作用也最强。结论硒、锌在吸收、代谢等方面可能存在相互抑制作用;血清硒、锌含量较低会促进人食管癌细胞的增殖,而增加硒、锌的摄入可提高血清硒、锌的含量且可能抑制癌细胞的增殖。     

缺锌并补锌对大鼠睾丸及血清睾酮的影响

目的　为了解锌缺乏及补锌对大鼠睾丸的重量及血清睾酮的影响。　方法　将出生后断乳一周的SD大鼠随机分为缺锌组、配喂组、对照组、补锌组和高锌组五组 ,缺锌组、对照组和高锌组分别用缺锌饲料 (锌含量 <1mg/kg)、常锌饲料 (锌含量为 5 0mg/kg)和高锌饲料 (锌含量为 15 0mg/kg)喂养 8周 ,补锌组用缺锌饲料喂养三周后改用高锌饲料喂养五周 ,配喂组用常锌饲料喂养 ,给料量按缺锌组前一天实际进食量添加。 8周后处死 ,用极谱法测定血清中锌含量 ,用原子吸收分光光度法测定睾丸中锌含量 ,采用双抗体放射免疫分析法测定血清中睾酮的含量。　结果　缺锌组大鼠睾丸及血清中锌含量降低 ,睾丸重量减轻。血清中睾酮含量下降 ,缺锌大鼠补锌后可恢复正常。　结论　说明锌缺乏直接影响睾丸及血清中锌的水平 ,从而影响大鼠睾丸的发育及睾酮的分泌与合成。     

面包内补充叶酸不影响年轻妇女的锌吸收

有研究显示，谷物中添加叶酸可减少神经管缺陷的发病率。但也有研究显示叶酸可干扰锌的吸收，这引起了对婴儿、怀孕妇女、老年人等高危人群体内锌状态的关注。探究了添加叶酸对含高和低浓度锌的精粉中锌吸收的影响。研究结果表明，锌的吸收在食用锌含量低的面包和低浓度锌的精粉中锌吸收的影响。研究结果表明，锌的吸收在食用锌含量低的面包时依据叶酸含量的不同没有明显的差异性，食用锌含量高的面包时亦如此。锌的吸收和叶酸的含量间无显著相关性。结论为无论精粉面包中锌含量是高或低，加入常量的叶酸并不影响锌的吸收。     

锌营养支持对缺锌大鼠局部创伤后生长激素水平的影响

目的在局部创伤状态下，观察锌营养支持对缺锌大鼠生长激素水平的影响。方法80只雄性SD大鼠分为4组，全部饲喂低锌(4μg／g)人工半合成饲料，制备缺锌模型。1周后处死1组大鼠作为伤前对照(组1，n=8)。其他3组(每组分别为24只)大鼠在背部固定部位造成约占总体表面积15％的深Ⅱ度局部烫伤。此后，组2继续饲喂低锌饲料，组3和组4分别改喂足锌(含锌10μg／g)和高锌(80μg／g)饲料，并与组2对比。分别于烫伤后的1，3和7d，每组各处死大鼠8只，测定血清、肝脏、肾脏中的锌含量及血清生长激素水平。结果组2大鼠创伤后血清锌和生长激素水平明显下降，3d后生长激素迅速回升，但血清锌始终未恢复正常。足锌组大鼠生长激素下降幅度显著低于缺锌组；高锌组大鼠血清锌和生长激素水平则分别上升为伤前的2．5倍和1．8倍。3组大鼠肝、肾组织中锌含量均明显升高。结论膳食锌营养支持能显著改善局部创伤大鼠的缺锌症状，提高生长激素水平，加速创伤愈合，不失为一种经济实用的临床辅助治疗手段。     

缺锌及补锌对大鼠甲状腺激素的影响

目的了解锌缺乏及补锌对大鼠甲状腺激素的影响。方法将出生后断乳1周的SD大鼠随机分为缺锌组、配喂组、对照组、补锌组和高锌组,缺锌组、对照组、高锌组分别用缺锌饲料(Zn含量<1mg/kg),常锌饲料(Zn含量为50mg/kg)和高锌饲料(Zn含量为150mg/kg)喂养8周,补锌组用缺锌饲料喂养3周后改用高锌饲料喂养5周,配喂组用常锌饲料喂养,给料量按缺锌组前一天实际进食量添加。8周后处死,用极谱法测定血清中锌的含量,用放射免疫法测定血清中FT3、FT4的含量。结果缺锌使大鼠血清中锌含量显著降低,血清中FT3含量下降,补锌后恢复正常,缺锌对FT4无影响。结论缺锌引起甲状腺激素FT3下降,而FT4不受影响。     

不同水平饲料锌与热暴露对大鼠某些脑区锌、铜、铁含量的影响

选用４８只ＳＤ雄性大鼠随机等分３组，即Ａ组、Ｂ组和Ｃ组。再从每组中分出８只用于高温暴露，另８只用于室温对照，在ＡＩＮ－９３Ｍ饲料配方基础上，以碳酸锌为锌源，配制成Ａ、Ｂ、Ｃ组锌饲料。每千克饲料锌含量测定值：Ａ组为９２．２ｍｇ，Ｂ组４５．６１ｍｇ，Ｃ组２１．７０ｍｇ。根据动物分组，饲以各组大鼠相应水平锌饲料１４天后，将用于高温暴露的大鼠置于高温室（Ｔｄｂ４０℃，Ｔｗｂ３０．８℃）连续暴露３小时。用原子吸收分光光度计火焰法测定大鼠海马、大脑皮层和小脑Ｚｎ、Ｃｕ、Ｆｅ含量。实验结果发现：①高温暴露可使海马铜含量显著增加：②高温暴露后，海马铜含量比小脑和大脑皮层铜含量高，而在室温对照大鼠，小脑铜含量却比大脑皮层和海马铜含量高。③摄入不同水平饲料锌主要影响小脑铜的含量，对铁的影响较小。④中、高水平膳食锌摄入可使热应激大鼠小脑铜含量降低     

边缘性锌缺乏对大鼠肥胖的影响

目的观察边缘性锌缺乏对大鼠肥胖的影响。方法 SPF级成年雄性SD大鼠32只,随机分为4组,低锌组喂饲含6 mg/kg锌的边缘性锌缺乏饲料,中锌组喂饲含10 mg/kg锌的边缘性锌缺乏饲料,低锌对饲组和对照组喂饲正常锌含量的AIN-93M饲料。喂养6周后,处死动物。测血锌、血脂、血清瘦素含量,肝脏总抗氧化能力(T-AOC)、超氧化物歧化酶(SOD)、丙二醛(MDA)水平。结果低锌组大鼠第5周起血锌含量明显低于低锌对饲组和对照组(P0.05),成功建立边缘性缺锌模型。第6周时,低锌组大鼠脂体比明显高于低锌对饲组和对照组(P0.05);低锌组和中锌组大鼠肝脏MDA含量明显高于对照组(P0.05);低锌组和中锌组大鼠肝脏TAOC、SOD水平明显低于对照组(P0.05)。结论边缘性锌缺乏可增加肥胖发生的风险,缺锌组大鼠体内氧化应激升高可能是边缘性锌缺乏增加肥胖风险的主要原因。     

锌对热应激大鼠垂体POMC mRNA表达的影响

目的：通过锌对热应激大鼠垂体阿黑皮素原（ＰＯＭＣ）ｍＲＮＡ表达的影响研究，探讨锌对热应激大鼠的保护机理。方法：２０只ＳＤ雄性大鼠随机等分４组，即高锌高温暴露组（Ａ组）、中锌高温暴露组（Ｂ组）、低锌高温暴露组（Ｃ组）和正常锌室温对照组（Ｄ组）。在ＡＩＮ－９３Ｍ饲料配方基础上，以碳酸锌为锌源，配制成高锌、中锌、低锌和正常锌饲料，每公斤饲料锌含量测定值分别为９２．２ｍｇ、４５．６１ｍｇ、２１．７０ｍｇ和４５．６１ｍｇ。４组大鼠在室温下饲以相应饲料１４天后，将Ａ、Ｂ、Ｃ组大鼠置于高温室（Ｔｄｂ４０℃，Ｔｗｂ３０．８℃）中连续暴露３小时。用Ｎｏｒｔｈｅｒｎｂｌｏｔ杂交分析法（探针为地高锌标记的ＰＯＭＣｃＲＮＡ），观察垂体ＰＯＭＣｍＲＮＡ表达水平。结果：（１）高温应激可使大鼠垂体ＰＯＭＣｍＲＮＡ表达水平增高；（２）高锌摄入可使热应激大鼠垂体ＰＯＭ－ＣｍＲＮＡ表达水平升高，而低锌摄入则相反。结论：锌对热应激大鼠垂体ＰＯＭＣ基因有调控作用，作用环节可能在转录水平上     

Folate derived from cecal bacterial fermentation does not increase liver folate stores in 28-d folate-depleted male Sprague-Dawley rats

This study assessed the ability of rats to absorb and store the folate synthesized by cecal bacteria. Male weanling Sprague-Dawley rats were folate depleted by feeding a low folacin AIN93G formulated basal diet for 28 d; they were then fed repletion diets containing folate (0.25-1.0 mg/kg diet), dietary fiber (DF; wheat bran, oat bran, ground corn, wheat germ) or undigested and fermented dietary material (UFDM; polydextrose, inulin) in the presence and absence of an antibiotic (succinylsulfathiazole). Fermentation was stimulated by DF and UFDM and reduced by the antibiotic. In the absence of succinylsulfathiazole, the increase in liver folate (during the repletion phase) was proportional only to the folate content of the diet and did not vary with added DF or UFDM. Adding succinylsulfathiazole lowered total folate excretion from 13.8 +/- 8.2 to 4.8 +/- 2.9 nmol/d (pooled diets, P < 0.00001) in agreement with its role in inhibiting bacterial folate synthesis. In addition, succinylsulfathiazole lowered liver folate in rats fed control and test diets approximately equally with a mean decrease from 11.6 +/- 2.5 to 7.5 +/- 2.5 nmol/g wet liver (pooled diets, P < 0.00001), suggesting that the antibiotic also affected rat folate absorption and/or metabolism. Increased bacterial fermentation and excretion as well as increased bacterial folate production in the presence of added DF and UFDM were demonstrated by increased volatile fatty acid content in cecal and fecal samples (P < 0.000001) and increased diaminopimelic acid, muramic acid and folate in feces (P < 0.00001). The magnitude of these changes depended on the type of DF and UFDM. These results show that bacterially synthesized folate is not substantially absorbed and stored in the liver of Sprague-Dawley male rats.     

Effect of dietary ascorbic acid, cholesterol and PCB on cholesterol and bile acid metabolism in a rat mutant unable to synthesize ascorbic acid

The effect of acute or chronic ascorbic acid deficiency on the activity of hepatic cholesterol 7 alpha-hydroxylase and fecal excretion of bile acids was investigated in ODS-od/od (OD) rats (a rat mutant unable to synthesize ascorbic acid) fed a purified basal diet or purified diets containing either cholesterol (2%) or polychlorinated biphenyl (PCB) (200 mg/kg). In OD rats, the dietary requirement of ascorbic acid to maintain normal growth and normal levels of cholesterol in serum and liver is about 300 mg of ascorbic acid/kg diet. In OD rats fed the basal diet, acute or chronic ascorbic acid deficiency did not affect the activity of hepatic cholesterol 7 alpha-hydroxylase and fecal excretion of bile acids. However, in OD rats fed diets containing either cholesterol or PCB, acute ascorbic acid deficiency caused a higher level of serum cholesterol, a lower activity of hepatic cholesterol 7 alpha-hydroxylase and a lower excretion of fecal bile acids than in OD rats fed a basal diet containing an adequate level of ascrobic acid. It is concluded that acute ascorbic acid deficiency causes a hypercholesterolemia due to the depression of bile acid synthesis in OD rats fed a purified diet with cholesterol or PCB.     

A model to produce pure zinc deficiency in rats and its use to demonstrate that dietary phytate increases the excretion of endogenous zinc

An early effect of zinc deficiency in rats is loss of appetite with consequent malnourishment. To obviate the need for pair-feeding, rats were fed liquid semipurified diets by gastric tube feeding. Rats tube fed a zinc-deficient diet at a daily rate of 90-110 g/kg thrived for 6-7 days and then rapidly became seriously ill. In contrast rats fed the deficient diet ad libitum stopped growing after 3 days but remained relatively healthy. Animals tube fed a zinc-replete diet or the deficient diet with subcutaneous injections of zinc grew normally and suffered no ill effects. Rats tube fed the deficient diet and supplemented parenterally with zinc excreted significantly more endogenous zinc into small intestinal luminal washings and into feces than unsupplemented rats. Sodium phytate, added to the tube feed in three groups of rats fed the deficient diet and supplemented daily with 0, 0.33 and 3.3 mg Zn/kg, significantly increased the zinc content of luminal washings in all three groups, increased fecal zinc excretion in two groups and lowered body zinc levels, estimated by femur zinc, in two groups. Tube feeding provides a means to study: 1) pure zinc deficiency without malnourishment of other nutrients; and 2) the excretion of endogenous zinc into the gastrointestinal tract.     

Rat bioassay of wheat bran folate and effects of intestinal bacteria

This study estimates the folate endogenous to a food material (wheat bran) and examines the role of intestinal bacteria in the rat bioassay for folate. After a 4-wk folate depletion period, rats were fed for an additional 4 wk basal diets with or without 0.5% phthalylsulfacetamide and with 100, 200 or 300 g of wheat bran; or 50, 100 or 150 g of xylan; or 0, 0.25, 0.50 or 0.75 mg of folic acid added per kg of basal diet. Xylan increased both liver and fecal folate, and this effect was nearly eliminated by phthalylsulfacetamide. Wheat bran contributed 1.6 micrograms of available folate per g of wheat bran without phthalylsulfacetamide in an apparently valid slope-ratio analysis. With the addition of phthalylsulfacetamide, liver folate increased in rats fed wheat bran diets and decreased in rats fed folic acid diets. The slope-ratio analysis for wheat bran folate with phthalylsulfacetamide became invalid due to a lack of intersection. Phthalylsulfacetamide had no effect on fecal folate excretion from rats fed the wheat bran diets. Further studies are needed on a variety of foods with and without phthalylsulfacetamide to evaluate the effect and importance of intestinal folate synthesis in the rat.     

The absorption of pteroylpolyglutamate and intestinal pteroylpolygammaglutamyl hydrolase activity in zinc-deficient rats

The effect of dietary zinc deficiency on pteroylpolygammaglutamyl hydrolase (folate hydrolase) activity and on pteroylpolyglutamate absorption was studied in rats. Three groups of male Sprague-Dawley rats (zinc-deficient, restricted-fed and ad libitum-fed controls) were fed a semipurified 25% egg white protein diet. The zinc-deficient group received 0.7 mg zinc/kg diet, whereas restricted-fed and ad libitum-fed control groups received 106 mg zinc/kg diet. After 6 wk of feeding, intestinal mucosal folate hydrolase activity was determined, and the absorption of pteryl-U[14C]glutamylhexaglutamic acid [(14C]PteGlu7) and [3H]pteroylglutamic acid [(3H]PteGlu) was measured after intragastric administration. The intestinal mucosal folate hydrolase activity of zinc-deficient rats was not significantly reduced compared with two control groups. No significant differences in the absorption of [14C]PteGlu7 and [3H]PteGlu were found among the three groups. These results indicate that intestinal folate hydrolase is not zinc dependent in rats and the intestinal absorption of pteroylpolyglutamate is not reduced in zinc-deficient rats.     

Relationship between riboflavin intake and excretion in female rats after weaning of the litter

Six groups of female rats which gave birth to offspring of 8 young (or adjusted to 8) were fed diets containing 2, 4, 6, 8, 12, or 16 mg of riboflavin per kg of dry matter. Seventeen days after birth, young were withdrawn from the mothers and these were placed in metabolic cages and excreta (urine and feces) were daily collected for 17 days. The activity coefficient of blood glutathione reductase was 1.45 in 17 days old young of group 2 whereas it was 1.12 in young of other groups. The coefficient was 1.09 in female rats at the end of the experiment. 5 and 6 days after excreta collection began urinary excretion of riboflavin reached a peak in females of groups 4 to 16. At the end of the experiment, females which were fed 8 mg of riboflavin/kg or more had an urinary excretion of the vitamin which reached a plateau at 50 micrograms/day. On the other hand fecal excretion of riboflavin markedly increased as the intake did. Data suggested that the intestinal absorption of riboflavin is limited but also that the requirement of riboflavin in lactating rats is 8 mg/kg of diet whereas it is 2 mg/kg for maintenance.     

Effect of dietary picolinic acid on the metabolism of exogenous and endogenous zinc in the rat

The excretion of 65Zn was compared by metabolic balance studies in adult male rats fed purified diets containing 0.8 mmol Zn/kg diet, with and without 40 mmol picolinic acid per kilogram diet, after single intragastric (i.g.) and intraperitoneal (i.p.) doses of the isotope. In a third experiment picolinic acid was introduced for 3 d into the diet of rats prelabeled with 65Zn. The urinary excretion of total zinc was increased by the ingestion of picolinic acid in all three experiments. The urinary and fecal outputs of 65Zn were both consistently greater in picolinic acid-fed rats than in the corresponding control animals. This was particularly marked after i.p. injection of the tracer, and the specific activities of urine and feces from the treated rats were both increased. When picolinic acid was introduced into the diet of prelabeled rats there was a delay of 24 h in the urinary response and 48 h in the fecal response. The residual 65Zn levels were reduced in several tissues from the picolinic acid-fed rats, especially after i.p. administration of the isotope. These observations indicate that dietary picolinic acid increases the turnover of endogenous zinc in addition to enhancing the absorption and excretion of ingested metal, and this has implications for its use in cases of zinc deficiency.     

Dietary cellulose, zinc and copper: effects on tissue levels of trace minerals in the rat.

This study was designed to examine the effect of graded levels of cellulose, zinc and copper on tissue mineral levels. Tissue mineral levels were assayed by atomic absorption spectrophotometry in samples collected from a study which involved 12 treatments in a 3 X 2 X 2 factorial arrangement. This study involved three levels of cellulose (0, 8, and 16% of the diet), two levels of Cu (deficient and adequate; 2 and 18 mg/kg of diet, respectively), and two levels of Zn (marginal and abundant; 10 and 120 mg/kg of diet, respectively). Six weanling, male Sprague-Dawley rats were assigned to each treatment and after 9 weeks they were killed. Reductions of tissue Cu content were observed in the serum, liver, tibia and testis of the rats fed the Cu-deficient diets. The Fe content of the tibia and testis was reduced, but that of liver was elevated in the rats fed Cu-deficient diets. Reductions in tibial Zn levels were observed in the rats fed marginal-Zn as compared to those fed the abundant-Zn diets; and in the rats fed Cu-adequate as compared to those fed Cu-deficient diets. Increases in cellulose resulted in increased liver and testicular Cu content only in rats fed the Cu-deficient diets. Additions of cellulose appeared to have no adverse effect on the distribution of Zn, Cu and Fe in tissues which are sensitive to dietary deficiencies. With the exception of rats fed the copper-deficient, marginal zinc diets, the rats fed the other diets demonstrated a small reduction in serum zinc values as cellulose was increased.     

甲鱼蛋粉调节大鼠血清胆固醇的基础研究

目的　研究甲鱼蛋粉对高胆固醇血症大鼠血清胆固醇的调节作用。方法　将 5 0只健康雄性SD大鼠按体重和血清胆固醇水平随机分成 5组 ,每组 10只 ,分别接受正常饲料、高脂饲料、高脂饲料加甲鱼蛋粉灌胃 (低、中、高剂量分别为 0 75、1 5 0、3 0 0 kgBW)处理 ,实验周期为 2 4周 ,实验期末 ,收集大鼠粪便 ,股动脉取血 ,酶法测定血清胆固醇 (TC)、高密度脂蛋白胆固醇 (HDL C)和低密度脂蛋白胆固醇 (LDL C)的含量 ,气相色谱法检测粪便胆固醇、粪甾醇、粪甾烯 ,循环酶法测定总胆汁酸的含量。结果　与高脂饲料组相比 ,中剂量和高剂量的甲鱼蛋粉均能显著降低 (P <0 0 5 )高胆固醇血症大鼠血清TC ,且剂量为 1 5 0g kgBW时能显著降低血清LDL水平 ;两剂量组均显著增加粪便胆固醇、粪甾醇和粪甾烯以及胆汁酸的排出。结论　甲鱼蛋粉是通过增加粪便固醇类以及胆汁酸的排出来达到降低模型大鼠血清胆固醇的作用