维生素A缺乏对大鼠铁代谢影响

目的 研究维生素A(VA)缺乏对大鼠铁营养状况和肝脏转铁蛋白受体(TfR)mRNA表达的影响.方法 雄性SD大鼠52只,按体重随机分为4组,每组13只,Fe和VA正常对照组(I组),Fe正常VA完全缺乏组(II组),Fe正常VA轻度缺乏组(III组),Fe和VA轻度缺乏组(IV 组).喂饲8周后处死,测定血清VA、血红蛋白、血清铁、血清转铁蛋白受体、血清铁蛋白、肝脏铁含量,脾脏铁含量,并用逆转录聚合酶链反应(RT-PCR)法检测各组大鼠肝脏转铁蛋白受体(TfR)mRNA的表达.结果 结果与对照组比较,VA缺乏使血清铁、血清铁蛋白含量显著降低(P<0.05).血清转铁蛋白受体水平、脾脏铁含量显著升高(P<0.05).VA缺乏时肝脏TfRmRNA表达显著增强.结论 维生素A缺乏可能通过影响铁吸收、储存、转运变改体内铁的营养状况,VA缺乏时,肝脏可能通过铁调节蛋白(IRE-IRP)途径使TfR mRNA的表达水平增加.     

维生素A缺乏对大鼠铁营养状况的影响

目的 研究维生素A(VA)缺乏对大鼠铁营养状况的影响及其可能的机制。方法 雄性Wistar大鼠40只．按体重随机分为IVA和铁缺乏组，ⅡVA完全缺乏组，ⅢVA轻度缺乏组，Ⅳ VA正常对照组。实验动物喂饲8周后处死，测定血清VA、血清铁、铁蛋白、血红蛋白、肝内总铁含量，并用逆转录一聚合酶链反应(RT-PCR)法检测各组大鼠肝脏转铁蛋白mRNA的表达情况。结果 维生素A缺乏显地降低血清铁蛋白、血红蛋白和肝内总铁含量。抑制肝脏转铁蛋白mRNA的表达。结论 维生素A缺乏可能通过降低肝脏转铁蛋白mRNA的表达水平从而抑制了铁的吸收和转运。     

维生素A缺乏对大鼠十二指肠DMT1,FPN1 mRNA表达的影响

目的研究维生素A(VA)缺乏对大鼠十二指肠二价金属离子转运蛋白(DMT1),膜铁转运蛋白(FPN1)mRNA表达的影响,为进一步研究维生素A缺乏影响铁代谢的相关机制提供基础。方法雄性SD大鼠52只,按体重随机分为4组,每组13只,Ⅰ组VA正常对照组,Ⅱ组VA完全缺乏组,Ⅲ组VA轻度缺乏组,IV组VA和铁轻度缺乏组。实验动物喂饲8w后处死,测定血清VA、血红蛋白、血清铁、血清铁蛋白,并用逆转录—聚合酶链反应(RT—PCR)法检测各组大鼠十二指肠二价金属离子转运蛋白(DMT1),膜铁转运蛋白(FPN1)mRNA表达的情况。结果 VA缺乏可使血清铁、血清铁蛋白含量显著降低。VA缺乏时十二指肠二价金属离子转运蛋白(DMT1)、膜铁转运蛋白(FPN1)mRNA的表达显著增强。结论 VA缺乏可能通过多种途径使大鼠十二指肠DMT1、FPN1 mRNA的表达增强,需要进一步研究证实。     

铜缺乏对大鼠铁代谢影响的研究

目的研究铜缺乏对大鼠铁营养状况和肝脏转铁蛋白受体mRNA及铁调素mRNA的影响。方法 48只雄性SD大鼠按体重随机分为4组,每组12只,正常对照组(Ⅰ组),铁正常铜完全缺乏组(Ⅱ组),铁正常铜轻度缺乏组(Ⅲ组),铁/铜轻度缺乏组(IV组)。喂饲8周后处死,取大鼠肝脏、脾脏和血清,测定血红蛋白,血清铜、血清铁、血清转铁蛋白受体、血清铁蛋白、肝脏铁和铜含量、脾脏铁和铜含量,并用逆转录-聚合酶链反应(RT-PCR)法检测各组大鼠肝脏转铁蛋白受体(TfR)和铁调素mRNA的表达水平。结果与正常对照组相比,铜缺乏使血清铁、血清铁蛋白含量显著降低(P0.05),血清转铁蛋白受体水平、肝脾脏铁含量显著升高(P0.05),铜缺乏时肝脏TfRmRNA表达增强,而肝脏铁调素mRNA表达下降。结论铜缺乏可能通过影响铁吸收、储存、转运来影响体内铁的营养状况。铜缺乏对大鼠铁调素mRNA的表达与IRE-IRP途径调节的转铁蛋白受体mRNA的表达均产生影响。     

维生素A缺乏对大鼠脂质过氧化和抗氧化系统的影响

目的 :　研究维生素 A(VA)缺乏对 3w龄大鼠的脂质过氧化和抗氧化系统的影响。方法 :　健康 Wistar雄性大鼠 33只 ,按体重随机分为 A(VA完全缺乏组 ) ,B(VA轻度缺乏组 ) ,C(VA正常对照组 )三组。每组 1 1只 ,实验期为 84d。观察指标有 :血清 VA,血清、肝脏及脑组织的超氧物岐化酶 (SOD)活性 ,全血、肝脏及脑组织的谷胱甘肽过氧化物酶 (GSH- Px)活性 ,血清、肝脏及脑组织的丙二醛 (MDA)含量 ,并采用电子自旋共振 (electron spin resonance,ESR)和自旋捕捉技术直接测定大鼠肝组织中的氧自由基。结果 :　 A、B组大鼠血清、肝脏及脑组织 SOD活性明显下降 ,全血、肝脏及脑组织 GSH- Px活性明显降低 ,血清、肝脏及脑组织 MDA含量显著升高 ,ESR图谱出现了 N- H偶合的三组双峰波。结论 :　 VA完全或轻度缺乏均可以使大鼠脂质过氧化反应明显增强 ,而抗氧化能力明显减弱     

维生素A水平对孕期大鼠脂质过氧化及抗氧化系统的影响

目的研究维生素A(VA)水平对孕期大鼠脂质过氧化及抗氧化系统的影响.方法健康雌性受孕SD大鼠24只,按体重随机分为A(VA缺乏组),B(正常对照组),C(VA5倍剂量组),D(VA15倍剂量组)四组.每组6只,饲以实验合成饲料,实验期为合笼前两周至孕期第19天.观察指标有血清和肝脏中VA含量、丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性.结果D组大鼠血清和肝脏中SDD活性明显下降(P＜0.05),MDA含量显著升高(P＜0.05).结论大剂量的VA摄人可使孕期大鼠SOD活性下降,脂质过氧化反应明显增强.而VA轻度及5倍过量似对孕期大鼠脂质过氧化无影响.     

管饲对缺锌大鼠体内锌与维生素A相互作用的实验研究

饲料含锌二个水平(1.41、100ppm),含维生素A(VA)三个水平(0、7、46mg/kg),将SD雄性大鼠44头分为六组。管饲喂养18天后,于实验第19天处死,测定各组大鼠血清及组织锌与VA的含量、血清AKP活力、总蛋白和Hb含量。结果表明,管饲缺锌饲料后,大鼠血清和组织中锌含量以及AKP活力明显降低,缺锌缺VA和缺锌正常VA组大鼠的血清VA含量亦明显降低。缺锌大剂量VA组大鼠的血清锌虽然低于对照组,但明显高于VA缺乏和正常的缺锌大鼠,该组大鼠的血清VA含量耒见降低。上述结果提示,缺锌可影响大鼠肝脏VA的正常释放,使血中VA含量降低,但这一影响可能发生在血锌含量的某一“阈浓度”之下。实验还发现,不同剂量的VA对缺锌大鼠有不同的影响,VA缺乏,会加重缺锌损害,增加VA的摄入量,可明显减轻缺锌损害。     

维生素A缺乏对大鼠铁水平及Hepcidin、FP1与DMT1 mRNA表达的影响

目的研究维生素A(VA)缺乏时大鼠铁营养状况的变化,从分子水平探讨VA缺乏对大鼠铁代谢的影响。方法 16只成年健康雄性SD大鼠,随机分为对照组(Con)和VA缺乏组(-VA),每组8只,分别饲以正常饲料和VA缺乏饲料。连续喂养4周,脱椎处死,取血及肝、脾组织检测血红蛋白(Hb)含量、血清铁(SI)、血清铁蛋白(SF)及肝、脾组织铁含量。以β-actin为内参,半定量RT-PCR技术比较两组大鼠铁调素(Hepcidin)、膜铁转运蛋白1(FP1)和二价金属离子转运蛋白(DMT1)肝组织mRNA的表达水平。结果 VA缺乏组SI、SF和Hb显著低于对照组(P0.05),肝、脾铁含量显著高于对照组(P0.05);Hepcidin及DMT1mRNA在肝组织中表达水平显著增加(P0.05)。结论 VA缺乏致使Hepcidin表达水平的升高,导致肝、脾铁储量增加而机体循环铁量和铁营养水平下降。     

补充维生素A和铁对孕妇铁营养状况的影响

目的　研究补充维生素 A、铁对孕妇铁营养状况的影响。方法　对 1 6 7名孕中期妇女进行铁和维生素 A营养状况的横断面调查并随机分成 4组 :对照组 (复合维生素 B片每日一片 ) ;补充维生素 A组 (1 1 0 0 μg/d) ;补充铁组 (6 0 mg/d元素铁 ) ;补充维生素 A和铁组 (VA1 1 0 0μg/d,Fe6 0 mg/d) ,共补充 1 0 w。结果　被调查孕妇孕中期维生素 A轻度缺乏率为 0 .6 % ,贫血患病率为 7.8% ,贮存铁缺乏率为 6 .2 %。血清 VA水平补充前各组正常 ,补充后对照组明显下降 ,但仍维持在正常范围。补 VA、补铁及补 VA+铁组血清 VA与补充前无明显差异 ,仍保持恒定。各组补充前后 Hb均在正常范围 ,差别不显著。血清铁蛋白、游离红细胞原卟啉及运铁蛋白饱和度补充后的改善效果均以补充 VA铁组优于单独补 VA或补铁组。结论　孕期同时补充 VA和铁对改善铁的营养状况优于单纯补铁。     

维生素A缺乏对大鼠铁调节蛋白2影响

目的 探讨维生素A缺乏对大鼠铁调节蛋白2(IRP2)mRNA及铁蛋白(Fn) nRNA和转铁蛋白受体(TfR)mRNA表达影响.方法48只雄性SD大鼠按体重随机分为4组,每组12只,对照组、维生素A完全缺乏组;维生素A边缘缺乏组;铁及维生素A边缘缺乏组;喂养8周后,麻醉处死大鼠,取组织和血清,进行相关指标和基因表达检测.结果与对照组( 1.50 +0.41) μmol/L比较,维生素A完全缺乏大鼠血清维生素A(0.22±0.26) μmol/L水平明显降低(P＜0.05);与对照组比较,维生素A完全缺乏组大鼠血清铁(2.26 +0.72)lμg/mL明显降低;维生素A完全缺乏组大鼠肝脏IRP2、TfR表达水平分别为(1.53±0.18)、(0.62±0.06)与对照组相比明显升高,FnmRNA (0.52±0.08),明显低于对照组(P＜0.05).结论维生素A缺乏通过改变IRP2表达、IRP-RNA结合活性,在转录后水平改变TfR和Fn mRNA表达,影响铁稳态.     

不同锌营养状况对大鼠铁代谢的影响

目的研究不同锌营养状况对大鼠铁代谢和肝脏铁调节蛋白(IRP)mRNA、铁蛋白(Fn)mRNA及转铁蛋白受体(TfR)mRNA的影响。方法 40只雄性SD大鼠按体重随机分为4组,每组10只,铁和锌正常对照组(ZA组),铁正常锌缺乏组(ZD组),铁和锌正常配饲组(PF组),铁正常锌过量组(ZE组)。喂饲8周后麻醉处死,取大鼠肝脏、脾脏和血清,测定血红蛋白,血清锌、血清铁、血清转铁蛋白受体、血清铁蛋白、肝脏铁和锌含量、脾脏铁和锌含量,并用逆转录-聚合酶链反应(RT-PCR)法检测各组大鼠IRP2 mRNA和肝脏TfR mRNA以及Fn mRNA的表达水平。结果与对照组相比,锌过量使肝脏和脾脏铁含量、血清铁水平显著降低(P<0.05);锌缺乏使肝脏铁含量、血清转铁蛋白受体水平显著增高(P<0.05),同时,血清铁水平显著降低(P<0.05);锌缺乏时肝脏IRP mRNA及TfR mRNA表达显著增强。结论锌缺乏可能通过影响铁吸收、储存、转运来影响体内铁的营养状况。锌缺乏通过改变IRP2表达、IRP-RNA结合活性,在转录后水平改变TfR mRNA和FnmRNA表达,影响铁稳态。     

Iron deficiency in young rats alters the distribution of vitamin A between plasma and liver and between hepatic retinol and retinyl esters.

We assessed whether iron deficiency alters the concentration of vitamin A (VA) in plasma or liver and the chemical distribution between hepatic unesterified and esterified retinol. Weanling male Sprague-Dawley rats (n = 10/group) were allocated to one of four diet groups: low iron (ID3, 3 mg of elemental iron/kg diet), marginal iron (ID15, 15 mg/kg), control diet food-restricted to the ID3 group (FR, 35 mg/kg), and control diet ad libitum consumption (AD, 35 mg/kg). Both ID3 and FR rats grew less than AD and ID15 rats. At the end of 5.5 wk, plasma retinol concentrations of the ID3 and FR rats were reduced >40% compared to ID15 and AD rats [Kruskal-Wallis test (K-W), P < 0.0042)]. Paradoxically, the hepatic VA concentration was greater in FR rats, with accumulation of more retinyl esters and retinol compared to the other dietary groups. Concentrations of hepatic retinyl esters and retinol did not differ among the other groups, but the molar ratio of hepatic retinyl esters to retinol was greater in ID3 rats (20.1 +/- 1.4) compared to ID15 rats (13.8 +/- 1.6, P = 0.02), AD (11.3 +/- 2.1, P < 0.0042) and FR (9.5 +/- 1.1, P < 0.0042). Iron deficiency may cause changes in liver and plasma VA that are refractory to VA intake, and thus a benefit may be derived from combining iron and VA supplements during nutrition interventions.     

铜缺乏对大鼠铁代谢的影响

目的研究铜缺乏对大鼠肝脏铁调节蛋白2(IRP2)、转铁蛋白受体(TfR)及铁蛋白(Fn)mRNA的影响。方法 40只雄性SD大鼠按体重随机分为4组,每组10只,对照组(Ⅰ组),铜完全缺乏组(Ⅱ组),铜边缘缺乏组(Ⅲ组),铁及铜边缘缺乏组(IV组)。喂养8周后处死,取大鼠组织和血清,进行相关指标和基因表达检测。结果与对照组比较,铜缺乏使大鼠血清铁和血清铁蛋白含量显著降低(P<0.05),血清转铁蛋白受体水平明显升高,铜缺乏时大鼠肝脏IRP2、TFR mRNA表达水平明显升高,Fn mRNA明显降低(P<0.05)。结论铜缺乏通过影响铁吸收、储存、转运而影响大鼠体内铁的营养状况。铜缺乏影响大鼠IRP2 mRNA表达与IRE-IRP结合活性,在转录后水平改变TfR和Fn mRNA的表达,影响机体的铁稳态。     

Effect of soybean hull iron on growth, iron bioavailability, and behavioral function in anemic rats induced by iron deficiency during gestation or lactation

Bioavailability of iron in soybean hull was investigated by hemoglobin regeneration efficiency (HRE), body iron status and maze test in rat pups with iron-deficiency anemia (IDA) induced by iron deficiency of dams during gestation or lactation (GID or LID group, respectively) and normal pups (N group). The soybean hull repletion diet (SH) and purified control diet (PC) as the experimental diets contained the same amount of iron (35mg/kg diet) and the pups in each group were divided into two subgroups by diet sources. The normal (N-SH), gestation iron deficiency (GID-SH), lactation iron deficiency (LID-SH) groups fed SH were significantly higher in food intake and growth than each of their respective control groups (N-PC, GID-PC, LID-PC) fed PC. After the feeding, hemoglobin concentrations approached normal value in all groups, but HRE were significantly higher with SH irrespective of iron deficient period. IDA rats in either lactation or gestation, when compared to normal rats, resulted in lower serum iron and transferrin saturation. Iron concentrations in both liver and spleen were significantly lower in LID-PC group than LID-SH and N-PC groups. The maze test showed a learning defect in either LID group, but GID groups were not significantly different in comparison with N groups. These results suggest that IDA in lactation may influence more serious growth and development than those in gestation, soybean hull iron has the higher bioavailability in normal and IDA-induced rats, and thus soybean hull is effective as source of iron supplement.     

LIVER VITAMIN A MOBILIZATION DURING ZINC DEFICIENCY AND RESTRICTED FOOD INTAKE

Zinc-deficient rats, compared to pair-fed controls, had decreased plasma vitamin A and retinol-binding protein (RBP), with liver vitamin A normal and liver RBP depleted. The hypothesis was therefore advanced that synthesis of liver RBP declines in zinc deficiency as a result of the lower growth rate (i.e. food intake and utilization) of the deficient rats.     

维生素A和铁缺乏对大鼠红系造血影响的比较

采用体外培养红系祖细胞(BFU-E、CFU-E),观察维生素A缺乏(VAD),或铁缺乏(ID)对断乳期大鼠红系造血的影响,结果发现VAD和ID大鼠的BFU-E及CFU-E集落数明显低于正常组,ID组的BFU-E及CFU-E集落数及每一集落的细胞数均明显低于正常及VAD组;补充VA和铁剂后BFU-E及CFU-E集落数明显增加,提示VAD和ID可能通过不同机制引起骨髓红系祖细胞增殖分化抑制。     

大鼠的实验性铁与锌营养缺乏

目的观察铁锌同时缺乏和单独缺乏对大鼠铁锌营养状况的影响。方法按照2×2析因设计,将4w龄雄性wistar大鼠随机分为4组:缺铁缺锌组(F0Z0):喂以低铁低锌饲料(铁7.10mg/kg,锌5.14mg/kg),自由进食;单纯缺铁组(F0Z1):喂以低铁饲料(铁7.10mg/kg,锌40mg/kg);单纯缺锌组(F1Z0):喂以低锌饲料(锌5.14mg/kg,铁40mg/kg);铁锌正常组(F1Z1):喂以铁锌正常饲料(铁40mg/kg,锌40mg/kg);后3组均与F0Z0组对喂。喂养42d后,处死大鼠,分别测定Hb、Hct、血清铁、血清锌、肝脏铁、肝脏锌、胫骨锌等指标。结果实验结束时F0Z0组大鼠的Hb平均水平降至82.36g/L,血清锌0.78μg/ml,成功建立缺铁缺锌大鼠模型。4组大鼠的各项指标水平大多以F0Z0组最低,F0Z1组或F1Z0组次之,F1Z1组最高;铁缺乏可导致大鼠血清铁、肝脏铁含量明显下降,也可降低肝脏锌水平;锌缺乏能显著降低机体肝脏锌、胫骨锌水平;在体重、Hb、Hct、血清锌这四项指标上存在铁锌交互作用。结论大鼠铁锌同时缺乏时铁锌营养状况最差,缺锌可能会增加对铁的吸收利用,缺铁会减少体内锌储存量。     

Iron deficiency and marginal vitamin A deficiency affect growth,hematological indices and the regulation of iron metabolism genes in rats

Iron deficiency and marginal vitamin A (VA) deficiency frequently coexist and affect billions of people, mostly children and women, worldwide. The effects of these micronutrient deficiencies alone and in combination on hematologic, biochemical and molecular indices of iron and VA status were investigated in a 2 x 2 randomized blocked study conducted in growing male Sprague-Dawley rats. From 3-8 wk of age, rats were fed one of four purified diets that were either adequate or restricted in iron (Fe) and adequate or marginal in VA: (+)Fe(+)VA, 20.3 and 0.367 micro g/g, respectively, denoted control diet; (-)Fe(+)VA, 3.34 and 0.405 micro g/g; (+)FeVA(m), 22.2 and 0.051 micro g/g; or (-)FeVA(m), 3.03 and 0.055 micro g/g. Weight-matched rats fed adequate micronutrients were included to control for possible confounding effects of Fe deficiency on growth and feed efficiency. Iron restriction reduced (P < 0.05) weight gain, feed efficiency, blood hemoglobin and hematocrit. Plasma and liver iron and plasma transferrin saturation were reduced by approximately 50%, whereas liver transferrin mRNA and protein and transferrin receptor mRNA were elevated, as was liver ferritin light-chain protein and light-chain mRNA. Liver heavy-chain ferritin mRNA, hemopexin, ceruloplasmin and cellular retinol-binding protein mRNA were not affected by iron or VA restriction. Although marginal VA deficiency did not exacerbate indices of poor iron status during iron deficiency, iron deficiency was associated with lower plasma retinol and elevated liver VA concentrations. These results are consistent with an impaired mobilization of liver retinol during iron deficiency as well as multiple alterations in iron metabolism.