硒对人鼻咽癌细胞辐射效应的抑制作用

本文研究晒的体外辐射防护作用。硒以亚硒酸钠（Ｎａ＿２ＳｅＯ＿３）形式溶于人鼻咽低分化鳞癌细胞株（ＣＮＥ－２）的培养液中（最终浓度０．５８ｍｍｏｌ／ＬＮａ＿２ＳｅＯ＿３），培养１５～１６ｈ，然后细胞接受２Ｇｘγ射线照射，将细胞接种于９６孔微量细胞培养板内，每孔５０个细胞，２４孔为一组，各加含硒或不含硒培养液。继续培养４８ｈ，在倒置显微镜下观察记录每孔内细胞克隆（≥８个细胞）数。结果发现加硒放射组与单纯放射组比较，克隆抑制率分别为３５．６８％和５０．７５％，两者差异显著（Ｐ＜０．０１），提示硒对体外培养细胞显然有辐射防护作用。     

硒加抗癌药对人肝癌细胞生长的影响

研究亚硒酸钠（Ｎａ_２ＳｅＯ_３）和丝裂霉素（ＭＭＣ）、盐酸阿霉素（ＡＤＭ）对ＱＧＹ—７７０３人肝癌细胞生长的影响。结果表明：终浓度为１μｇ／ｍｌ的Ｎａ２ＳｅＯ３，可明显抑制肝癌细胞的生长增殖、减少细胞对甲胎蛋白（ＡＦＰ）的分泌；１μｇ／ｍｌ的Ｎａ２Ｓｅ０３与１．５μｇ／ｍｌ的ＭＭＣ或１５μｇ／ｍｌ的ＡＤＭ联合应用对肝癌细胞生长增殖的抑制作用，不论是细胞生长的抑制率、还是肝癌细胞分泌ＡＦＰ的抑制率，均明显高于各自的单独应用效果，差异有显著性意义（Ｐ＜０．０５）．并随着培养时间的延长、抑制程度持续增强。提示Ｎａ_２ＳｅＯ_３与抗癌药联合应用。具有良好的协同或相加抑癌、抗癌效应。对临床应用有一定的实际意义。     

硒锗联合对酒精致大鼠肝脏脂质过氧化的影响

采用体外和体内实验以酒精诱导大鼠肝脏脂质过氧化为模型，研究了（Ｎａ＿２ＳｅＯ＿３）和锗（羧乙基锗倍半氧化物，Ｇｅ－１３２）联合应用的协同抗氧化作用。结果表明，酒精在体外和体内均可导致大鼠肝脏脂质过氧化。体外研究发现将硒和锗同时使用时（Ｎａ＿２ＳｅＯ＿３，２０μｍｏｌ／Ｌ＋Ｇｅ－１３２，１０．５ｍｍｏｌ／Ｌ），表现出比使用相同剂量单一的硒Ｎａ＿２ＳｅＯ＿３，２０μｍｏｌ／Ｌ）或锗（Ｇｅ－１３２，１０．５ｍｍｏｌ／Ｌ）具有更强的抗氧化作用。体内研究将硒和锗剂量减半同时使用（Ｎａ＿２ＳｅＯ＿３，０．０５５ｍｇ／ｋｇ＋Ｇｅ－１３２，１００ｍｇ／ｋｇ），具有类似如单一的较高剂量硒（Ｎａ＿２ＳｅＯ＿３，０．１１ｍｇ／ｋｇ）的抗氧化作用和比使用单一的较高剂量锗（Ｇｅ－１３２，２００ｍｇ／ｋｇ）更强的抗氧化作用。本次研究结果表明硒（Ｎａ＿２ＳｅＯ＿３）和锗（Ｇｅ－１３２）在体外及体内均具有协同抗氧化作用。     

硒的化学形态对大鼠肝T_45’－脱单碘酶活力的影响

用低硒地区施硒肥（Ｎａ＿２ＳｅＯ＿３）粮饲料（Ｓｅ０．１００ｍｇ／ｋｇ）和硒含量相近的补硒（Ｎａ＿２ＳｅＯ＿３）粮饲料（Ｓｅ０．０９９ｍｇ／ｋｇ）分别喂养大鼠８周，观察不同化学形态硒对动物肝Ｔ＿４５′－脱单碘酶（ＩＤ－Ｉ）活力、肝硒含量及血谷胱甘肽过氧化物酶（ＧＳＨ－ｐｘ）活大的影响。结果表明，硒肥粮组与补硒粮组相比较，肝ＩＤ－Ｉ活性明显高（Ｐ＜０．０１），肝硒含量亦高，但没有显著意义，而血ＧＳＨ－ｐｘ活力却略低；各指标的硒肥／补硒两组之比值为肝ＩＤ－Ｉ活力１．８２、肝硒含量１．２５、血ＧＳＨ－ｐｘ活力０．８３。证明施硒肥粮中结合态硒（硒蛋氨酸）较无机硒－Ｎａ＿２ＳｅＯ＿３更有利于肝ＩＤ－Ｉ的合成     

亚硒酸钠与硒蛋氨酸对砷诱导人外周血淋巴细胞遗传毒性保护作用比较

为了探讨硒作为拮抗砷毒害的化学干预剂，拮抗砷对机体损伤，降低肿瘤发病率的机理，我们采用ＳＣＥ实验和ＤＮＡ合成抑制实验，研究证实预加５×１０－７、１×１０－６ｍｏｌ／ＬＮａ２ＳｅＯ３和同时加１×１０－６ｍｏｌ／Ｌ硒蛋氨酸能明显减轻Ａｓ２Ｏ３诱导人外周血淋巴细胞ＳＣＥ频率。预加５×１０－６ｍｏｌ／ＬＮａ２ＳｅＯ３和同时加１×１０－６、５×１０－６ｍｏｌ／Ｌ硒蛋氨酸能明显拮抗Ａｓ２Ｏ３对ＤＮＡ合成抑制作用。硒对砷损伤人细胞遗传物质保护作用的机理尚待进一步研究。     

硒的化学形态对大鼠肝T45‘—脱单碘酶活力的影响

用低硒地区施硒肥（Ｎａ２ＳｅＯ３）粮饲料（Ｓｅ０．１００ｍｇ／ｋｇ）和硒含量相近的补硒（Ｎａ２ＳｅＯ３）粮饲料（Ｓｅ０．０９９ｍｇ／ｋｇ）分别喂养大鼠８周，观察不同化学形态硒对动物肝Ｔ４５＇－脱单碘酶（ＩＤ－Ｉ）活力、肝含量及血谷胱甘肽地氧化物酶（ＧＳＨ－Ｐｘ）活力的影响。结果表明，硒肥粮组与补硒粮组相比较，肝ＩＤ－Ｄ活性明显高（Ｐ＜０．０１），肝硒含量亦主同，但没有显著意义，而血ＧＳＨ－Ｐｘ活力     

保健食品中硒的化学形态分析

基于２，３－二氨基萘（ＤＡＮ）试剂对Ｓｅ（Ⅳ）的选择性测定，比较了ＡＰＤＣ－ＣＨＣｌ_３萃取法、直接分析法和加标法分析保健品中Ｓｅ（Ⅳ）的差异，从而建立了加标法测定保健品中Ｓｅ（Ⅳ）的方法。硝酸—高氯酸—硫酸体系将硒蛋白中以负二价形式存在的硒氧化到四价后测定总硒，用差减法获得样品中不同化学形态硒的含量     

硒与脱碘酶及其研究技术（二）

硒与脱碘酶及其研究技术（二）西安医科大学李综述徐光禄审校关于Ⅰ型酶中硒参入的机制，根据既往对硒参入蛋白质机制的研究，有两种可能性。一种为翻译后修饰学说，一种为直接参入学说。前者认为，在预防缺硒性肝坏死方面，Ｈ２Ｓｅ、ＨｅＳｅＯ３和硒蛋氨酸具有同等效力...     

硒,锗对低硒饲料喂养大鼠的脂质过氧化作用的影响

为了解硒、锗抗脂质过氧化的联合作用，用克山病区粮喂养Ｗｉｓｔａｒ大鼠１２周，通过在饲料中加入一定剂量的Ｎａ２ＳｅＯ３和Ｇｅ－１３２观察其体内自由基代谢情况。结果表明：加硒加锗能降低大鼠肝、肾组织中自由基含量，降低心脏、肝脏、肾脏中脂质过氧化物（ＬＰＯ）含量，提高血液中谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）活力，而且硒、锗之间表现出一定的协同作用。     

亚硒酸钠与硒蛋氨酸对砷诱导人外周血淋巴细胞遗传毒性保护作…

为了探讨硒作为拮抗砷毒害的化学干预测，拮抗砷对机体损伤，降低肿瘤发病的机理，我们采用ＳＣＥ实验和ＤＮＡ合成抑制实验，研究证实预加５×１０＾－７、１×１０＾－６ｍｏｌ／ＬＮａ２ＳｅＯ３和同时加１×１０＾－６ｍｏｌ／Ｌ硒蛋氨酸能明显减轻Ａｓ２Ｏ３诱导人外周血淋巴细胞ＳＣＥ频率。     

纳米硒对肉鸡生长和抗氧化的影响

目的:研究纳米硒和亚硒酸钠对肉鸡生长和抗氧化的影响。方法:岭南黄雌雄混合雏780羽按试验要求分为13组,每组4个重复,每个重复15羽。将纳米硒和亚硒酸钠两种硒源分别以0.1、0.2、0.3、0.4、0.5、1.0mg/kg六个硒水平添加到基础日粮中,配制成12种试验日粮,基础日粮作对照。结果:(1)亚硒酸钠在0.2～0.5mg/kg添加水平肉鸡生长处于高峰平台,1.0mg/kg硒添加水平肉鸡生长显著低于0.2～0.4mg/kg硒添加水平。纳米硒添加1.0mg/kg,肉鸡生长仍然保持在高峰平台。硒添加浓度在0.1～0.3mg/kg时,亚硒酸钠和纳米硒对肉鸡生长无显著差异;硒添加浓度在0.4～1.0mg/kg时,纳米硒组肉鸡生长显著高于亚硒酸钠组(P<0.05)。(2)硒添加浓度在0.1～0.4mg/kg时,两种硒对GSH-Px活性和全血硒无显著差异(P>0.05);在0.5和1.0mg/kg硒水平上,纳米硒组GSH-Px活性和全血硒显著高于亚硒酸钠组(P<0.05)。(3)硒添加浓度在0.1～0.3mg/kg时,两种硒源对T-AOC、MDA和活性氧的影响无显著差异;硒浓度在0.4～1.0mg/kg硒时,纳米硒组T-AOC显著高于亚硒酸钠组(P<0.05),MDA和活性氧显著低于亚硒酸钠组(P<0.05)。结论:纳米硒用于肉鸡的Weinberg剂量-效应的最适剂量范围宽于亚硒酸钠,高剂量添加时比亚硒酸钠具有更强的营养生物学作用,对肉鸡的安全性更高。     

维生素B6对硒的生物利用率影响的研究Ⅳ．对大鼠体内不同化学形式硒利用率及脂质过氧化物的影响

４周龄雄性大鼠饲缺维生素Ｂ６（ＶＢ６）缺硒酪蛋白蔗糖基础饲料，３周后按体重把动物分成１０组，即基础饲料组、基础饲料中补充含硒０．２５ｍｇ／ｋｇ饲料的硒酸钠组、亚硒酸钠组、ＤＬ－硒蛋氨酸组或硒胱氨酸组，在此基础上每种饲料又分成补充或不补充盐酸吡哆醇２．５０μｇ／ｇ饲料两组。实验期为４周。补ＶＢ６各组的红细胞、骨骼肌和心肌中硒水平和谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）活性均显著高于相应缺ＶＢ６各组，ＶＢ６对饲硒酸钠、亚硒酸钠和硒胱氨酸大鼠肝硒和ＧＳＨ－Ｐｘ水平没有影响；但当补充硒蛋氨酸时，与补ＶＢ６大鼠相比缺ＶＢ６大鼠的肝硒水平较高而ＧＳＨ－Ｐｘ活性显著降低。本研究结果进一步证明，ＶＢ６与血浆硒的转运和利用有关，并且参与了硒蛋氨酸在肝脏中的代谢过程     

Comparative toxicity and tissue retention of selenium in methionine-deficient rats fed sodium selenate or L-selenomethionine

Selenium (Se) toxicity is known to be affected by level of intake of the mineral, but there are conflicting reports on the relative toxicities of the various chemical forms of Se. We monitored Se toxicity in rats fed Torula yeast-based diets containing 0.1, 0.5 or 2.5 micrograms Se/g of diet as either sodium selenate (Na2SeO4) or L-selenomethionine (SeMet). Half the diets were supplemented to contain adequate dietary methionine (Met). Weights were monitored weekly for 6 (Met-adequate) or 7 (Met-deficient) wk, at which time the rats were killed. There were no significant differences in final weight among Met-adequate rats, regardless of level or form of dietary Se. Methionine-deficient rats all gained significantly less weight than their Met-adequate counterparts. Selenosis was most severe in the Met-deficient rats fed 2.5 micrograms Se/g of diet as Na2SeO4, as indicated by significantly impaired weight gains. Nonetheless, Se retention in serum, heart, brain, bone, testes, colon, skin, lungs and pancreas was greater in rats fed SeMet than in those fed Na2SeO4, and Met deficiency further intensified this trend. The kidney was the only organ in which Se levels were markedly higher in the severely poisoned Met-deficient rats fed Na2SeO4. Further research is needed to determine whether elevated kidney Se levels are related to the greater toxicity observed in the Met-deficient rats fed Na2SeO4.     

Nutritional availability and chronic toxicity of selenocyanate in the rat

To evaluate nutritional availability and chronic toxicity of KSeCN, female postweanling rats were fed casein-based diets plus 0.1, 0.5, 2.5, 5 and 10 mg Se/kg as KSeCN for 6 wk, or 0.1, 0.5 and 10 mg Se/kg as Na2SeO3. A control group was fed the basal diet (Se = 0.04 mg/kg) and one group was fed the basal diet plus 5 mg Se/L as KSeCN in the drinking water. There were no differences in weight gain and diet consumption among groups fed 2.5 mg Se/kg or less. At 5 and 10 mg Se/kg, rats showed depression in weight gain and diet consumption. After wk 6 there were no abnormalities of the major organs of rats fed 2.5 mg Se/kg or less. Spleen enlargement was observed at 5 and 10 mg Se/kg, and liver damage and kidney enlargement at 10 mg Se/kg. Se content in the blood, liver and kidney of rats fed KSeCN was generally somewhat lower than for those fed Na2SeO3 at the same levels. The availability of Se from KSeCN for glutathione peroxidase formation in blood, liver and kidney was comparable to that of Na2SeO3. Plasma thyroxine in groups fed 10 mg Se/kg was 40% of that in the control group, but was not altered at lower Se levels.     

Selenium absorption and retention from a selenite- or selenate-fortified milk-based formula in men measured by a stable-isotope technique

The present study was designed to determine the apparent absorption and retention of the inorganic Se compounds SeO3(2-) and SeO4(2-), which are commonly used for Se fortification of clinical nutrition products and infant formulas. Ten healthy men were fed a milk-based formula labelled with 40 microg Se as 74SeO3(2-) or 76SeO4(2-) on two consecutive days using a randomised crossover design. Se stable-isotope analysis of 9 d complete collections of urine and faeces was used to calculate apparent Se absorption and retention. Se retention from 74SeO3(2-) (41.0 (SD 8.4) %) and from 76SeO4(2-) (46.0 (SD 7.9) %) was not significantly different (P > 0.05). However, Se absorption was significantly higher from SeO4(2-) than from SeO3(2-) (91.3 (SD 1.4) % v. 50.2 (SD 7.8) %, P < 0.05). Urinary excretion of the administered dose was 9.2 (SD 1.8) % for 74SeO3(2-) and 45.3 (SD 8.2) % for 76SeO4(2-) (P < 0.05). Urinary Se excretion kinetics differed significantly for the two Se compounds; 90 % of the total urinary Se was excreted after 121 h for 74SeO32- and after 40 h for 76SeO42- These results suggest that although Se absorption and urinary excretion differ for SeO3(2-) and SeO4(2-), both Se compounds are equally well retained when administered at a relatively low dose (40 microg Se). The nutritional impact of Se fortification of foods would thus be expected to be similar when SeO4(2-) or SeO3(2-) are used.     

硒对正常小鼠免疫功能的影响

<正> 近年来微量元素对机体的作用已越来越受重视,市场上也出现了不少含微量元素的食品和药物。硒是谷胱甘肽过氧化物酶的基本成分,对机体有多方面的作用。硒对机体免疫功能也有作用。缺硒可导致血凝抗体降低。对羊红细胞免疫应答反应降低,机体对疾病的抵抗力降低,补硒可纠正或提高     

The tissue disposition of zinc and copper following repeated administration of cadmium and selenium to rats

Female rats were divided into four groups of five rats each including one control group (C). The animals were administered Na2SeO3 (Se), (CdCl2 Cd), and Na2SeO3 + CdCl2 (Cd + Se). Sodium selenite was given intragastrically at a dose of 0.5 mg Se/kg every day and cadmium chloride was injected subcutaneously every other day at a dose of 0.3 mg Cd/kg for 2 weeks. Exposure of rats to Cd caused an increase in the concentration of copper in the kidneys, blood, and liver and a decrease in the lung, but increased the concentration of zinc in the liver and brain and diminished it in the muscles and bones. In animals exposed to Se an increase in the copper concentration was observed in blood and brain; zinc was increased in the blood, heart, brain, and stomach, but decreased in the kidneys. Exposure of rats to Cd + Se resulted in an increase of copper in the kidneys and a decrease in the spleen, lungs, stomach, muscles and bones. Se prevented the cadmium-induced diminution of the zinc levels in the muscles and bones.     

Effect of selenium repletion on glutathione peroxidase protein level in rat liver

We have previously reported that liver glutathione peroxidase (GSH-Px, EC 1.11.1.9) protein level and activity decrease exponentially during Se deficiency. To determine the effect of Se repletion on these parameters, Se-deficient rats were repleted with 0.1 or 0.5 mg Se/kg diet as Na2SeO3 in a 30% torula yeast-based diet and were killed 0, 1, 2, 3, 5, 7 or 14 d later. GSH-Px protein was quantitated using anti-GSH-Px antibodies. Dietary repletion with 0.5 mg Se/kg diet increased GSH-Px protein and activity significantly (P less than 0.05) after 1 d. After 5 d for GSH-Px protein and 7 d for activity the rate of increase slowed, and at d 14 neither GSH-Px protein nor activity was significantly different from that of Se-adequate rats. Repletion with 0.1 mg Se/kg diet did not significantly increase GSH-Px protein or activity until 14 d. To examine the short-term effect of Se repletion, Se-deficient rats were injected intravenously with 15 or 60 micrograms Se as Na2SeO3 and killed 1, 3, 6, 12 or 24 h later. Only rats injected with 60 micrograms Se and killed 24 h later had a significant increase in GSH-Px activity along with a marginally significant increase in GSH-Px protein. These response curves indicate that homeostatic processes control the level of GSH-Px. The lack of an increase in GSH-Px until 24 h after Se administration implies that additional metabolic events after a rise in cellular Se may be necessary prior to an increase in GSH-Px synthesis in Se-deficient rats.     

大蒜多糖及其硒化产物抗氧化活性的比较研究

目的比较大蒜多糖与硒化大蒜多糖对经过氧化氢(H2O2)诱导损伤的大鼠嗜铬瘤细胞株(PC12)的保护作用。方法用H2O2建立PC12细胞损伤模型,应用四氮唑蓝(MTT)比色法检测PC12细胞的活力;化学比色法测定细胞培养液中乳酸脱氢酶(LDH)释放量、细胞内和细胞培养液中丙二醛(MDA)含量及超氧化物歧化酶(SOD)的活性。结果硒化大蒜多糖、大蒜多糖500μg/ml及以上剂量组和亚硒酸钠12.50μg/ml及以上剂量组均能有效抑制由H2O2引起的细胞存活率的下降(P<0.01)。硒化大蒜多糖、大蒜多糖2000μg/ml可显著降低LDH释放量和细胞培养液及细胞内的MDA含量,以及提高SOD活性(P<0.01),表现出良好的抗氧化活性,而硒化大蒜多糖的抗氧化作用更为明显(P<0.05)。结论硒化大蒜多糖对经H2O2诱导损伤的PC12细胞具有保护作用,这种保护作用明显优于大蒜多糖或单纯硒,其作用机制可能与提高PC12细胞的抗氧化能力有关。     

Selenium-mercury interaction during intestinal absorption of 75Se compounds in chicks

The effects of inorganic (HgCl2) and organic (CH3HgCl) mercury on the intestinal absorption of Se compounds [Na2(75)SeO3, Na2(75)SeO4, L-[75Se]methionine ([75Se]Met)] were determined in 3-wk-old White Leghorn cockerels by the in vivo ligated duodenal loop procedure. The intraduodenal dose contained 0.05 microCi 75Se, 0.01 mM Se, 150 mM NaCl and 0-1.0 mM Hg. In the presence of 1 mM inorganic Hg in the intraduodenal dose, the absorption of the inorganic 75Se compounds was only about 65% of that in the control group, whereas only a slight inhibitory effect on [75Se]Met absorption was observed. Methylmercury had no effect on [75Se]selenite absorption. Precipitation of the 75Se-selenite in the intestinal lumen partly explained the direct interaction between inorganic Hg and Se compounds. Absorption of [75Se]Met and [75Se]selenite was also determined in chicks fed after hatching a purified diet supplemented with varying amounts of Hg (0-500 mg/kg) and Se (0-4 mg/kg). Dietary Hg significantly reduced the transfer of [75Se]selenite to body by enhancing the accumulation of the isotope in the intestinal tissue. Dietary Hg did not affect the absorption of [75Se]Met, but altered the whole-body distribution of this Se compound. Because interaction between Se and Hg was observed mainly between the inorganic compounds and with use of a manyfold excess of Hg over Se, the data suggest that intestinal interaction between these metals is not of great nutritional importance.