富含硒玉米对低硒大鼠硒和GSH—Px活性的影响

为了研究富含硒玉米对低硒粮饲料喂养大鼠血硒状态的影响，观察了补充富含硒玉米或亚硒酸钠时和停止补硒后大鼠血硒水平和谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）活性的变化。结果显示：①两种补硒形式均可有效地增高血浆、红细胞的硒水平和红细胞的ＧＳＨ－Ｐｘ活性；②富含硒玉米增高和维持血浆和经细胞硒水平作用与亚硒酸钠相同；③富含硒玉米升高红细胞ＧＳＨ－Ｐｘ活性的作用低于亚硒酸钠，但停止补硒后两维持ＧＳＨ－Ｐｘ活性作     

克山病病区粮喂大鼠对紫阳高硒玉米硒的生物利用率

用耗竭/补充/耗竭的设计,以克山病病区低硒粮饲料(含硒6μg/kg)喂养大鼠6周后,观察了补充紫阳高硒玉米(含硒7.241mg/kg)或亚硒酸钠硒(饲料含硒分别为221和223μg/kg)时以及停止补硒后,大鼠组织和血液硒水平以及谷胱甘肽过氧化物酶(GSH-px)活性的变化,评估了紫阳高硒玉米硒的相对生物利用率。结果表明:以血浆、肾、肝和心肌硒含量为指标时,高硒玉米硒的平均相对生物利用率(补硒2、4和6周时)与亚硒酸钠硒相似,分别为99、107、100和104%(亚硒酸钠定为100%);但以红细胞硒为指标时,高硒玉米硒的生物利用率(120%)高于亚硒酸钠硒;以心肌和红细胞 GSH-px 活性为指标时,其生物利用率(72和84%)低于亚硒酸钠硒。至再停止补硒3周时,高硒玉米维持组织硒水平和 GSH-px 活性的作用与亚硒酸钠相似。     

硒酵母利亚硒酸钠对克山病病区粮喂养大鼠血小板血栓素的影响

应用克山病病区低硒粮饲料喂养大鼠１４周，探讨补硒（亚硒酸钠或硒酵母）对血小板血栓素生成的影响。结果表明，补充两种硒制剂均可明显增高低硒大鼠血浆硒水平和血小板ＧＳＨ─Ｐｘ活性，降低ＡＤＰ诱导的血小板ＴＸＡ２形成和血浆ＴＸＡ２水平，两种硒制剂的作用程度相似；补硒对血浆前列环素水平无显著影响。     

硒对克山病病区粮喂养大鼠血小板聚集性和5—HT释放反应的影响

用克山病病区低硒粮饲料喂养大鼠14周,探讨补硒(亚硒酸钠或硒酵母)对血小板聚集性和5—HT释放反应的影响。结果表明,补充两种硒制剂均能增加低硒大鼠血浆硒水平和血小板GSH—Px活性,降低ADP诱导的血小板聚集性和5—HT释放反应;两者的影响程度相似;补硒对血小板5—HT含量无显著影响。     

补硒对低硒克山病病区居民血浆甲状腺激素水平的影响

给低硒克山病病区居民每日口服２００μｇ亚硒酸钠１２周，测定红细胞硒含量，谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）活性的血浆Ｔ３、Ｔ４及ｒＴ３水平，探讨硒对甲状腺激光水平的影响。结果表明：补硒显提高红细胞硒含量和ＧＳＨ－Ｐｘ活性；补硒组血浆Ｔ３明显升高，ｒＴ２明显降低，而Ｔ４无明显改变。红细胞硒含量与血浆Ｔ３呈明显正相关（ｒ＝０．５４７，ｎ＝３８，Ｐ〈０．００１）和血浆ｒＴ３呈显负相关（ｒ＝－０．４２     

克山病病区居民血小板血栓素、聚集性和形态的改变及补硒的作用

对比研究了克山病病区和非病区居民的硒状态、血栓素(TXA_2)水平以及血小板聚集性形态,并观察了补硒的影响。发现:(1)血硒水平低的病区居民血小板GSH-Px活性也低;血浆TXA_2、血小板TXA_2生成和聚集性均显著高于非病区;血小板形态有异常,出现变形和团聚血小板。(2)给病区居民补硒(亚硒酸钠,200μgSe/d)12周后,红细胞硒和GSH-Px活性显著增高,血浆TXA_2、血小板TXA_2生成和聚集性均显著低于未补硒居民,但血浆前列环素和β-血小板球蛋白(βTG)、血小板βTG含量和释放率无显著变化;补硒可明显减轻病区居民血小板的形态改变。提示,病区低硒居民血小板的高活化反应是克山病发病的一个危险因素;补硒预防克山病发病的机理之一,在于缓解病区人体血小板的高反应性,从而消除心肌围血管病变发生的基础。     

硒与GSH联合对氟致大鼠脂质过氧化作用的影响

目的　研究抗氧化剂硒及与不同剂量 GSH联合对氟所致脂质过氧化作用的影响。方法　采用动物实验。结果　饮含氟化钠 (15 0 mg/ L)水可使大鼠肝、肾及血清中 L PO含量显著增加 ;SOD活性、GSH- Px活性、GSH含量均显著下降 ;饮含氟水同时给亚硒酸钠 ,可使血清中 L PO含量显著下降 ;SOD活性、GSH- Px活性、GSH含量显著升高。说明硒对氟引起的脂质过氧化有拮抗作用。饮含氟水同时给 Se与不同剂量 GSH后 ,结果显示 :Se与低、中、高 3个剂量 GSH均可使血清中 L PO含量显著下降 ,全血中 SOD活性显著增强 ,呈剂量—效应关系 ,使肝、肾及全血中 GSH- Px活性不同程度增强 ,表明 Se与 GSH联合可有效拮抗氟所致的脂质过氧化作用 ,恢复机体抗氧化能力。结论　 1氟可引起大鼠肝、肾及全血中脂质过氧化物含量升高 ,抗氧化能力下降 ;2硒及与不同剂量 GSH联合具有不同程度拮抗氟诱导的脂质过氧化作用 ,恢复机体的抗氧化能力     

克山病病区居民血小板血栓素,聚集性和形态的改变及补…

对比研究了克山病病区和非病区居民的硒状态、血栓素（ＴＸＡ２）水平以及血小板聚集性形态，并观察了补硒的影响。发现：（１）血硒水平低的病区居民血小板ＧＳＨ－Ｐｘ活性也低；血浆ＴＸＡ２、血小板ＴＸＡ２生成和聚集性均显著高于非病区；血小板形态有异常，出现变形和团聚血小板。（２）给病区居民补硒（亚硒酸钠，２００μｇＳｅ／ｄ）１２周后，红细胞硒和ＧＳＨ－Ｐｘ活性显著增高，血浆ＴＸＡ２、血小板ＴＸＡ２生成和聚集     

硒酵母和亚硒酸钠对克山病病区粮喂养大鼠血小板血栓素的影响

应用克山病病区低硒粮饲料喂养大鼠１４周，探讨补硒对血小板血栓素生成的影响。结果表明，补充两种硒制剂均可明显增高低硒大鼠血浆硒水平和血小板ＧＳＨ－Ｐｘ活性，降低ＡＤＰ诱导的血小板ＴＸＡ２水平，两种硒制剂的作用程度相似；补硒对血浆前列环素水平无显著影响。     

碘硒缺乏对大鼠甲状腺抗氧化酶活性影响

应用2×2析因实验设计将 Wistar 大鼠随机分为四组,测定了喂养12周及30周大鼠甲状腺中四种抗氧化酶活性及脂质过氧化物含量。结果表明,甲状腺中四种抗氧化酶活性(Se—GSH—Px,SOD,CAT,GST)于低碘两组明显高于补碘两组,而硒除含硒酶(Se—GSH—Px)外对其余三种酶活性均无影响。补硒能明显提高 Se—GSH—Px 活性,但低碘因素增高活性的幅度更为突出;低碘高硒使GSH—Px 活性增高最明显。脂质过氧化物含量于低碘组亦明显高于补碘组,硒对此影响不明显。提示在缺碘时甲状腺组织抗氧化能力呈代偿性增强,但仍不能克服缺碘所致 LPO 增高对组织造成的损伤。     

Availability of selenium in dough and biscuit in comparison to wheat meal

We studied the availability of selenium in processed foods and whole wheat diets for restoring the Se content and glutathione peroxidase (GSHPx) activity in the blood and liver of selenium-depleted rats. The Se content in the rat diets ranged from 225 to 342 micrograms Se/kg diet. Different selenium sources and different Se amounts had little influence on the Se levels in the blood and liver of repleted rats. Se from processed foods did not completely restore the GSHPx activity in whole blood and liver as happened with Se coming from wheat. These results indicate that it is the milling processes of the flour production, and not the cooking, which decrease the availability of Se for GSHPx synthesis in rats.     

硒蛋氨酸对大鼠全血谷胱甘肽过氧化物酶活性影响的动态观察

用人工合成饲料喂养大白鼠,控制硒、蛋氨酸含量,动态观察谷胱甘肽过氧化物酶(简称 GSH-Px)的活性。结果表明:GSH-Px 活性与饲料中硒及蛋氨酸含量均有密切关系。在常硒条件下,低蛋氨酸能降低 GSH-Px 活性。在低硒条件下,低蛋氨酸能进一步降低 GSH-Px 活性。     

Tolerance of diets deficient or excessive in selenium by Syrian hamsters

Syrian hamsters were fed torula yeast (TY) diets with 8 selenium (Se) supplement levels (0.0-10.0 ppm Se as sodium selenite) or casein (C) diets with 5 supplement levels (0.0-5.0 ppm Se as sodium selenite) for 25 weeks. Whole blood Se, plasma glutathione peroxidase (GSH-Px) activity and erythrocyte GSH-Px activity were measured after 5, 10, 15 and 25 weeks. At 25 weeks hematology was examined and tissue samples analyzed for Se and evaluated for histopathological lesions. While survival was not influenced by dietary Se, food consumption and body weight gain were altered in animals given TY, as those fed 0.0, 0.05 or 10.0 ppm Se consumed less diet. Weight gains at 25 weeks were highest in animals at the 0.1 ppm Se level and reduced in those given unsupplemented TY or 10.0 ppm Se supplements. Hemoglobin, hematocrit and red blood cell counts were reduced in females fed the lowest and highest Se supplements with TY diets. With both C and TY, whole blood Se rose with increasing dietary Se and in the case of TY, Se was elevated with each feeding increment, except between the 0.05 and 0.1 ppm or the 0.25 and 0.5 ppm levels. Plasma GSH-Px increased with rising Se up to 10 ppm, and erythrocyte GSH-Px activity increased up to 5 ppm Se. Erythrocyte GSH-Px values were higher in animals fed C diets. Histopathological observations were normal at all Se levels. Syrian hamsters tolerated dietary Se from 0.05 to 5.0 ppm Se for 25 weeks of observation without detrimental effects.     

Glutathione peroxidase activity in patients with rheumatoid arthritis and in normal subjects: effects of long-term selenium supplementation

The effects of dietary supplementation with selenium were studied in 6 patients with severe, active rheumatoid arthritis (RA) and in 6 healthy control subjects. Initial concentrations of Se in red blood cells and in serum, and the activity of the Se-dependent enzyme glutathione peroxidase (GSH-Px) in red blood cells, serum, and granulocytes were significantly lower in RA patients compared with controls. During Se supplementation, however, the differences in Se levels and in GSH-Px activity between the 2 groups disappeared, except that, in RA patients, GSH-Px activity in granulocytes increased but remained significantly lower than in controls.     

饲料低硒对大鼠血清VE含量的影响

用分别补充100ppm VE 的大骨节病区低硒粮配制的低硒饲料和加饲料饲硒养并繁殖大鼠,组织学上未发现母代或子代大鼠有肝坏死和骨骼肌病变。在母代大鼠中,低硒组的血硒含量明显地低于加硒组(P<0.01),而血清 VE 含量在低硒与加硒组间几乎相同。提示低硒不影响母代大鼠的血清 VE 含量。在子代大鼠中,各组动物血硒含量的变化与其母代基本相同;而低硒组的血清 VE 含量明显地高于加硒组(P<0.05),并且血清 VE 含量与血硒含量之间呈负相关关系(r=-0.658,P<0.05)。结果表明饲料低硒能使子代低硒大鼠血清 VE 含量增加。     

Bioavailability to rats of selenium in milk of cows fed sodium selenite or selenited barley

The nutritional availability of Se to rats in two experimental Finnish milks were compared to that in American milk naturally high in Se. The experimental milks had their Se content increased by feeding cows either sodium selenite (selenited milk) or selenited barley (selenited-barley milk). Weanling male rats were fed a low-Se milk powder diet for 4 weeks followed by continued depletion or repletion with graded levels of Se as sodium selenite (standard) or different milks for 4 weeks. Plasma Se level and plasma and liver glutathione peroxidase (GSH-Px) activities were used as criteria of body Se status. The bioavailability of Se was calculated with the slope-ratio method. The Se in the selenited-barley milk was significantly (p less than 0.01) more available than that in the selenited milk when the plasma Se level was the response criterion. On the other hand, the bioavailability of Se from the various milks was not different when plasma or liver GSH-Px activities were used as the response criteria. Overall bioavailability for the selenited milk, selenited-barley milk and American milk was only slightly less than that for the standard (sodium selenite = 1.00), showing that milk is a relatively readily available source of dietary Se.     

Effect of selenium supplementation on selenium balance in the dependent elderly

Although trace minerals are necessary constituents of enzymes, dietary requirements of these nutrients for the elderly are unknown. This study measured selenium balance in six dependent elderly men before and after five weeks daily administration of 200 micrograms organically-bound selenium; dietary selenium intake averaged 62.1 +/- 7 micrograms/day during both study periods. Selenium status was assessed not only chemically but also biologically as red cell and platelet glutathione peroxidase activities. Plasma selenium averaged 8.8 +/- 0.8 micrograms% (normal: 10 +/- 2 micrograms %) when intake derived from dietary sources alone and increased during medicinal supplementation to an average of 12.8 +/- 1.9 micrograms %. The rise in plasma selenium was not associated with an increase in red cell or platelet glutathione peroxidase activity. The effect of selenium supplementation on in vivo platelet aggregability was studied by measuring plasma levels of beta-thromboglobulin and platelet factor 4, two proteins secreted concomitant with aggregation. beta-thromboglobulin diminished 7.5 +/- 11.0 ng/ml and platelet factor 7.6 +/- 11.0 ng/ml during selenium supplementation despite no change in platelet glutathione peroxidase activity. These data support the concept that selenium nutritional status should be assessed not only by blood selenium content but also by selenium-dependent enzyme activity or selenium-dependent biologic effect.     

Antihuman plasma glutathione peroxidase antibodies: immunologic investigations to determine plasma glutathione peroxidase protein and selenium content in plasma

Plasma glutathione peroxidase (GSHPx) (glutathione: H2O2 oxidoreductase) is a unique selenoglycoprotein. Treatment of this enzyme with glycopeptidase F partially deglycosylates it and establishes the presence of N-linked sugar moieties. Antibodies raised in a rabbit against the purified enzyme from plasma were found to be specific, noninhibitory, and capable of precipitating the enzymatic activity. The antibodies precipitated greater than 90% of the GSHPx activity of normal plasma, thus indicating that the selenoenzyme is the main if not the sole GSHPx activity of plasma. The antibodies did not precipitate RBC GSHPx. A slight cross-reactivity of the antibodies was found with rat plasma GSHPx. A GSHPx activity precipitation assay of normal plasma in the presence of selenium (Se)-deficient plasma indicates that no cross-reactive protein in the Se-deficient plasma interferes with the precipitation of the GSHPx activity from normal plasma. Thus, GSHPx protein as well as activity is deficient in plasma in the absence of Se. Antibodies against GSHPx either from RBCs or from plasma were used to specifically immunoprecipitate most of the GSHPx activity from RBCs or plasma, respectively, in healthy individuals to determine the amount of Se associated with the protein. GSHPx accounts for approximately 15% of the Se in RBCs and 12% of the Se in plasma. Thus, in normal individuals, these proteins account for only a fraction of plasma and RBC Se.     

氟中毒大鼠心电图改变及其硒的影响

为观察氟中毒大鼠心电图变化及其Ｓｅ的影响，两组Ｗｉｓｔａｒ大鼠饮用１．５８、２．６３ｍｇ／Ｌ高Ｆ＾－水，另两组鼠饮高Ｆ＾－水加饲０．０２５ｍｇ／ｋｇＳｅ饲料，在实验前及实验４、８、１２个月进描记心电图。结果两组大鼠随摄氟时间延长Ｔ波降低，Ｑ－Ｔ间期缩短。