克山病病区粮食中补充蛋氨酸对大鼠膳食硒生物利用的影响

为研究在克山病病区粮食中补充蛋氨酸对大鼠组织硒和谷胱甘肽过氧化物酶 (GPX)活性的影响 ,用克山病病区生产的低硒粮食为主配成低硒基础饲料 ,其硒含量为 0 .0 0 7mg/kg。在此基础上添加不同量的硒蛋氨酸 ,使饲料硒水平分别达到 0 .0 0 7、0 .0 6和 0 .5 0 mg/kg。每一硒水平又分别补充或不补充 4g/kg DL -蛋氨酸 ,配制成含不同硒和蛋氨酸的 6种饲料 ,分别喂养雄性 Wistar断乳大鼠 8周。结果在饲料硒水平为0 .0 0 7mg/kg时 ,补充蛋氨酸组动物除肌肉硒含量低于未补充组外 ,其它组织硒含量和各组织 GPX活力与不补充蛋氨酸动物无显著差异 ;在饲料硒水平为 0 .0 6 mg/kg时 ,补充蛋氨酸组动物组织中的硒含量出现了重新分布 ,最明显的是补充蛋氨酸组动物肌肉的硒含量减少 ,而肝脏和血硒含量增加 ,且各组织中 GPX活力显著大于未补充蛋氨酸组的动物 ;在饲料硒水平为 0 .5 0 mg/kg时 ,补充蛋氨酸组动物组织中硒含量有不同程度下降 ,但 GPX活力仍保持不变。研究结果认为病区粮食中蛋氨酸不足时 ,机体首先利用膳食中的硒蛋氨酸(谷类食物中硒的主要形式 )以替代蛋氨酸参与组织蛋白质的合成。补充蛋氨酸后 ,硒蛋氨酸即可发挥其应有生理功能。进一步提示病区粮食中蛋氨酸不足可能是与克山病发病有关的另一因素。     

大鼠硒耗竭过程中不同组织硒蛋白利用硒的优先性

以低硒酵母配制的低硒基础饲料（含硒量为０．０１ｍｇ／ｋｇ）和在此基础上加亚硒酸钠配成硒水平为０．５０ｍｇ／ｋｇ的足硒饲料来喂养雄性Ｗｉｓｔａｒ断乳大鼠。于０、１、２、４、６、８、１２、１５、１７、１９、２０和２４周时处死大鼠取其组织,分别对各种组织中的硒、细胞内谷胱甘肽过氧化物酶（ｃＧＰＸ）、细胞外谷胱甘肽过氧化物酶（ｅＧＰＸ）、磷脂氢谷胱甘肽过氧化物酶（ＰＨＧＰＸ）、Ⅰ型脱碘酶（ＩＤⅠ）和Ⅱ型脱碘酶（ＩＤⅡ）活性进行动态观察。结果发现睾丸中的硒和脑垂体中的ｃＧＰＸ在耗竭过程中降低速度较其它组织慢,且降低幅度较小;而硒蛋白中ＩＤⅠ和ＰＨＧＰＸ对硒的利用优先于ｃＧＰＸ和ｅＧＰＸ,ＰＨＧＰＸ和ＩＤⅠ的功能可能比ｃＧＰＸ和ｅＧＰＸ更重要。     

氟对大鼠硒代谢的影响

为研究氟和硒的相互作用，按３×３析因实验设计，将氟和硒相配成９种实验饲料（氟水平为１、１５和６０ｍｇ／ｋｇ饲料，硒水平为０．０３、０．３和５．０ｍｇ／ｋｇ饲料），分别给予雄性Ｗｉｓｔａｒ大鼠，饲养１３周。结果显示：氟（６０ｍｇ／ｋｇ）虽对食用不同硒水平饲料大鼠体重增长和进食量无影响，但氟可缓解动物因硒中毒而引起全血谷胱甘肽含量和肛谷胱甘肽过氧化物酶活力下降，并且组织中有硒含量减少和毛硒含量增加的趋势。另一方面可见硒（５．０ｍｇ／ｋｇ饲料）能降低氟在骨骼中的积蓄。由此可认为氟和硒在体内存在拮抗作用。     

Bioavailability of selenium from raw and cooked ground beef assessed in selenium-deficient Fischer rats.

The literature on the bioavailability of selenium (Se) from meats, especially beef, is meager, and that which existed when this research began suggested that Se was not highly bioavailable. In addition, much of the analytical values for Se in beef predated the Food and Drug Administration's 1973 approval of Se as an additive to feeds and mineral premixes of livestock.

One hundred and thirty-six weanling female Fischer 344 rats were divided into two dietary groups: the selenium deficient group in which animals were fed a torula yeast (TY) basal diet which contained 0.008 mg/kg Se and the control group in which animals were fed the TY diet to which was added 0.10 mg/kg Se as sodium selenite.

After 6 weeks of dietary treatment liver glutathione peroxidase (GSHPx) activity had fallen in the Se-deficient rats to 2.4% of that of control rats. At this time (week 6) rats from the Se-deficient TY diet were refed diets containing 0.10 mg/kg Se as selenite, selenate, raw or cooked ground beef that had been freeze-dried. During the Se-repletion period rats were sacrificed at weeks 1, 3, 5 and 8. Liver GSHPx activity and total Se levels in liver and muscle tissue were the criteria of Se bioavailability. After 8 weeks of Se resupplementation the recovery of liver GSHPx activity compared to the control animals (set at 100%) were selenite (98%, p > 0.05), selenate (117%, p < 0.05), raw beef (127%, p < 0.05) and cooked ground beef (139%, p < 0.05). Total Se in both liver and muscle tissue reflected the liver GSHPx activity with the total Se concentration in tissues being highest for cooked beef.

The data suggest that bioavailability of Se from ground beef is greater than that from either selenite or selenate.     

Modulation of selenium-dependent glutathione peroxidase by perfluorodecanoic acid in rats: effect of dietary selenium

Forty-eight male Sprague-Dawley rats fed a diet containing 0.4, 0.2 or 1.0 mg of selenium (Se)/kg of diet were injected with a single dose (35 mg/kg) of perfluorodecanoic acid (PFDA) in corn oil and killed 2 wk later. Control animals were pair-fed and treated with an equal volume of vehicle. PFDA treatment significantly increased Se-dependent glutathione peroxidase (Se-GSHPx) activity in liver cytosol of rats fed the 0.04 mg of Se/kg of diet but not in rats fed the other diets. The increase in liver cytosolic Se-GSHPx activity in rats fed 0.04 mg of Se/kg of diet paralleled increases in Se content and serum Se-GSHPx activity. Determination of Se-GSHPx by an enzyme-linked immunosorbent assay showed that PFDA caused a decrease in Se-GSHPx protein in rats fed 0.2 or 1.0 mg of Se/kg of diet but not in rats fed 0.04 mg of Se/kg of diet. Further analysis revealed that the ratio of Se-GSHPx activity to antibody-reactive protein was increased by PFDA in all three groups. The in vitro addition of PFDA directly to the assay mixture for Se-GSHPx activity did not produce any effect. Reduced glutathione was significantly increased by PFDA treatment in all three groups. These data show that PFDA affects the Se content, Se-GSHPx activity and Se-GSHPx protein in rat liver and that the effect is dependent on the dietary/hepatic Se level.     

不同硒水平饲料对大鼠肝脏谷胱甘肽过氧化物酶和脱碘酶活性的影响

为了解不同饲料硒水平对大鼠肝脏中谷胱甘肽过氧化物酶和脱碘酶活性的影响及确定它们发挥最佳活性时的最低饲料硒水平。５４只体重为５０～６０ｇ的雄性断孔Ｗｉｓｔａｒ大鼠分成９组，分别喂以９种含硒水平为０．０１，０．０２，０．０３，０．０４，０．０５，０．０６，０．１，０．２和５ｍｇ／ｋｇ的不同饲料。实验持续２０周。９组动物２０周的体重增长除５ｍｇ／ｋｇ饲料组与０．１、０．２ｍｇ／ｋｇ饲料组之间有差异外，其余均没有显著性差异。谷胱甘肽过氧化物酶的活性随着饲料硒水平的升高而升高，当饲料硒含量为０．１，０．２和５ｍｇ／ｋｇ饲料时，活性达到最高。因此它发挥正常活性范围的最低饲料硒需要量为０．１ｍｇ／ｋｇ。９个组脱碘酶的活性（ｎｍｏｌ／ｍｉｎ．ｇ）在０．０５至０．２ｍｇ／ｋｇ饲料时活性最高，在５ｍｇ／ｋｇ饲料时酶活性降低，发挥最佳活性最低饲料硒需要量为０．０５ｍｇ／ｋｇ。     

Effects of dietary zinc and cadmium on tissue selenium concentration and glutathione peroxidase activity in rats fed DL-selenomethionine or sodium selenite.

The effects of dietary zinc (Zn) and cadmium (Cd) on tissue selenium (Se) concentration and glutathione peroxidase (GSH-Px) activity were studied in weanling male Wistar rats. One group of rats was fed a purified diet based on casein and sucrose, and the other rats used in a 2 x 2 x 2 factorial arrangement of treatment were fed this diet supplemented with 0.1 mg Se/kg, either as DL-selenomethionine or sodium selenite and plus 100 mg Zn/kg as zinc sulfate or 5 mg Cd/kg as cadmium chloride or both for 4 weeks. Se concentrations in plasma, erythrocytes, muscle, heart, and liver were significantly elevated by Zn. Cd significantly decreased Se concentration in muscle. Addition of Zn to the diets markedly increased (p less than 0.001) hepatic GSH-Px activity. However, Cd in the diets produced a significant increase (p less than 0.001) in erythrocyte GSH-Px activity. These results indicate that Zn level of marginal deficiency (8.6 mg/kg diet) can decrease Se availability and a small excess of Zn increases Se availability for hepatic GSH-Px activity.     

Effects of dietary copper, cadmium, iron, molybdenum and manganese on selenium utilization by the rat

The possible antagonistic effects of different dietary concentrations of copper (1.3-200 mg/kg), cadmium (1-5 mg/kg), iron (20-500 mg/kg), molybdenum (0.3-50 mg/kg) and manganese (0.2-200 mg/kg) on selenium utilization by the rat were studied by the measurement of the absorption and organ distribution of dietary selenium as [75Se]selenite and by effects on organ glutathione peroxidase (GSH-Px: EC 1.11.1.9) activity. Although a high concentration of copper (200 mg/kg) in the diet did not alter the percentage absorption and total-body retention of doses of 75SeO3(2)- by rats, after such treatment tissue 75Se distribution was changed and was lower total selenium in some tissues. After copper treatment (200 mg/kg diet) GSH-Px activity of liver, testis, kidney and whole blood was also lower. Dietary cadmium, iron, molybdenum and manganese at the concentrations investigated had no significant effects on selenium metabolism. Thus it is unlikely that copper, cadmium, iron, molybdenum and manganese at normal dietary concentrations will have a major effect on selenium metabolism in the rat, especially if adequate amounts of selenium are being consumed.     

Effects of dietary selenium on DMBA-induced carcinogenesis in rats fed a diet high in mixed fats

The effects of selenium intake on 7,12-dimethylbenz(a)anthracene (DMBA)-induced mammary carcinogenesis were examined in rats fed a diet high in mixed fats and representative of that consumed in North America. Six groups of 20 rats were fed an AIN-76 diet modified to contain 20% fat from lard:corn oil (3:1 wt/wt) and various amounts of selenium (0.1, 0.035, 0.1, 1.0, 2.0 or 4.0 mg Se/kg diet). At wk 5, animals in groups 2-6 were dosed with 4.32 mg of DMBA. Serum clinical parameters and the activities of plasma selenium-dependent and total glutathione peroxidase (GSHPx), erythrocyte GSHPx and superoxide dismutase (SOD) were determined every 4 wk for 25 wk. The extent of lipid peroxidation was determined by measuring urinary malondialdehyde during wk 13 and 24, and erythrocyte malondialdehyde at wk 25. Erythrocyte GSHPx was found to be a better indicator of selenium status than plasma activity, while SOD did not vary with dietary selenium. The group of animals fed 4.0 mg Se/kg diet had reduced numbers of tumors (P less than 0.01), but this reduction was associated with evidence of chronic selenium toxicity. Variations in GSHPx activity with dietary selenium did not result in differences in tumor incidence, nor in changes in lipid peroxidation in the other groups. Thus, nontoxic levels of selenium do not appear to offer any protective effect during carcinogenesis in rats fed a casein-based diet similar in fat content to that consumed by North Americans.     

Effect of chronic ethanol consumption on selenium status and utilization in rats

Effects of chronic ingestion of 2 levels of alcohol on selenium (Se) utilization were determined in initially Se-depleted rats. Male weanling rats were fed ad lib a Se deficient (0.012 mg/kg) basal diet for 4 weeks and then were meal-fed low or marginally adequate Se in the form of high Se yeast for 4 weeks. During Se repletion, ethanol, which replaced medium-chain triglycerides in the diet, provided 10 or 20 percent of food energy. The basal diet provided 80% of food energy as well as adequate protein, vitamins and minerals. In rats given adequate Se moderate chronic ethanol consumption did not influence Se absorption or retention, but increasing ethanol level raised Se in liver and whole blood in a linear fashion and in kidney in a quadratic manner. In this rat model measures of Se status were reduced by low Se intake, not chronic moderate ethanol ingestion.     

亚硒酸钠和硒蛋氨酸的毒性比较

目的　比较亚硒酸钠和硒蛋氨酸毒性差异以及探讨硒中毒的指标。方法　将断乳Wistar大鼠随机分为 7组 ,每组 14只 ,雌雄各半。其中一组为对照组 ,另外六组分别给予含硒 3、6、10mg kg的亚硒酸钠或硒蛋氨酸饲料 ,于第 12周将其处死。结果　当饲料硒水平达到 3mg kg时 ,动物肝脏出现病理变化 ,在Se6mg kg时 ,体重才出现下降。饲料硒水平为 6、10mg kg时 ,同一饲料硒水平的亚硒酸钠组大鼠体重小于硒蛋氨酸组。饲料硒水平为 3、6mg kg时 ,硒蛋氨酸组大鼠的肝脏病理改变轻于亚硒酸钠组 ,雄性大鼠轻于雌性。亚硒酸钠组较硒蛋氨酸组或雌性大鼠较雄性大鼠在肝脏体重比方面变化更为明显。除雌性大鼠肝脏谷胱甘肽过氧化物酶 (GPX)活性随硒水平升高而降低外 ,其它补硒各组肝、红细胞、血浆GPX活性具有随硒水平的升高而升高的趋势。结论　大鼠硒中毒的剂量为Se 3mg kg,硒蛋氨酸的毒性小于亚硒酸钠 ,雌性大鼠对硒毒性更为敏感     

Effect of selenite, vitamin E and N,N'-diphenyl-p-phenylenediamine on liver organic solvent-soluble lipofuscin pigments in mice

The present experiment was designed to investigate the effect of selenium (Se) supplementation, as sodium selenite, on organic solvent-soluble lipofuscin pigment (OLP) accumulation and glutathione peroxidase (GSH-Px) activity in the livers of mice fed varying levels of vitamin E or N,N'-diphenyl-p-phenylenediamine (DPPD). Four groups of 16 female, weanling mice each were fed either a vitamin E-deficient diet, a diet supplemented with 30 mg/kg or 300 mg/kg vitamin E (as RRR-alpha-tocopheryl acetate), or a diet supplemented with 30 mg/kg DPPD. Each diet contained 0.05 ppm Se. At 5 months of age, eight animals from each dietary group were supplemented with an additional 0.1 ppm Se, as sodium selenite, in their drinking water. The remaining animals were fed their original diets through the 9-month experimental period. Selenite supplementation resulted in a significant increase in OLP concentration and GSH-Px activity in the liver of mice fed vitamin E- or DPPD-supplemented diets. Normal levels of vitamin E and DPPD (30 mg/kg) were not sufficient to protect against the oxidative effects of selenite; however, 10 times the normal level of vitamin E (300 mg/kg) markedly suppressed this oxidative effect.     

Effects of dietary selenium and vitamin E on hepatic mixed-function oxidase activities and in vivo covalent binding of aflatoxin B1 in rats

Male weanling fischer-344 rats were fed a selenium (Se)-vitamin E (VE) deficient Torula yeast basal diet or that diet supplemented with a graded levels of SE (0.2-6.0 ppm as Na2SeO3) or VE (100 iu/kg as all-rac-2-tocopheryl acetate), or both, for 4 or 6 weeks. Se deficiency and excess (6.0 ppm) markedly depressed in vivo covalent binding of aflatoxin (AFB1) to macromolecules in livers of rats killed 2 hours after an i.p. dose of 1 mg/kg tritiated AFB1. VE supplementation had no effect. Prior phenobarbital (PB) treatment generally decreased adducts without changing diet-related trends. Some hepatic enzyme capabilities were also measured. Cytochrome b5 content and cytochrome c reductase activity were unaffected by diet. VE increased cytochrome P-450 content, ethylmorphine N-demethylase and benz(alpha)pyrene hydroxylase activities; all these were unaffected by Se levels. Se deficiency and excess (but not VE deficiency) increased glucuronyl transferase. PB induction affected all diet groups and was more in agreement with MFO activity than transferase. Adduct formation was more consistently related to transferase activity than to MFO activities. The contrasting effects of SE and VE on AFB1 adducts in rats and chicks are discussed.     

大鼠脱碘酶、硒蛋白P和硒蛋白W正常表达所需的最低饲料硒水平

目的　研究能满足大鼠脱碘酶、硒蛋白 P和硒蛋白 W合成所需的饲料硒水平。方法　以低硒酵母合成饲料加不同剂量的亚硒酸钠配成硒水平分别为 0 .0 1、0 .0 2、0 .0 3、0 .0 4、0 .0 5、0 .0 6、0 .1 0和 0 .2 0 mg/kg的 8种饲料喂养雄性 wistar断乳大鼠。 2 0周时杀死大鼠取其组织 ,分别对各种组织中的 型、 型和 型脱碘酶、硒蛋白 P的 m RNA以及硒蛋白 W的 m RNA的水平进行测定。结果　能满足大鼠各组织 型、 型和 型脱碘酶发挥最佳活性时的最低饲料硒水平为0 .0 5mg/kg,而硒蛋白 P的 m RNA以及硒蛋白 W的 m RNA正常表达所需的最低饲料硒水平分别为 0 .0 5和 0 .0 6mg/kg。结论　饲料硒水平达到 0 .1 mg/kg可满足大鼠脱碘酶、硒蛋白 P和硒蛋白 W的合成。     

Effect of dietary methionine on tissue selenium and glutathione peroxidase (EC 1.11.1.9) activity in rats given selenomethionine

1. The effect of dietary methionine on the utilization of selenium from dietary selenomethionine [( Se]Met) for tissue Se deposition and for glutathione peroxidase (EC 1.11.1.9; GSH-Px) synthesis was studied in male weanling rats. 2. When rats were given 0.5 mg Se as [Se]Met/kg diet supplemented with 0, 4 or 9 g methionine/kg, Se in plasma, erythrocytes, liver and muscle increased significantly over the 20 d period for all methionine-treatment groups. The increases in erythrocyte and muscle Se, however, were significantly higher in rats fed on the methionine-deficient diet compared with the methionine-supplemented diets. 3. In contrast to the increases in tissue Se, GSH-Px activity in liver, plasma and muscle decreased in methionine-deficient rats given 0.5 mg Se as [Se]Met/kg whereas GSH-Px activity was maintained or increased in rats supplemented with methionine. 4. The percentage of tissue Se associated with GSH-Px was calculated from the measured Se concentration and GSH-Px activity. A significantly lower percentage of Se was associated with GSH-Px in methionine-deficient rats compared with methionine-supplemented rats. 5. These results show that Se from dietary [Se]Met is preferentially incorporated into body proteins rather than used for GSH-Px synthesis when methionine is limiting in the diet. 6. These results further suggest that [Se]Met might not be the optimum Se compound to use for Se supplementation because metabolism of dietary [Se]Met to a biochemically active form, such as GSH-Px, was impaired when [Se]Met was provided in diets low in methionine.     

Influence of dietary methionine on the metabolism of selenomethionine in rats

To determine the influence of methionine on selenomethionine (SeMet) metabolism, weanling male rats were fed for 8 wk a basal diet marginally deficient in sulfur amino acids, containing 2.0 micrograms selenium (Se)/g as DL-SeMet and supplemented with 0, 0.3, 0.6 or 1.2% DL-methionine. Increased dietary methionine caused decreased selenium deposition in all tissues examined but increased glutathione peroxidase (GSHPx, EC 1.11.1.9) activity in testes, liver and lungs. A positive correlation was found between dietary methionine and the calculated percentage of selenium associated with GSHPx. In a second experiment, 75SeMet was injected into weanling male rats which had been fed the basal diet containing 2.0 micrograms selenium as DL-SeMet with or without the addition of 1.0% methionine. The selenoamino acid content of tissues and the distribution of 75Se in erythrocyte proteins were determined. In comparison to the rats fed the basal diet without added methionine, significantly more 75Se-selenocysteine was found in liver and muscle, more 75Se was found in erythrocyte GSHPx and less 75Se was found in erythrocyte hemoglobin of rats fed 1.0% methionine. These data suggest that methionine diverts SeMet from incorporation into general proteins and enhances its conversion to selenocysteine for specific selenium-requiring proteins, such as GSHPx.     

Dietary selenium requirement of fingerling channel catfish

Two experiments were conducted in aquaria to determine the minimum dietary selenium requirement of fingerling channel catfish (Ictalurus punctatus). Casein-gelatin diets containing graded levels of supplemental selenium (as Na2SeO3) ranging from 0 to 15 mg/kg were fed to catfish for 15 weeks in experiment 1 to broadly define their selenium requirement and toxicity levels. Although growth of catfish was affected by dietary selenium level, significant differences in weight gain were not easily discernible due to variability among the groups of fish. Weight gain data generally indicated that the basal diet containing 0.06 mg Se/kg diet caused growth depression, and a supplemental selenium level of 15 mg/kg also caused a reduced growth response, which indicated selenium toxicity. Selenium concentrations in edible muscle tissue increased almost linearly with increasing dietary selenium levels. Liver and plasma selenium-dependent glutathione peroxidase (Se GSH-Px) activities indicated the selenium requirement of fingerling channel catfish was between 0.1 and 0.5 mg Se/kg diet. In experiment 2, casein-gelatin diets containing incremental levels of supplemental selenium were fed to catfish for 14 weeks to more precisely determine their minimum dietary selenium requirement. Growth data and liver and plasma Se GSH-Px activities indicated that the minimum selenium requirement of fingerling channel catfish fed adequate vitamin E was 0.25 mg Se/kg dry diet. Based on these data, it appears that selenium supplementation of commercial catfish feeds is warranted.     

Type I iodothyronine deiodinase activity after high selenium intake, and relations between selenium and iodine metabolism in rats.

Type I iodothyronine deiodinase (I-D), which catalyzes the production of the thyroid hormone 3,3',5-triiodothyronine from thyroxine, has recently been identified as a selenoenzyme. It is therefore of interest to investigate the relationships between selenium and iodine metabolism. In the livers of Se-deficient rats I-D activity was inhibited; the production of 3,3',5-triiodothyronine and 3,3'-diiodothyronine from added thyroxine was decreased by greater than 95% relative to Se-adequate controls. The hepatic I-D activity was also reduced in rats fed a diet with a low iodine concentration. Unaltered glutathione peroxidase activities in liver and plasma of these rats suggest, however, that with normal Se intake this metabolic pathway of Se is not affected by iodine depletion. When rats were administered 75Se-labeled selenium at levels equal to the amounts ingested from diets with Se concentrations of 0.3 or 2 mg Se/kg, greater Se concentrations were found in the thyroid and liver of the animals receiving the higher dosage. The thyroidal 3,3',5-triiodothyronine and thyroxine concentrations, however, were comparable in rats fed diets with 0.3 mg Se/kg diet as selenite and 2 mg Se/kg as selenite or L-selenomethionine. The measurement of the hepatic I-D and glutathione peroxidase activities in these animals showed that excessive Se supply does not elevate the activities of the two enzymes but might even have the opposite effect. At high Se intake tissue Se concentration cannot therefore be used as indicator of the selenoenzyme activities.     

大鼠谷胱苷肽过氧化物酶发挥最佳活性所需的最低饲料硒水平

目的　测定大鼠谷胱苷肽过氧化物酶活性达到最高时所需的饲料硒水平。方法　以低硒酵母配制低硒基础饲料 ,在此基础上加不同剂量的亚硒酸钠配成 8种不同硒水平的饲料来喂养雄性 Wistar断乳大鼠。饲料硒水平分别为 0 .0 1、0 .0 2、0 .0 3、0 .0 4、0 .0 5、0 .0 6、0 .1 0和 0 .2 0mg/kg。 2 0周时处死大鼠 ,分别对各种组织中的硒 ( Se)、细胞内谷胱苷肽过氧化物酶 ( c GPX)、细胞外谷胱甘肽过氧化物酶 ( e GPX)、磷脂氢谷胱甘肽过氧化物酶 ( PHGPX)活性进行测定。结果　在Wistar大鼠的各种组织中 c GPX发挥最佳活性时的最低饲料硒水平高于其它两种硒蛋白。雄性Wistar大鼠发挥最佳 c GPX活性所需最低饲料硒水平为 0 .2 0 mg/kg,e GPX和 PHGPX发挥最佳活性所需的最低饲料硒水平分别为 0 .0 4和 0 .0 5mg/kg。结论　确保满足雄性大鼠 c GPX、e GPX和 PHGPX三种硒蛋白合成的饲料硒水平为 0 .2 0 mg/kg。     

Dietary selenium intake controls rat plasma selenoprotein P concentration

The purpose of this study was to determine the effect of dietary selenium on selenoprotein P concentration. Selenoprotein P was quantitated in plasma by radioimmunoassay. Selenium-dependent glutathione peroxidase activity in plasma and liver 105,000 x g supernatant was measured for comparison. Weanling male rats were fed a selenium-deficient diet or a control diet that contained 0.5 mg selenium/kg as Na2SeO4. The concentration of selenoprotein P fell at approximately the same rate in the rats fed the selenium-deficient diet as did plasma glutathione peroxidase activity. Groups of weanling rats were fed different levels of selenium for 8 wk. Selenoprotein P concentration was proportional to dietary selenium level up to 0.1 mg/kg and was a greater percentage of control values than was glutathione peroxidase activity. No increment in selenoprotein P concentration occurred between 0.1 and 0.5 mg selenium/kg diet. These results indicate that the concentration of selenoprotein P in the plasma is directly dependent on selenium supply in the diet up to 0.1 mg/kg. There is overlap between the dietary selenium ranges in which selenoprotein P concentration and glutathione peroxidase activity increase, but the selenoprotein P range is lower than the glutathione peroxidase range.