Relation between erythrocyte selenium concentrations and glutathione peroxidase (EC 1.11.1.9) activities of New Zealand residents and visitors to New Zealand.

1. Erythrocyte, plasma and whole blood selenium concentrations and glutathione peroxidase (EC 1.11.1.9; GSHPx) activities were measured (1) in 104 healthy New Zealand residents living in Otago, a low-soil-Se area (2) in sixty-four surgical patients, including nineteen patients on total parenteral nutrition and twenty-three cancer patients (3) in fifty-two 'overseas subjects' (twenty-five visitors to Otago from outside New Zealand and twenty-seven Otago residents on return from overseas travel). 2. Blood Se concentrations reflected dietary Se intake; means for Otago patients, healthy subjects and overseas subjects were different 0.043, 0.059, 0.136 micrograms Se/ml blood respectively) and mean for overseas residents was greater than for New Zealand overseas travellers. 3. Erythrocyte Se concentration was always greater than plasma Se, and plasma Se was a smaller proportion of erythrocyte Se for patients compared with the controls. 4. GSHPx activities were different in the three groups, and varied directly with erythrocyte Se until a plateau was reached at approximately 0.14 micrograms Se/ml erythrocytes. 5. Overseas subjects showed no relationship between erythrocyte Se and GSHPx activity. This agrees with some overseas studies and the significance of this finding is discussed. 6. Plasma Se concentration remained the most sensitivie index of short-term changes in Se status, and erythrocyte Se and GSHPx activities for long-term changes in New Zealand subjects. Use of these measurements for overseas subjects with higher blood levels is discussed.     

Effects of supplementation with high-selenium wheat bread on selenium, glutathione peroxidase and related enzymes in blood components of New Zealand residents

The effects of supplementation with high-Se wheat bread on selenium (Se) concentrations, glutathione peroxidase (EC 1.11.1.9, GSHPx) activities and related enzymes in the prevention of lipid peroxidation were studied. Four New Zealand women were supplemented with 200 micrograms Se daily for 8-13 weeks followed by a post-dosing period of 9-12 weeks. GSHPx activities increased in whole blood, erythrocytes, plasma and platelets of all subjects but increases were considerably less than those of Se concentrations in whole blood, plasma and erythrocytes. During the post-dosing period Se concentrations and GSHPx activities fell to levels which were in most cases somewhat higher than baseline values. Glutathione-S-transferase activities in erythrocytes, plasma and platelets did not change during the study, nor did superoxide dismutase in erythrocytes and platelets, erythrocyte catalase or plasma alpha-tocopherol. Thus Se supplementation of healthy New Zealand subjects increased GSHPx activities but did not produce any adaptive changes in other components of the lipid peroxidation defense mechanisms.     

Effect of chemical form of selenium on tissue glutathione peroxidase activity in developing rats

Two experiments were conducted to determine the effect of various forms of selenium (Se) on the activity of glutathione peroxidase (GSHPx) in liver, heart, kidney and eyes of the developing rat. In experiment 1, throughout mating, pregnancy and lactation, female rats consumed one of three diets: basal (less than 0.05 microgram Se/g); selenite (0.15 microgram Se/g) and selenomethionine (0.15 microgram Se/g). Some pups born to dams in the basal group were also given intraperitoneal doses of saline, selenite or selenomethionine. GSHPx activity was measured in tissues from fetuses, 7-d-old and 14-d-old nursing pups and the dams. In all tissues studied, GSHPx activity was highest in the 14-d-old pups whose mothers were in the selenomethionine group. Rat pups given intraperitoneal selenite (3 micrograms/kg body weight) had higher liver and kidney GSHPx activity than pups given the same amount of selenium as intraperitoneal selenomethionine. In experiment 2, all dams were fed the same basal diet, and pups were weaned to diets containing one of two levels of selenium (0.1 or 0.2 microgram/g), one of three forms of selenium (selenite, selenomethionine or selenocystine) or no added selenium. After 14 d of repletion, the highest level of hepatic GSHPx activity occurred in the selenite group and the lowest in the basal diet group. After 21 d of repletion, renal GSHPx activity was lowest in the basal group followed by the selenocystine group. The highest tissue selenium concentration was found in kidney tissues of the selenocystine group. These data support the hypothesis that these dietary forms of selenium are differentially available for GSHPx activity.     

Brazil nuts: an effective way to improve selenium status

BACKGROUND: Brazil nuts provide a rich natural source of selenium, yet no studies have investigated the bioavailability of selenium in humans. OBJECTIVE: We investigated the efficacy of Brazil nuts in increasing selenium status in comparison with selenomethionine. DESIGN: A randomized controlled trial was conducted with 59 New Zealand adults. Participants consumed 2 Brazil nuts thought to provide approximately 100 mug Se, 100 mug Se as selenomethionine, or placebo daily for 12 wk. Actual intake from nuts averaged 53 mug Se/d (possible range: 20-84 mug Se). Plasma selenium and plasma and whole blood glutathione peroxidase (GPx) activities were measured at baseline and at 2, 4, 8, and 12 wk, and effects of treatments were compared. RESULTS: Plasma selenium increased by 64.2%, 61.0%, and 7.6%; plasma GPx by 8.3%, 3.4%, and -1.2%; and whole blood GPx by 13.2%, 5.3%, and 1.9% in the Brazil nut, selenomethionine, and placebo groups, respectively. Change over time at 12 wk in plasma selenium (P < 0.0001 for both groups) and plasma GPx activity in the Brazil nut (P < 0.001) and selenomethionine (P = 0.014) groups differed significantly from the placebo group but not from each other. The change in whole blood GPx activity was greater in the Brazil nut group than in the placebo (P = 0.002) and selenomethionine (P = 0.032) groups. CONCLUSION: Consumption of 2 Brazil nuts daily is as effective for increasing selenium status and enhancing GPx activity as 100 mug Se as selenomethionine. Inclusion of this high-selenium food in the diet could avoid the need for fortification or supplements to improve the selenium status of New Zealanders.     

An evaluation of the bioavailability of selenium in high-selenium yeast.

The bioavailability of selenium (Se) in high-Se yeast (SeY) was evaluated by measuring tissue Se accumulation and glutathione peroxidase (GSHPx) activity. For 4 weeks, 4-week-old male Wistar rats were fed a Torula yeast-based Se-deficient diet (basal diet) or a diet supplemented with a graded level (0.04, 0.08, 0.16, and 0.32 microgram/g) of Se as either sodium selenite or SeY, which was obtained from two different sources. Se supplementation did not influence growth, hematological values, or serum biochemical tests. Se contents and GSHPx activities in the liver, serum, and erythrocytes increased gradually with increases of the supplemented Se. At lower Se levels (0.04 and 0.08 microgram/g), selenite produced higher Se deposition and higher GSHPx activities than SeY did, but at a higher Se level (0.32 microgram/g), SeY showed higher measures. Strong correlations were detected between the supplementary Se levels and the tissue Se contents or GSHPX activities when the regression was fitted to this equation: R-Rb = m log X + k, where R represented tissue Se content or GSHPx activity in rats fed the diet supplemented with Se at X level, Rb corresponding mean value in rats fed the basal diet, m slope, and k constant. The bioavailability of Se in SeY, as assessed by slope ratio analysis using selenite as a reference Se, was 135% to 165% in the tissue Se content and 105% to 197% in the GSHPx activities. These results indicate that Se in SeY is more bioavailable than selenite Se, and therefore it is the preferred form for supplementation.     

Effectiveness of selenium supplements in a low-selenium area of China

BACKGROUND: Selenium is an essential micronutrient with a recommended dietary allowance for adults of 55 mug/d. It functions as an essential constituent of selenoproteins. Although there is no evidence of selenium deficiency in the United States, people in many other areas of the world are selenium deficient, with the consequence that they are unable to express their selenoproteins fully. OBJECTIVE: We carried out a supplementation trial in a selenium-deficient population in China to assess the requirement for selenium as selenite and as selenomethionine. DESIGN: One hundred twenty subjects with an average selenium intake of 10 mug/d were randomly assigned and administered tablets containing no selenium or amounts as high as 66 mug Se/d for 20 wk. Plasma was sampled before supplementation and at 4-wk intervals during supplementation and was assayed for the 2 plasma selenoproteins, glutathione peroxidase and selenoprotein P. RESULTS: Full expression of glutathione peroxidase was achieved with 37 mug Se/d as selenomethionine and with 66 mug/d as selenite. Full expression of selenoprotein P was not achieved at the highest doses of either form. CONCLUSIONS: Full expression of selenoprotein P requires a greater selenium intake than does full expression of plasma glutathione peroxidase. This suggests that selenoprotein P is a better indicator of selenium nutritional status than is glutathione peroxidase and that the recommended dietary allowance of selenium, which was set with the use of glutathione peroxidase as the index of selenium status, should be revised. Selenium as selenomethionine had nearly twice the bioavailability of selenium as selenite.     

On supplementing the selenium intake of New Zealanders. 2. Prolonged metabolic experiments with daily supplements of selenomethionine, selenite and fish

1. The daily intake of selenium by three subjects was supplemented with 100 microgram Se as selenomethionine (Semet-Se) or sodium selenite (selenite-Se)/d for 10-11 weeks, or with 65 microgram Se as in mackerel (Scomber japonicus) (fish-Se)/d for 4 weeks. 2. Urinary and faecal excretion of Se was measured and also Se concentration in whole blood, plasma and erythrocytes. Measurements on blood were made at intervals after supplementation had ceased. 3. Selenite-Se was not as well absorbed (0.46 of the intake) during the first 4 weeks as Semet-Se (0.75 of the intake) and fish Se (0.66 of the intake). 4. Blood Se increased steadily with Semet-Se, from 0.08 to 0.18 microgram Se/ml, but more slowly with selenite-Se, reaching a plateau in 7-8 weeks at 0.11 microgram Se/ml. Plasma Se increased more rapidly with Semet-Se than with selenite-Se, so that initially with Semet-Se plasma Se was greater than erythrocyte Se. 5. Daily urinary excretion increased with all forms of supplement, with initially a greater proportion of absorbed selenite-Se being excreted than Semet-Se or fish-Se. A close relationship was found between plasma Se and 24 h urinary excretion. The findings suggested that there was a rapid initial excretion of presumably unbound Se then a slower excretion of residual unbound, loosely bound or bound Se. 6. Total retentions of 3.5 mg selenite-Se and 4.5 mg Semet-Se were large when compared with an estimate of body content of 6 mg Se, derived in another paper (Stewart, Griffiths, Thomson & Robinson, 1978). Retention of Semet-Se and fish-Se appeared to be reflected in blood Se, whereas for selenite-Se, blood Se reflected retention for only a short period after which Se appeared to be retained without altering the blood Se. This suggested that Semet-Se and selenite-Se were metabolized differently. 7. A double blind-dosing trail with 100 microgram Semet-Se was carried out for 12 weeks on twenty-four patients with muscular complaints in Tapanui, a low-Se-soil area. Blood Se increased in the experimental group (from 0.067 to 0.143 microgrm Se/ml); clinical findings were not conclusive and will be presented elsewhere. 8. Bood Se was measured in New Zealand residents before travelling to Europe or to North America. On return their blood Se was increased, and depending upon the period of time spent outside New Zealand some values reached concentrations found in visitors and new settlers to New Zealand. 9. The results from these studies and the earlier studies of single and multiple dosing have been used to look at the various criteria in use for assessing Se status of subjects. It is suggested that plasma Se be used in preference to 24 h urinary excretion, and in addition to whole blood Se and glutathione peroxidase (EC 1.11.1.9) activity.     

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。     

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.     

Selenium supplementation affects the retention of stable isotopes of selenium in human subjects consuming diets low in selenium

Twenty-nine women and fifteen men from an area of low Se intake (South Island of New Zealand) consumed 100 micrograms stable 74Se, as selenate given in water after an overnight fast, and blood was collected for 3 weeks. They were then divided into five groups and supplemented with 0, 10, 20, 30 and 40 micrograms Se/d (as selenomethionine) for 5 months. After 5 months, they received a second dose of 74Se identical to the first. Supplementation significantly altered retention of 74Se in the plasma, but not in the erythrocytes or platelets. Subjects receiving the placebo retained the greatest amount, and subjects receiving 30 micrograms supplemental Se/d retained the least 74Se. Supplementation resulted in relatively more isotope being retained in a medium molecular mass protein considered to be albumin, and relatively less in another fraction considered to be selenoprotein P. The lack of many observed changes in retention of stable Se, and the shift in retention among the plasma proteins, suggests that supplemental Se was not being used to replete critical pools of Se, probably because of adaptation to low Se intake.     

Selenium metabolism and platelet glutathione peroxidase activity in healthy Finnish men: effects of selenium yeast, selenite, and selenate

The mean dietary selenium intake in Finland increased from 40 to 100 micrograms/d in 1987 because of the addition in 1985 of selenium to fertilizers. A selenium-supplementation study was performed in 1987 on the same men as were followed in a 1981 study that had a similar design (200 micrograms Se/d). Selenite and selenate, but not selenium yeast increased platelet glutathione peroxidase (GSHPx) activity by 30% compared with placebo, much less than the 70% found in the previous study. Selenium yeast and selenite increased plasma selenium after 11 wk from 1.39 mumol/L to peak values of 2.15 and 1.58 mumol/L, respectively. Only yeast selenium was incorporated into red cells. From a regression plot based on present and literature data, it was estimated that the plasma selenium concentration needed to achieve maximal platelet GSHPx activity was 1.25-1.45 mumol/L. At the present selenium intake in Finland, 100 micrograms/d, GSHPx activity is saturated in plasma and red cells and almost saturated in platelets.     

我国人民硒需要量的研究 五、硒生理需要量的再研究和有关硒需要量问题的讨论

对本所12名职工分别补充不同剂量的亚硒酸钠(8人)和硒蛋氨酸(4人),每组男女各半。实验膳供给硒量男女分别为48.3±20.2和42.8±20.4μg/日。实验结果表明:不论补充哪一种形式的硒和补充剂量的大小,受试者血浆GSHpx活力在实验期始终保持不变。因此,本次观察天然膳食所得男子摄入量≤48.3和以往用补充的方法在低硒地区的结果是一致的,但若单独考虑本次实验结果成年男子应为60μg。此外,为了确定实验对象血浆硒水平是否在补充前已达到最高恒定水平,给另一组6人(男女各半),每天补充相当于20μg硒的亚硒酸钠,结果显示:受试者血浆硒对补充的硒有反应,在男女分别摄入硒的量达到68.3±20.2和62.8±20.4μg/日时,血浆硒达到最高恒定水平。文内简单地讨论了血浆GSHpx和补充亚硒酸钠后血浆硒的最高恒定水平的营养意义。     

慢性硒中毒大鼠硒蛋白的变化

在低硒酵母配制的低硒饲料的基础上,加亚硒酸钠配成含硒量为０．２和５．０ｍｇ／ｋｇ（适硒和高硒）的两组饲料来喂养雄性断乳Ｗｉｓｔａｒ大鼠。在实验２０周末处死大鼠,测定组织器官的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、硒蛋白Ｐ和硒蛋白Ｗ以及组织硒含量,并对所有大鼠的肝脏进行病理学检查。结果发现高硒饲料组大鼠的体重明显低于适硒饲料组。高硒组动物组织中硒含量明显高于适硒组。两组动物肝脏无明显病理学差异,但高硒组大鼠的血浆ｅＧＰＸ活性,肾脏、心脏和睾丸中的ｃＧＰＸ活性,肝、肾和甲状腺的ＩＤⅠ活性,心脏和睾丸中的ＰＨＧＰＸ活性以及大鼠体重明显低于适硒饲料组。提示它们可以作为硒中毒的早期生化指标。     

Longitudinal selenium status in healthy British adults: assessment using biochemical and molecular biomarkers

Human selenium (Se) requirements are currently based on biochemical markers of Se status. In rats, tissue glutathione peroxidase-1 (Gpx1) mRNA levels can be used effectively to determine Se requirements; blood Gpx1 mRNA levels decrease in Se-deficient rats, so molecular biology-based markers have potential for human nutrition assessment. To study the efficacy of molecular biology markers for assessing Se status in humans, we conducted a longitudinal study on 39 subjects (age 45 +/- 11) in Reading, UK. Diet diaries (5 day) and blood were obtained from each subject at 2, 8, 17 and 23 weeks, and plasma Se, glutathione peroxidase (Gpx3) enzyme activity, and selenoprotein mRNA levels were determined. There were no significant longitudinal effects on Se biomarkers. Se intake averaged 48 +/- 14 microg/d. Plasma Se concentrations averaged 1.13 +/- 0.16 micromol/l. Plasma Se v. energy-corrected Se intake (ng Se/kJ/d) was significantly correlated, but neither Gpx3 activity v. Se intake (ng Se/kJ/d) nor Gpx3 activity v. plasma Se was significantly correlated. Collectively, this indicates that subjects were on the plateaus of the response curves. Selenoprotein mRNAs were quantitated in total RNA isolated from whole blood, but mRNA levels for Gpx1, selenoprotein H, and selenoprotein W (all highly regulated by Se in rodents), as well selenoprotein P, Gpx3, and phospholipid hydroperoxide glutathione peroxidase were also not significantly correlated with plasma Se. Thus selenoprotein molecular biomarkers, as well as traditional biochemical markers, are unable to further distinguish differences in Se status in these Se replete subjects. The efficacy of molecular biomarkers to detect Se deficiency needs to be tested in Se-deficient populations.     

A comparison of methods of assessment of dietary selenium intakes in Otago, New Zealand

The aims of the present study were (1) to compare three methods of assessment of dietary Se intake, i.e. chemical analysis of duplicate diets, diet records and a food-frequency questionnaire (FFQ) designed specifically for Se, and (2) to determine dietary Se intakes of residents of Otago, New Zealand. The FFQ was completed by 110 free-living adults. Diet records (3 d) and duplicate diet collections were carried out by forty-three of these subjects chosen on the basis of low blood Se concentration, and during a period when consumption of the high-Se foods fish, kidney, liver and Brazil nuts was discouraged. Mean Se intakes were similar for duplicate diet analysis (29 (SD 13) micrograms/d) and diet record assessments (28 (SD 15) micrograms/d). Estimates of intakes from the FFQ for the subgroup of forty-three subjects were higher (51 (SD 26) micrograms/d) than those from duplicate diets and diet records. Values from duplicate diet analysis and diet record assessments were strongly correlated (r 0.7, P = 0.0001), but difference plots indicated a lack of agreement between the two methods. Thus, diet record assessment was not adequate for predicting dietary Se intakes of individuals. Significant correlations were found for relationships between Se intake from duplicate diets (microgram/kg body weight per d) and plasma Se, Se intake from diet records (microgram/d and microgram/kg body weight per d) and plasma Se; and Se intake from the FFQ and whole-blood Se. Se intakes from duplicate diets and diet records were similar to those reported previously for New Zealanders, but lower than the recommended intakes in the USA (National Research Council, 1989), Australia (Truswell et al. 1990) and the UK (Department of Health, 1991) and the World Health Organization/Food and Agriculture Organization/International Atomic Energy Agency (1996) normative requirement.     

Selenium and vitamin E supplementation: activities of glutathione peroxidase in human tissues

Twenty-seven New Zealand women received daily for 4 wk, 200 micrograms selenium as sodium selenite, 170 mg alpha-tocopherol acetate, or a placebo. Se supplementation raised platelet selenoglutathione peroxidase (Se-GSHPx, p less than 0.001) and also Se and Se-GSHPx in whole blood and plasma. Se concentrations and Se-GSHPx activities in liver biopsies taken after supplementation were greater (p less than 0.05) for the Se group and a good correlation was found between Se and Se-GSHPx in liver and muscle for all subjects. Platelet Se-GSHPx correlated well with Se and Se-GSHPx in liver, indicating its suitability for assessing Se bioavailability. This is the first reported study of relationships between Se and Se-GSHPx in human liver and muscle tissue and platelet Se-GSHPx after Se supplementation. These observations verify in man relationships observe in animal studies, giving support to assumptions made in methods for assessing Se status and bioavailability in man, in particular the use of platelet GSHPx.     

中国成人硒需要量研究

目的 探讨使人体血浆硒蛋白P(SEPPI)达到饱和的硒摄入量,以评估硒需要量,为膳食硒参考摄入量DRIB的修订提供参考.方法 时98名低硒健康受试者(体重平均58kg)进行为期40w的双盲补硒实验.随机分为七组,补硒(以硒蛋氨酸形式)剂量分别为0、21、35、55、79、102和125 μg/d.定期检测血浆中谷胱甘肽...     

Glutathione peroxidase and selenium deficiency in patients receiving home parenteral nutrition: time course for development of deficiency and repletion of enzyme activity in plasma and blood cells

The time course for the depletion of red blood cell (RBC) and plasma glutathione peroxidase (GSHPx) activity in five patients receiving home parenteral nutrition was documented. During the development of the RBC GSHPx deficiency, enzymatic activity and protein content decreased. Plasma and RBC selenium content were similarly decreased as was cellular metabolism of exogenous hydrogen peroxide. When the replacement of Se (selenious acid) began, there was a rapid increase (within 6 h) in plasma GSHPx activity. Platelet and granulocyte (PMN) GSHPx activity, which were low when Se replacement began, became normal within a time consistent with the kinetics of platelet and PMN production. RBC GSHPx did not become normal for 3-4 mo. This is consistent with the time course for RBC production. It appears that the repletion of blood cell GSHPx requires the formation of these cells in the presence of Se.     

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.     

硒蛋白对糖尿病小鼠血糖、Ca2+转运以及NO系统影响的实验研究

目的研究硒蛋白对糖尿病小鼠血糖、Ca2+转运及NO系统的调控作用.方法体重(20.3±1.7)g昆明种雄性小鼠,腹腔注射200mg/kgbw,2%的四氧嘧啶造糖尿病(DM)模型.实验分6组正常对照组(Ⅰ)、正常+硒蛋白组(Se 100μg/kgbw)(Ⅱ)、糖尿病对照组(Ⅲ)、DM+硒蛋白低剂量组(Se 100μg/kgbw)(Ⅳ)、DM+硒蛋白高剂量组(Se 300μg/kgbw)(Ⅴ)、DM+亚硒酸钠组(Se 100μg/kgbw)(Ⅵ).结果Ⅴ组血糖(20.4±6.3)mmol/L明显低于Ⅲ组(45.3±3.3)mmoi/L,P＜0.05;肾脏三磷酸腺苷酶(Ca2+-ATPase)活性,Ⅴ组0.90±0.5明显高于Ⅲ组(0.35±0.1)μmol/(h·mg prot),P＜0.05;一氧化氮合酶(NOS)活性,Ⅴ组(25.0±4.3)U/ml明显低于Ⅲ组(35.2±4.4)U/ml,P＜0.05.结论补硒剂量为Se 300μg/kgbw的硒蛋白能够显著的降低糖尿病小鼠血糖、提高肾脏Ca2+-ATPase活性和降低血浆NOS活性.