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.     

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.     

Effect of low lysine diet on rat protein metabolism.

Prolonged lysine deficiency resulted in inhibition of growth of the rat and in lowered levels of albumin and beta-globulins, but not of total liver proteins. The apparent incorporation of [3H]lysine into total and chromosomal liver proteins, however, was increased in lysine deficient rats relative to pair-fed controls. The concentration of free lysine in neither serum nor liver was altered in lysine deficient rats. The specific radioactivity of liver free lysine 2 hours after administration of [3H]lysine was noticeably elevated in the deficient rats. However, when the pool of liver free lysine is considered, synthesis of all proteins studied was inhibited. The largest inhibitory effect was seen in serum albumin and total liver protein synthesis. Inhibition of snythesis of nuclear chromatin protein was less pronounced. The data indicate an adaptive mechanism operates to preserve liver lysine in rats fed lysine deficient diets for a prolonged period. In spite of retention of lysine, the synthesis of liver and serum proteins was inhibited.     

Influence of diet on growth in the rat

Twenty-eight-day old male Sprague Dawley rats were fed, either ad libitum or in restricted amounts, isoenergetic diets containing 2%, 5%, 10%, 15%, 25%, or 50% lactalbumin protein and 5%, 11.9%, or 21.1% fat for 8 weeks and were then killed. Weekly food consumption and body weight, terminal weight, body water and lipid, and liver weight, DNA, RNA, protein, and lipid were measured. The growth rate increased progressively with each increase in the level of dietary protein up to 25% protein and then declined. Growth was also accelerated by a high fat diet but was retarded by restriction of energy intake. Total body lipid correlated directly with the level of fat in the diet. Multiple regression analysis of the type: Y = beta0 + beta1X1 + beta2X2 + B3X3 + B4X4 where Y = rate of weight gain X1 = dietary protein level, X2 = protein efficiency ratio, X3 = appetite factor, and X4 = energy/protein ratio, showed that the maximum rate of weight gain of 58.8 g/week occurred when the diet contained 23% protein. Growth rate declined when the diet contained a higher protein level.     

Impact of maternal seafood diet on fetal exposure to mercury, selenium, and lead.

Umbilical cord blood from 1,023 consecutive births in the Faroe Islands showed a median blood-mercury concentration of 121 nmol/l (24.2 micrograms/l); 250 of those samples (25.1%) had blood-mercury concentrations that exceeded 200 nmol/l (40 micrograms/l). Maternal hair mercury concentrations showed a median of 22.5 nmol/g (4.5 micrograms/g), and 130 samples (12.7%) contained concentrations that exceeded 50 nmol/g (10 micrograms/g). Frequent ingestion of whale meat dinners during pregnancy and, to a much lesser degree, frequent consumption of fish, and increased parity or age were associated with high mercury concentrations in cord blood and hair. Blood-mercury levels were slightly lower if the mother had occasionally ingested alcoholic beverages. Mercury in blood correlated moderately with blood selenium (median, 1.40 mumol/l). Increased selenium concentrations were associated with intake of whale meat, alcohol abstention, delivery after term, and high parity. Lead in cord blood was low (median, 82 nmol/l), particularly if the mothers had frequently had fish for dinner and had abstained from smoking.     

硒碘对大鼠谷胱甘肽过氧化物酶活力及甲状腺激素代谢的影响──Ⅱ．硒碘营养状态对大鼠甲状腺激素代谢的影响

用四种硒水平饲料和两种碘含量饮水饲养大鼠观察了其甲状腺激素（ＴＨ）代谢。硒组间肝脏、肾脏Ⅰ型脱碘酶（ＩＤⅠ）活力、血清Ｔａ含量差异显著；两碘组间甲状腺重量、甲状腺过氧化物酶（ＴＰＯ）活力。甲状腺碘含量、肾脏ＩＤⅠ及大脑Ⅱ型脱碘酶（ＩＤⅡ）活力差异明显；Ⅰ－（不加碘）组中甲状腺ＩＤⅠ活力与血清三碘甲腺原氨酸（Ｔａ）含量呈显著正相关。提示硒缺乏通过ＩＤⅠ影响ＴＨ代谢继而影响大脑ＩＤⅡ活力并可加重碘缺乏的效应；低碘时甲状腺ＩＤⅠ在维持循环Ｔａ含量中起重要作用；碘缺乏有可能增加硒缺乏的效应；硒、碘对ＴＨ代谢的影响可能在一定程度上取决于自身和对方的营养状态。     

Effect of dietary methionine on utilization of tissue selenium from dietary selenomethionine for glutathione peroxidase in the rat

To study the effect of dietary methionine on the bioavailability of Se from selenomethionine ([Se]Met), weanling rats were first loaded with Se by feeding 0.5 mg Se as [Se]Met per kg diet of a low methionine (0.17% by analysis) torula yeast-based diet for 21 d, and then were fed an Se-deficient diet (less than 0.02 mg Se/kg) supplemented with 0, 0.4 or 0.9% methionine for 28 d. Plasma, liver and muscle Se increased 2.6-, 2.5- and 2.2-fold, respectively, during [Se]Met supplementation, and then the tissue Se declined exponentially during the Se-deficient diet period. Plasma, liver and muscle glutathione peroxidase (GSH-Px) activities decreased 43-50% during the [Se]Met supplementation period in spite of the increase in tissue Se. When these [Se]Met-loaded rats were fed the Se-deficient diet and supplemented with methionine, tissue GSH-Px activities increased significantly within 3 to 7 d, but then decreased for the remainder of the experiment. Calculation of the percentage of tissue Se present as Se in GSH-Px indicated that substantial Se from dietary [Se]Met was stored in tissues in a form different from GSH-Px when a low methionine diet was fed. These results indicate that the dietary methionine level can modulate the availability of Se from dietary [Se]Met and from stored tissue [Se]Met; the inability of stored [Se]Met to provide Se for GSH-Px synthesis over a prolonged period of time suggests that [Se]Met may not be an optimum form for Se supplementation.     

不同剂量硒对染铅孕鼠仔代生长发育影响

目的 探讨不同剂量硒对染铅孕鼠仔代性别分化、生长发育和青春期启动的影响.方法 SD大鼠随机分为5组,自受孕1～20d,中毒组孕鼠自由饮用含2mg/ml醋酸铅的双蒸水,硒拮抗组在此基础上分别自由饮用含2,4,8μg/ml亚硒酸钠的双蒸水,对照组自由饮用双蒸水.自然分娩后各组母鼠均饮用双蒸水并哺乳,观察仔鼠性别比例、出生后4,22d生存率、肛殖距离(AGD)和青春期启动的情况.结果 4μg/ml硒拮抗组仔鼠的生长发育和青春期启动与对照组比较差异无统计学意义(P>0.05),各组仔鼠的性别比例和肛殖距离差异无统计学意义(P>0.05).结论 4μg/ml亚硒酸钠可明显拮抗2mg/ml醋酸铅对仔鼠生长发育和青春期启动的毒性,孕期适宜的硒营养补充量可明显改善有铅暴露史孕鼠仔代的生长发育和青春期启动.     

硒碘联合作用对机体甲状腺激素代谢的影响机制探讨

用克山病病区粮以及分别加 Se 或/和加 I 喂饲大鼠,并观察机体甲状腺激素的代谢变化。结果发现,缺 I 可显著降低循环和肝脏的 T_4水平,循环总 T_3受 Se、I 影响不十分明显,但 FT_3变化较大。缺 Se 使肝 I 型5′-脱碘酶活性下降,并使肝 T_3生成减少,但因此引起 T_4堆积的现象只能在缺 Se加 I 组中出现。甲状腺组织的甲状腺激素水平因缺 I 而减少,但缺 Se 并未使其进一步下降,反而有较大幅度的升高,且同时使甲状腺肿胀加剧。循环促甲状腺激素(TSH)有相对稳定循环T_3水平的作用。TSH 与 T_4负相关。研究提示,不同 Se、I 营养状况对循环和组织甲状腺激素代谢影响不同,肝组织内源性甲状腺激素受 Se 水平影响较大。     

硒对大鼠眼晶体脂质过氧化作用影响的实验研究

用晶体培养方法研究硒与光照射诱发的晶体脂质过氧化作用的关系。结果表明经光照射２４～４５ｈ后晶体丙二醛（ＭＤＡ）含量显著升高（Ｐ＜０．０５）。培养液中含适宜硒浓度（１．１５μｍｏｌ／Ｌ）可使光照射晶体的丙二醛含量减少，并在一定硒浓度范围内经光照射晶体的丙二醛含量与培养液中硒浓度呈负的剂量反应关系。两组在不同硒浓度培养液中培养的晶体经光照射后谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ），超氧化物歧化酶（ＳＯＤ）的活性无明显差别。推测硒能抑制光照射诱发的晶体脂质过氧化作用，硒对晶体的保护可能是通过谷胱甘肽过氧化物酶以外的其它途径。     

Effect of vitamin E,selenium and age on lipid peroxidation events in rat cerebrum

The effect of 8 and 20 weeks of dietary vitamin E (200 IU/kg diet) and/or selenium (0.2 ppm) supplementation or deficiency on oxidative processes in cerebrum of 1 and 15 month old male F344 rats was examined. After 8 weeks of treatment a 32-fold difference in plasma and a 3-fold difference in cerebrum alpha-tocopherol (a-T) level was found between vitamin E supplemented and deficient young rats. These differences were 1.8- and 1.5-fold, respectively, in old rats and increased to 8- and 2-fold differences, respectively, after an additional 12 weeks of treatment. Selenium deficiency had a significant effect on plasma glutathione peroxidase activity and a slight sparing effect on plasma a-T content. Endogenous lipid peroxides (thiobarbituric acid reactants present without incubation) in cerebrum were not correlated with a-T concentration or age. However, incubation of cerebrum homogenates with or without the addition of 0.1 mM Fe²⁺, 0.25 mM ascorbic acid, or 100 mg % acetaldehyde revealed that dietary vitamin E has a major role and selenium has a minor role in the protection against ex-vivo and possibly in vivo lipid peroxidation in cerebrum.     

Effect of an alpha-linolenic acid-rich diet on rat mammary tumor growth depends on the dietary oxidative status

To investigate whether the oxidative status of an 18:3(n-3) polyunsaturated fatty acid (PUFA)-enriched diet could modulate the growth of chemically induced rat mammary tumors, three independent experiments were performed. Experiments I and II examined the variation of tumor growth by addition of antioxidant (vitamin E) or a prooxidant system (sodium ascorbate/2-methyl-1,4-naphthoquinone) to a 15% linseed oil diet rich in 18:3(n-3). Experiment III addressed the role of PUFA in the tumor growth modulation by vitamin E. For this purpose, we compared the effect of vitamin E in 15% fat diets containing a high level of 18:3(n-3) (linseed oil, high-PUFA diet) or devoid of 18:3(n-3) (hydrogenated palm/sunflower oil, low-PUFA diet). In Experiments I-III, tumor growth increased in the presence of vitamin E compared with control (without vitamin E). Furthermore, it decreased when prooxidant was added. In contrast, no difference was observed when the diet was low in PUFA, suggesting that sensitivity of PUFA to peroxidation may interfere with tumor growth. This observation was supported by growth kinetic parameter analysis, which indicated that tumor growth resulted from variations in cell loss but not from changes in cell proliferation. These data show that, in vivo, PUFA effects on tumor growth are highly dependent on diet oxidative status.     

Effect of intermittent supplementation with selenate on selenium status of rats fed selenium-deficient diet

To examine the selenium (Se) status of rats intermittently supplemented with Se, we measured tissue Se contents and glutathione peroxidase (GPx) activities in rats fed a Se-deficient diet intermittently supplemented with selenate. In experiment 1, four groups of male 4-wk-old Wistar rats were fed a Torula yeast-based Se-deficient diet (Se content, < 0.01 microg/g) for 28 d. During the experimental period, the diet of each group was supplemented with sodium selenate (0.17 microg Se/g) for 0, 1, 2 or 7 d/wk. The tissue Se contents and GPx activities both increased gradually with an increase in frequency of the selenate supplementation, and significant linear regressions were observed between the frequency and these Se indices. In particular, the correlation coefficient in the liver and plasma indices was nearly equal to a value of 1.0. In experiment 2, three groups of rats were fed the Se-deficient basal diet for 28 d. Among these, one group was daily supplemented with sodium selenate to the Se-deficient diet at a level of 0.17 microg Se/g, and another group was intermittently supplemented with the selenate at a level of 1.19 microg Se/g for 1 d/wk. The tissue Se contents and GPx activities both were increased by the selenate supplementation and no significant difference was observed between daily and weekly supplementation in the Se indices except in erythrocyte Se. These results indicate that Se status in the growth period is dependent on total Se intake in this period and that weekly intermittent supplementation with Se can maintain adequate Se status.     

Effect of dietary selenium and vitamin E on the antioxiant defense systems of rat erythrocytes.

The effect of dietary selenium and vitamin E on the important cellular antioxidant defense systems was studied in rat erythrocytes. Weanling male Sprague-Dawley rats were fed a basal selenium and vitamin E deficient diet and supplemented with either none or 0.5 ppm selenium and either none or 45 ppm vitamin E for 35 or 40 days. Depletion of dietary selenium resulted in marked decrease of glutathione (GSH) peroxidase in the red cells, but the levels of GSH, catalase and superoxide dismutase were not significantly altered. The red cells of rats fed the basal diet deficient in both selenium and vitamin E had significantly lower levels of GSH and GSH peroxidase, but not of catalase and superoxide dismutase, than in those fed the basal diet and supplemented with either selenium, vitamin E or both. The results suggest that depletion of dietary selenium and vitamin may have a precipitate effect on lowering the levels of GSH and GSH peroxidase in rat erytyrocytes.