Effects of durum wheat dietary selenium on glutathione peroxidase activity and Se content in long-term-fed rats

A 120-day assay was made of Se concentration and glutathione peroxidase Se-dependent (GSHpx) activity in plasma, erythrocytes and liver of female Sprague-Dawley rats fed either a Torula diet (low Se content) or a durum wheat diet providing 28-405 micrograms of Se/kg diet. For all groups there was a strong increase for the first 20 days in plasma and liver Se; for the remaining period the increase was lower; erythrocyte Se increased, as before, in the first 60 days for groups fed 28-200 micrograms/kg diet, after this period it decreased in the groups fed high-Se diet. Plasma GSHpx activity was extremely sensitive to dietary Se levels and increased for up to 40 days of repletion, after which the trend was to plateau; liver and erythrocyte GSHpx activity increased continuously for up to 60 days of supplementation, it then remained constant. The correlation between Se in plasma, liver and erythrocytes and its GSHpx activity was statistically significant (p less than 0.001). These results suggested that in long-term-fed rats, a diet with levels of 100-400 micrograms/kg was sufficient to satisfy the rat's needs; there was no evidence of toxicity and, moreover, in all tissues, an amount of Se, probably bound to proteins with unknown functions, was present.     

Tolerance of low and high dietary selenium throughout the life span of Syrian hamsters

In lifetime studies on the effects of dietary selenium (Se) levels, Syrian hamsters were fed diets containing low (unsupplemented torula yeast), adequate (0.1 ppm Se supplemented from sodium selenite), or excessive (5 ppm Se supplemented from sodium selenite) levels of Se. A commercial ration was fed to separate groups. Male and female hamsters were assigned to each diet, and blood samples were collected at 54 and 79 weeks of age for determination of Se status. Body weights of male hamsters were generally highest in those fed unsupplemented diets and lowest in those fed 5 ppm Se supplements. Female weights did not differ between the three semipurified diets. Erythrocyte and plasma glutathione peroxidase and blood Se values increased with the increments in dietary Se at the 54- and 79-week measurements. Survival was approximately 40-45% lower in hamsters fed the commercial ration than in those fed semipurified diets, but was not altered by the Se level in the semipurified diet.     

Toxic effects of dietary selenium in the Syrian hamster

Selenium (Se) toxicity and utilization was evaluated in hamsters fed casein- and torula yeast-based diets. 4-week-old hamsters received semipurified diets for 21 days. In experiment I diets were supplemented with either 0.25, 10, 20, 40 or 80 ppm Se as sodium selenite (SS) and in experiment II diets were supplemented with 0.1, 5.0 or 10.0 ppm as SS or selenomethionine (SM). Blood and tissue Se concentrations and glutathione peroxidase (GSH-Px) activity were measured at the termination of the feeding period. In both studies growth rate was depressed and food consumption decreased in hamsters given diets supplemented with 10 ppm or greater SS. Mortality associated with Se toxicity occurred only in females fed the 80 ppm Se-supplemented diet. Whole blood and tissue Se concentrations rose with increasing dietary Se and occurred up to the 80 ppm Se level in blood. Liver, kidney and lung Se concentrations were higher in hamsters fed SM than for those fed SS. Plasma GSH-Px activity was not significantly affected by increasing dietary Se levels, and hamsters fed dietary Se levels above 10 ppm did not have increased erythrocyte GSH-Px activity associated with increased blood Se concentrations. Liver GSH-Px activity was higher in SM-fed hamsters. The results suggest that dietary Se, fed as SS, becomes toxic for Syrian hamsters at levels of 10 ppm and above.     

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.     

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.     

Effect of a glucosidase inhibitor on the metabolic response of diabetic rats to a high carbohydrate diet,consisting of starch and sucrose,or glucose

The metabolic consequences of the addition of BAY-g-5421 to a diet whose caloric value included 67% carbohydrate, comprising wheat starch (diet A), equal quantities of wheat starch and sucrose (diet B) or glucose (diet C) were studied in lean diabetic and non-diabetic rats. BAY-g-5421 led to a significant (30%) reduction in daily food intake of diabetic and non-diabetic rats fed diets A and B, respectively. In diabetic rats fed diets A and B with BAY-g-5421, daily urinary glucose was diminished ten-fold, while the post-prandial plasma glucose excursions were almost halved. Serum cholesterol, but not triglyceride concentrations, were reduced after five days, by the addition of BAY-g-5421 to diets A or B in non-diabetic rats, and in diabetic rats when the animals fed diets A and B were combined. BAY-g-5421 did not significantly alter the food intake, urinary glucose excretion, post-prandial plasma glucose excursions nor serum lipids in diabetic and non-diabetic rats fed diet C. These findings illustrate the therapeutic potential of BAY-g-5421 as an adjunct to the dietary management of diabetes mellitus.     

Dietary ascorbic acid and selenium relationships in the guinea pig

Plasma-, erythrocyte- and liver Se-dependent glutathione peroxidase (GPx) activity, ascorbic acid (AA) concentration, and erythrocyte and liver Se levels were analyzed in groups of guinea pigs fed a Torula yeast-based semipurified diet supplemented with either O (-AA), 200 (+AA), or 400 (++AA) mg of AA/kg of diet and either 0.05 (+Se) or 0.2 (++Se) ppm of Se for 24 days. Plasma, erythrocyte, and liver AA concentration were directly related to the levels of AA fed. There were 21.2 +/- 2.7% and 51.2 +/- 4.5% (p less than 0.0001) increases in erythrocyte and liver Se, respectively, in ++Se guinea pigs compared to +Se guinea pigs. Dietary AA had no effect on erythrocyte or liver Se levels. Plasma, erythrocyte, and liver GPx specific activities were significantly (p less than 0.001) increased in ++Se guinea pigs compared to +Se guinea pigs. In addition, liver, plasma, and erythrocyte GPx activities were directly related to the level of AA fed. These data indicate that dietary AA has no influence on tissue levels of Se but increases plasma, liver, and erythrocyte GPx activities in the guinea pig.     

High-fat diet feeding reduces the diurnal variation of plasma leptin concentration in rats

To investigate the response of plasma leptin and its diurnal variation to graded levels of dietary fat intake, adult (486.8+/-10.8 g), male rats (N = 52) were fed diets containing 12%, 28%, 44%, and 60% fat for 4 weeks. The body weight gain and abdominal fat pad weight were higher (P < .05) in groups fed diets containing 44% and 60% fat compared with the two diets containing less fat. There were no significant differences in terms of body weight or fat pad weight between animals fed the two diets with higher fat content or between animals fed the two lower-fat diets. Twenty-four-hour energy expenditure was not different among the dietary fat groups. After 3 days on the experimental diets, plasma leptin increased (P < .03) in all dietary groups. The increases in leptin in animals fed 12% and 28% fat diets occurred primarily in the morning. In contrast, in groups fed the two diets containing higher fat content, leptin levels increased mainly in the afternoon. As a result, the daily variation in leptin increased (P < .05) in the two groups fed lower-fat diets, but decreased (P < .04) in animals fed the two higher-fat diets. These data demonstrate that short-term high-fat diet feeding abolished the diurnal fluctuation of plasma leptin levels, which may prevent proper leptin function and eventually contribute to the development of obesity.     

硒和维生素E对大鼠心肌腺苷酸及氧化损伤的影响

目的：研究低硒（Ｓｅ）低维生素Ｅ（ＶＥ）饮食大鼠心肌腺苷酸含量和氧化损伤的关系。方法：使用高效液相测定心肌腺苷酸含量和使用生化方法测定心肌ＭＤＡ含量和ＳＯＤ、ＧＳＨ－Ｐｘ活性。结果：与补充Ｓｅ和／或ＶＥ饮食大鼠相比，低Ｓｅ低ＶＥ饮食大鼠心肌ＡＭＰ，ＡＤＰ含量无明显差异，而ＡＴＰ含量明显降低，ＭＤＡ含量增加，ＳＯＤ，ＧＳＨ－Ｐｘ活性降低，表明Ｓｅ和ＶＥ影响ＡＴＰ含量与其抗氧化作用有关，而其中以联合补充Ｓｅ和ＶＥ效果最佳     

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.     

多不饱和脂肪酸对饲低硒粮大鼠血浆游离脂肪酸的影响

以低硒及补硒粮饲料饲养大鼠４周后，给予豆油和鱼油（５０ｇ／ｋｇ）继续饲养４周，用ＨＰＬＣ法测定其血浆游离脂肪酸含量和组成。结果表明，单纯补豆油后血浆Ｃ１８：２、Ｃ１８：３及游离多不饱和脂肪酸含量明显增高，加油后同时伴有ＧＳＨ－Ｐｘ活性明显降低。饲料中补硒（０．１μｇ／ｇ）对上述变化具有不同程度地纠正作用。结果提示，在膳食硒不足的情况下，增加多不饱和脂肪酸饮食，机体抗氧化能力降低，同时ＦＦＡ含量和组     

A quantitative microscopic analysis of the myocardial interstitial tissue space and myocardial fiber diameter in rats with vitamin E and selenium deficiency

Vitamin E (E) and selenium (Se) are important antioxidant nutrients, preventing membrane damage by lipid hydroperoxides. In a previous study on E + Se deficient rats it was shown that plasma levels of lipoproteins increase dramatically. In continuation of this study a quantitative microscopic study was undertaken to determine the behavior of myocardial interstitial tissue space (ITS) in E + Se deficient rats as compared to control rats. Four rats fed on normal laboratory chow and 8 rats fed on basal diet supplemented with adequate E + Se served as control. Eight rats were fed on E + Se deficient diet. The animals were sacrificed after 13 to 20 weeks. Qualitative microscopic study showed patchy areas of hemorrhage, edema, infiltration of macrophages and myocardial damage consisting of pyknosis and coagulation necrosis in the deficient rats. Quantitative microscopic study of the apparently normal areas of myocardium of deficient rats showed a shrinkage of ITS (21.0 +/- 1.29% vs 16.51 +/- 4.62%, alpha = 0.01), whereas the ITS of normal laboratory chow and E + Se supplemented groups were similar. The myocardial fiber diameter was unchanged. Using Starling's hypothesis regarding fluid movement across capillary walls, several mechanisms could be advanced to explain this apparently paradoxical phenomenon. We contend that the interstitial fluid of normal areas of the myocardium is either absorbed by the adjacent damaged areas, or before extravasation of the intravascular proteins and swelling of ITS, the interstitial fluid is first absorbed by the intravascular compartment, due to capillary membrane damage.     

低硒对雄性大鼠性腺发育和分泌功能的影响

目的　研究雄性动物性腺的发育和功能与硒的关系。方法　分别以低硒饲料、补硒饲料和常规饲料喂养刚分窝的雄性Ｗ ｉｓｔａｒ 大鼠１４ 周和３９ 周后,分别采用２,３－二氨基萘（ＤＡＮ）荧光分光光度法和化学发光酶免疫法测定血和睾丸硒含量及血浆睾酮水平等指标。结果　饲养１４ 周后,低硒组大鼠不仅血和睾丸硒含量以及睾丸谷胱甘肽过氧化物酶（ＧＰｘ）活性显著低于对照组,而且其精囊腺重量、精囊腺指数和血浆睾酮水平等也显著低于对照组,但其睾丸中脂质过氧化物（ＬＰＯ）水平则显著高于对照组（ Ｐ ＜ ０．０５）。在低硒饲料中补充一定量的硒可在一定程度上纠正这些变化。饲养３９ 周后,低硒组精囊腺指数进一步降低,与对照组的差异达极显著程度（ Ｐ ＜ ０．０１）,甚至睾丸指数也降至显著低于对照组。结论　这些结果提示,硒不足对雄性动物性腺的发育和分泌功能有不良影响,适当补硒可作为男性不育症的辅助治疗手段。     

Relationship between magnesium and zinc levels of the diet and its protein utilization

Protein utilization of the diet was tested in relation to different levels of magnesium and zinc in rats. The experimental diets contained either a low (0.14 g Mg or 10 mg Zn/kg) or adequate (0.45 g Mg or 40 mg Zn/kg) level of Mg or Zn and two different quality protein sources: casein or wheat gluten. Net protein utilization and net protein radio indexes in case of casein were significantly lower for the diet containing a low level of Mg or Zn. For gluten diets, such differences were not observed. Digestibility of protein measured in rats fed a low Mg or Zn casein diet was the same as for the diets with an adequate content of these minerals. Rats fed low Mg or Zn casein diets showed a significantly lower plasma Mg or Zn and a lower liver DNA content in comparison to the rats on adequate Mg or Zn diets. The results indicate that the utilization of protein is affected by Mg and Zn content of the diet and that this relationship depends on the quality of protein.     

Time-course of changes in plasma lipids in diabetic rats fed diets high in fish or safflower oils

Adult male rats were maintained for 10 days on a standard chow diet or that diet supplemented with either safflower or marine fish oils, and then rendered diabetic with streptozotocin (40 mg/kg of body weight) and circulating metabolites determined over the next 3 days. Pre-diabetic concentrations of glucose and insulin did not differ between groups, and the severity of hyperglycaemia and lowering of insulin in streptozotocin-treated animals were also similar. Pre-diabetic concentrations of plasma free fatty acids and triacylglycerols were lower, and blood ketone bodies were higher in non-diabetic rats fed fish oil than in both other groups. However, following streptozotocin treatment, plasma free fatty acids rose significantly more in both groups of oil-fed animals than in chow-fed ones. Plasma triacylglycerols were unaltered from pre-treatment levels in rats fed chow, but rose considerably in both groups fed oil-supplemented diets. In a subsequent experiment it was shown that the increase in triacylglycerols persisted for up to 11 days after streptozotocin and the hypertriglyceridaemia was greatest in the fish oil group. The rise would seem to result from defective clearance of lipoproteins of dietary origin. It appears that fish oil-supplemented diets should be avoided in diabetics until the possibility of increased hypertriglyceridaemia has been excluded by controlled studies.     

Effects of dietary selenium and vitamin E on plasma lipoprotein cholesterol levels in male rats

Male Fischer-344 rats fed a diet deficient in both vitamin E and selenium (Se) for 20 weeks had higher levels of low-density lipoprotein cholesterol than age-matched rats fed an identical diet but supplemented with these micronutrients. The rats supplemented with both vitamin E and Se were switched to a diet deficient in both these micronutrients at week 20. These rats eventually developed elevated levels of low-density lipoprotein cholesterol compared to age-matched rats either continuously maintained on the diet supplemented with vitamin E and Se or rats switched (at week 20) from the vitamin E-and Se-deficient diet to a diet supplemented with both these micronutrients. In a second experiment, we found that Se deficiency alone was sufficient to significantly elevate low-density lipoprotein cholesterol. The basal diet used in these experiments had a very low cholesterol content and the observed alterations in lipoprotein cholesterol levels are likely to reflect alterations in the metabolism of endogenously synthesized cholesterol.     

Fish protein stimulated the fibrinolysis in rats

OBJECTIVE: We hypothesized that fish protein affects blood coagulation and/or fibrinolysis, and compared the activity and amounts of factors involved in blood coagulation and fibrinolysis in rats fed the fish protein, which was treated to remove water-soluble and ethanol-soluble elements, from sardine (sardine protein). METHODS: In the first experiment, rats were fed for 21 days an AIN-93G-based control diet, and diets in which the casein of the control diet was exchanged for sardine protein at 5, 10 and 20% levels. In the second experiment, rats were fed an AIN-93G control diet and diets containing 5% fish oil, 10% sardine protein or both (5% fish oil + 10% sardine protein) for 21 days. At the end of the experiments, blood coagulation time, hemostatic parameters and fibrinolysis parameters were measured. RESULTS: The activated partial thromboplastin time (APTT), which is an assay for blood coagulation time in the intrinsic blood coagulation pathway, of rats fed the 20% sardine protein diet was significantly prolonged compared to that of rats fed the control diet. The prolonged APTT by dietary sardine protein was due to a significant decrease of the activities of plasma blood coagulation factors VIII, IX, XI and XII. On the other hand, dietary sardine protein significantly increased the activity of tissue-type plasminogen activator, and the amount of plasma plasmin-alpha(2)-plasmin inhibitor complex, which are markers of activated plasmin. Moreover, we observed that the 20% sardine protein diet increased the amount of plasma D-dimer, which is a degraded product of the fibrin polymer by plasmin. In the second experiment, the APTT and PT of rats fed the F diet were prolonged compared to those of rats fed the control diet, however the concentration and amount of fibrinolytic parameters in the plasma were almost the same as those of rats fed the control diet. In contrast, the F+S diet not only prolonged APTT and PT, but also increased the concentration and amount of fibrinolytic parameters in plasma. CONCLUSIONS: We consider that the beneficial effects to health and amelioration of cardiovascular and cerebrovascular diseases by fish consumption are caused by a combination of the suppressing effect on blood coagulation of n-3 polyunsaturated fatty acids and the promoting effect on fibrinolysis of fish protein.     

Dietary protein source determines the degree of hypertension and renal disease in the Dahl salt-sensitive rat

Previous studies demonstrated that a whole-grain diet attenuated sodium-dependent hypertension and renal disease in Dahl salt-sensitive rats from the colony at the Medical College of Wisconsin (Dahl SS/Mcw rats) compared with rats maintained on a purified AIN-76A diet. The present experiments determined which component(s) of the grain diet prevented renal and cardiovascular disease. Male SS/Mcw rats were maintained on isocaloric diets identical to AIN-76A, except the source of protein (wheat gluten for casein), carbohydrate (wheat flour for sucrose), or fat (soybean oil for corn oil) was substituted in separate diets. Rats were maintained on the different diets from weaning and studied after 3 weeks on a high-salt (4.0% NaCl) diet. Substitution of the carbohydrate in the diet did not affect body weight, arterial pressure, or renal disease. Replacement of casein with wheat gluten significantly reduced body weight (258+/-7 versus 353+/-3 grams), mean arterial pressure (133+/-2 versus 153+/-2 mm Hg), and albumin excretion (9+/-1 versus 50+/-7 mg/d) to levels of rats fed the whole-grain diet (n=7 to 16/group). Replacement of the fat in the diet increased arterial pressure without affecting body weight or albumin excretion. The results of the present study indicate that dietary components other than sodium play an important role in the development of hypertension and renal disease in the Dahl SS/Mcw rat.     

Glucagon and insulin response to dietary carbohydrate in rainbow trout (Oncorhynchus mykiss)

The effects of high carbohydrate (CH) diets on circulating levels of insulin and glucagon were studied in rainbow trout (Oncorhynchus mykiss). Fish (76.87 +/- 8.11 g) were fed for 60 days with three isocaloric diets: control (C) (12% CH), W (28% CH mainly from wheat), and S (28% CH from wheat plus gelatinized starch). After the diet treatment, trout fed the enriched CH diets showed a higher hepatosomatic index and liver glycogen content than controls. In addition, plasma glucose levels were also higher but, on the contrary, circulating insulin levels were greater in the control group. After the period of diet adaptation, fish were sampled 3, 6, 9, and 24 h after food administration. Glycemia levels correlated with the dietary carbohydrate content, and were minimum in controls (from 96.02 +/- 3.77 to 118.97 +/- 6.08 mg/100 ml), followed by W group (from 124.60 +/- 7.46 to 172.19 +/- 11.36 mg/100 ml) and maximum in the S group (from 133.51 +/- 9.36 to 217.88 +/- 13.36 mg/100 ml). Postprandial glucagon profiles showed an inverse relationship with glycemia, indicating that the ingestion of glucose inhibits glucagon secretion. There were no significant differences in postprandial insulin levels between groups except for W group, which presented lower levels of circulating insulin 9 h after feeding. These results indicate that in trout fed a CH diet glucose affects the secretion of glucagon more than insulin during the postprandial period.     

Energetic efficiency and brown adipose tissue uncoupling protein of obese Zucker rats fed high-carbohydrate and high-fat diets: the effects of adrenalectomy

The influence of diet on the response of lean and obese fa/fa rats to adrenalectomy has been studied. Adrenalectomized and sham-operated rats were fed either a semi-synthetic high-carbohydrate (HC) or high-fat (HF) diet for 13 days. Energetic efficiency, calculated for measurements of energy storage and energy intake, was increased in obese rats fed both HC and HF diets and reduced close to values of lean rats after adrenalectomy. Brown adipose tissue mitochondrial GDP binding and uncoupling protein concentration were reduced in control obese rats fed both HC and HF diets. After adrenalectomy the level of GDP binding and uncoupling protein concentration were increased to levels of lean rats. Molar ratios of GDP binding to uncoupling protein were similar in lean and obese rats, were unaffected by adrenalectomy, but were elevated in rats fed the HC diet (0.40 +/- 0.02 vs 0.28 +/- 0.03). The data suggests that diet, but not obese genotype, may influence the masking of mitochondrial uncoupling protein.