Dietary selenium protection of methylmercury intoxication of Japanese quail

Summary Selenium, as sodium selenite, added at 5 ppm to purified diets of Japanese quail protected against methylmercury intoxication. Selenium fed simultaneously with methylmercury to quail for 9 weeks gave complete protection. However, feeding selenium with methylmercury for 4 weeks, followed by a diet containing only methylmercury, delayed the onset of methylmercury intoxication for 1–2 weeks as compared to quail not pretreated with selenium. On diets which contained 20 ppm of methylmercury but no selenium, over 90% mortality was observed for young quail within 2 weeks, and mature quail within 4 weeks. Methylmercury residues in liver, kidney, and brain are higher in male than female quail. High methylmercury content of these organs, or in produced eggs, does not indicate that birds will show evidence of methylmercury toxicosis.Approved by the Director of the New York State Agricultural Experiment Station for publication as Journal Paper No. 2012.     

Effects of selenium and methylmercury upon glutathione and glutathione-S-transferase in mice

The effect of selenium and methylmercury upon liver glutathione concentration and glutathione-S-transferase activity was investigated in mice. Intraperitoneal injections of methylmercury produced a decrease in liver glutathione and an increase in glutathione-S-transferase. The response to methylmercury was similar in both selenium-control and selenium-deficient animals. Selenium administered alone produced an increase in glutathione and glutathione-S-transferase activity in the selenium-deficient animals but had little effect in the selenium-control animals. However, in both selenium-control and selenium-deficient mice the injection of selenium prior to methylmercury reduced the effect of methylmercury upon glutathione-S-transferase. Furthermore, this study demonstrated that following methylmercury administration the liver glutathione level dropped drastically within 2 days, but that it was 6 days before the rise in glutathione-S-transferase activity reached a peak.The results from this study suggest that one of the interactions of selenium and methylmercury, which may be involved in the amelioration of methylmercury toxicity, occurs at the time both metals are metabolized in the liver.     

Role of selenium in mercury intoxication in mice

Studies were conducted to examine the effect of pre and post-treatment of selenium in mercury intoxication (20 micromole/ kg b.w. each given intraperitoneally) in mice in terms of lipid peroxidation (LPO), glutathione (GSH) content, activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT) and mercury concentration in liver, kidney and brain. No significant alteration was observed in all the organs examined after mercury or selenium treatment in LPO and GSH but administration of selenium (pre and post) resulted in an increase in the level of LPO and GSH. The activity of SOD was depleted in liver and kidney while that of GPx was lowered in liver of mercury exposed animals. Selenium administration resulted in restoration of the depletion of these enzymatic activities. The activity of CAT in liver and brain was enhanced both in mercury and selenium treated animals. Administration of selenium significantly arrested enhanced CAT activity. Kidney showed the highest mercury concentration among the organs examined. Administration of selenium resulted in further enhancement of mercury concentration in the tissues. An increase in selenium level in liver was observed after mercury treatment, which was also restored by mercury selenium co-administration. Our results indicate that the prooxidant effect of selenium was greater by its pretreatment.     

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。     

Bioavailability to rats of selenium in various tuna and wheat products

Bioavailability of selenium (Se) in tuna and wheat at various stages of processing was studied in rats. The protein source of the rat diets was torula yeast with Se supplied by either raw, precooked or canned tuna, or whole wheat flour, whole wheat bread or bran. Sodium selenite was used as the standard. Each Se source was fed at three levels: 0.05, 0.10 and 0.15 ppm. By using increase in glutathione peroxidase (GSH-Px) activity in liver, kidney and whole blood as an indicator of bioavailability, no differences were found among the three tuna products or among the three wheat products tested. However, significantly lower GSH-Px activity was found in the combined tuna groups as compared to the combined wheat groups, suggesting that selenium in wheat was more available than that in tuna. There was a significant increase in the liver Se content of rats fed all levels of Se in canned tuna and in kidney, blood and muscle Se of rats fed 0.10 and 0.15 ppm Se in canned tuna in comparison to the tissue Se content in rats fed these same levels of Se in raw or precooked tuna. Since this did not correspond with an increase in GSH-Px activity it was concluded that it did not represent increased bioavailability of canned tuna. Thus, food processing does not appear to affect Se availability, but Se appears to be more available in wheat than tuna.     

Metabolism of selenite in men with widely varying selenium status.

OBJECTIVE: This study was undertaken to investigate the metabolism of selenite in men with life-long intakes of deficient, adequate and excess selenium. METHODS: Stable isotopes of selenium were infused for five hours into Chinese men living in deficient, adequate or excessive selenium areas, and 24-hour urine and blood samples were collected daily for the next seven days. Stable isotopic selenium excretion was determined in urine and in whole plasma and plasma fractions. RESULTS: Even though there was a positive correlation of selenium intake with the urinary excretion of this element, this relationship was not linear over the entire range (deficient, adequate, excessive) of selenium intake. When the urine excretion was normalized internally within each group, a sharp increase in the slope of this relationship was found when long-term intake increased to adequate amounts, but the slope reached a plateau when the daily intake exceeded the adequate group. The plasma selenoprotein P fraction was labeled initially, but the incorporation in the glutathione peroxidase fraction subsequently increased by a small amount. A two-month dietary restriction of selenium of the subjects from the excess area did not result in a reduction of urinary excretion of infused selenite. CONCLUSION: A complex relationship exists between long-term intake of selenium and selenium status, and subjects living in the excess area are more saturated with selenium than anticipated. More than two months of depletion are required to affect urinary excretion of selenium.     

Alteration of inorganic mercury accumulation due to selenite in organs of mice fed methylmercury

Mice were fed methylmercury (10 nmol/g feed) and selenite (0, 8, 20 or 50 nmol/ml drinking water) for one or two weeks. Doses of selenite and duration of feeding were determining factors of total mercury and inorganic mercury concentrations in organs. Increasing the dose of selenite produced the following results: concentration of total mercury increased in the brain and liver and decreased in the blood, kidneys and spleen; concentration of inorganic mercury increased in the liver and spleen, decreased in the kidneys, and remained unchanged in the brain; the rate of inorganic mercury to total mercury increased in the liver and spleen, decreased in the brain, and remained unchanged in the kidneys. In every case, inorganic mercury in the blood was below the detection limit.     

Effect of chronic selenite supplementation on selenium excretion and organ accumulation in rats

We examined the effect of chronic selenite supplementation on whole body and selected organ selenium (Se) accumulation, urine excretion of total Se and trimethylselenonium ion, and Se balance in adult male rats. Animals were housed in metabolic cages and given either deionized water or water containing 4 micrograms of Se/mL as selenite for 30 d. Absorption of selenite was nearly complete, with only approximately 10% of ingested Se appearing in feces. There was a rapid rise in urinary Se that reached a plateau within a few days and accounted for 54 +/- 2% of the intake. Excretion of trimethylselenonium ion (TMSe) in urine increased rapidly, representing 35-40% of urinary Se in the supplemented animals compared with only 2% for the control group. In one experiment, rats were killed at 30 d and total carcass Se was measured using isotope dilution analysis. Supplemented rats had only a modest increase in whole body Se (94 +/- 4 micrograms Se vs. 66 +/- 3 in controls). Calculation of Se balance in the supplemented rats showed that approximately 35% of ingested Se could not be accounted for by urine plus fecal losses combined with the portion retained in the carcass. The results from this study demonstrate that under the condition of supplementation at 4 micrograms of Se/mL of drinking water, pathways other than urinary and fecal excretion may account for a substantial portion of Se loss.     

A human model of selenium that integrates metabolism from selenite and selenomethionine

Selenium (Se) metabolism is affected by its chemical form in foods and by its incorporation (specific vs. nonspecific) into multiple proteins. Modeling Se kinetics may clarify the impact of form on metabolism. Although the kinetics of Se forms have been compared in different participants, or the same participants at different times, direct comparisons of their respective metabolism in the same participants have not been made. The aim of this study was to simultaneously compare kinetics of absorbed Se from inorganic selenite (Sel) and organic selenomethionine (SeMet) in healthy participants (n = 31). After oral administration of stable isotopic tracers of each form, urine and feces were collected for 12 d and blood was sampled over 4 mo. Tracer enrichment was determined by isotope-dilution-GC-MS. Using WinSAAM, a compartmental model was fitted to the data. Within 30 min of ingestion, Se from both forms entered a common pool, and metabolism was similar for several days before diverging. Slowly turning-over pools were required in tissues and plasma for Se derived from SeMet to account for its 3-times-higher incorporation into RBC compared with Se from Sel; these presumably represent nonspecific incorporation of SeMet into proteins. Pool sizes and transport rates were determined and compared by form and gender. The final model consisted of 11 plasma pools, 2 pools and a delay in RBC, and extravascular pools for recycling of Se back into plasma. This model will be used to evaluate changes in Se metabolism following long-term (2 y) Se supplementation.     

硒多糖、亚硒酸钠对大鼠血硒浓度和肝细胞色素P_(450)单加氧酶系的影响

研究了一次和连续７天腹腔注射硒多糖、亚硒酸钠对大鼠血硒浓度及肝细胞色素Ｐ４５０、ｂ５、ＮＡＤ（Ｐ）Ｈ－细胞色素Ｃ还原酶、谷胱甘肽硫转移酶（ＧＳＴ）和谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）的影响；并比较了硒多糖与亚硒酸钠的作用。结果表明：一次腹腔注射Ｓｅ０．６ｍｇ／ｋｇ体重的硒多糖和亚硒酸钠后，血硒浓度迅速增加，在注射后２小时血硒浓度达到高峰，随后血硒浓度逐渐下降。亚硒酸钠在大鼠体内的吸收和排出均较硒多糖快。连续７天腹腔注射０．２ｍｇ／ｋｇ体重剂量硒多糖和亚硒酸钠后，硒多糖和亚硒酸钠组大鼠血硒浓度分别为对照组的２．６倍和２．１倍，其中硒多糖组的血硒含量显著高于亚硒酸钠组（Ｐ＜０．０５）；硒多糖和亚硒酸钠在体内、外均降低肝细胞色素Ｐ４５０、ｂ５的含量，抑制ＧＳＴ的活性，硒多糖的作用尤为显著，分别为对照组的５７％、７０％和６２％（Ｐ＜０．０５）。两种硒化合物对ＮＡＤ（Ｐ）Ｈ－细胞色素Ｃ还原酶无明显影响。硒多糖和亚硒酸钠均能显著增强ＧＳＨ－Ｐｘ的活性（Ｐ＜０．０５）。     

Chemical forms of selenium in rat tissues after administration of selenite or selenomethionine

The chemical forms of selenium (Se) were determined in erythrocyte and liver proteins after injection of 75Se as either sodium selenite or selenomethionine (Se-Met) in male weanling rats. Gel-filtration chromatography (Sephadex G-150) of erythrocyte lysate revealed labeling of four fractions corresponding to void volume proteins, glutathione peroxidase (GPx), hemoglobin (Hb) and low-molecular-weight materials. Acid hydrolysates of erythrocyte protein fractions and whole liver were analyzed by ion-exchange chromatography (Dionex DC6A). Void volume proteins contained principally selenocysteine (75Se-Cys) in [75Se]selenite-injected animals. This material contained both 75Se-Met and 75Se-Cys 1 d postinjection in 75Se-Met-injected animals, but primarily 75Se-Cys at 20 d afterwards. GPx contained 75Se as 75Se-Cys regardless of the selenium compound injected. Hb of 75Se-Met-injected animals contained principally 75Se-Met at both 1 and 20 d postinjection. In [75Se]selenite-injected animals, 75Se was present in hemoglobin as two unidentified forms. In acid hydrolysates of whole liver 75Se was recovered principally as 75Se-Cys from animals injected with [75Se]selenite. For animals injected with 75Se-Met, liver 75Se was present initially as 75Se-Met, but after 5 d the majority of liver 75Se was as Se-Cys. No differences were found in deposition of 75Se in liver, kidney, testes, erythrocytes or plasma in rats injected with labeled selenite or Se-Met, but a significantly greater retention was found in muscle of Se-Met-injected rats as compared to those given selenite.     

急性氯化甲基汞染毒大鼠脑某些抗氧化指标的变化

目的 对SD大鼠经腹腔注射氯化甲基汞(MeH必)的急性染毒方式，观察其对大鼠脑组织和血清某些抗氧化指标的变化。方法 用甲基汞对大鼠染毒24h后，断头处死，取血清和脑组织检测谷胱甘肽过氧化物酶(GSH—Px)和超氧化物歧化酶(SOD)活性及丙二醛(MDA)含量。结果 染毒24h后，5．00mg／kg和10．00mg／kg剂量的大鼠脑组织匀浆和血清中的GSH—Px活性和S0D活性下降，MDA含量上升。结论 甲基汞染毒24h后，GSH—Px和SOD活性下降，MDA含量上升，表明这种作用对MeHgCl引起的神经毒性有一定的敏感性。MeHgCl可使脑组织和血清中某些抗氧化指标发生变化。     

Effects of various dietary levels of selenium as selenite or selenomethionine on tissue selenium levels and glutathione peroxidase activity in rats

Weanling rats were fed a basal diet or this diet plus 0.2, 1.0, 2.0 or 4.0 mg/kg selenium (Se) as either selenite or selenomethionine (SeM). Except at the 0.2 mg/kg Se level, Se accumulated in all tissues at higher levels when SeM was fed than when selenite was given, and the magnitude of difference became more pronounced with increasing levels of dietary Se. This was particularly true for muscle and brain. Se levels in whole blood, testes, kidney and lungs were not significantly different between rats fed 0.2 mg/kg Se as selenite or as SeM, but the Se levels in liver, muscle and brain were higher in rats fed SeM. Although the tissue Se concentrations differed markedly, there were no differences in the glutathione peroxidase (GPX) activity in tissues of rats fed SeM rather than selenite. The percentage of Se associated with GPX was lower in all tissues from rats fed SeM than in those from rats fed selenite. These results indicate that the chemical forms of dietary Se can have a marked influence on biological responses, including bioavailability of dietary Se.     

Infuence of dietary calcium,selenium, and methylmercury on eggshell thickness in Japanese quail

Summary A high Ca, semi-purified diet promoted greater egg production with thicker shells in Japanese quail hens. 7 ppm of dietary Se depressed egg weights with no effect on eggshell thickness. The addition of 20 ppm of MHg to either a low or high Ca diet containing Se depressed both egg production and eggshell thickness. Se residues of liver, kidney, and brain in Se-MHg fed quail were significantly higher than in Se treated quail, probably reflecting the ability of Se to bind with Hg. CA, an enzyme required for the formation of the carbonate radical of Ca carbonate in egg-shells, was not reduced in the Se-MHg treated Japanese quail hens blood or oviducts.