硒化壳聚糖的制备及其表征

本研究将具有良好的生物相容性的壳聚糖无机硒酸进行硒化,并对其硒化产物进行结构表征。硒化壳聚糖的IR和UV光谱证明：硒化位点为壳聚糖碳6位上的羟甲基与碳2位上的氨基。硒化壳聚糖为低分子量水溶性物质,有望开发成为高效低毒的抗肿瘤有机硒药物。     

硒化壳聚糖抗K562细胞作用机制的初步探讨

应用分光光度法和放免法观察不同剂量硒化壳聚糖对K562细胞株抗氧化指标及cAMP、cGMP含量的影响,结果发现硒化壳聚糖可明显升高细胞内GSH-PX活力,降低SOD活性和MDA含量,升高cAMP含量,降低cGMP含量,升高cAMP/cGMP比值.降低K562细胞内脂质过氧化水平,升高cAMP/cGMP比值可能是硒化壳聚糖诱导K562细胞凋亡机制之一.     

富硒猫棒束孢菌丝的培养方法

目的制备富硒猫棒束孢,通过固体培养,实现无机硒向有机硒的生物学转化。方法在猫棒束孢常规培养过程中,加入无机硒化合物,采用高效液相色谱-电感耦合等离子体-质谱(HPLC-ICP-MS)法检测培养好的富硒猫棒束孢和非富硒猫棒束孢菌丝粉中有机硒含量,确定其生物转化率。结果 840 g小米和42 g葡萄糖中加入亚硒酸钠140 mg,平均可培养出富硒猫棒束孢菌丝粉280 g,所培养富硒猫棒束孢中有机硒含量为48.78μg/g,无机硒的的生物转化率为21.39%。结论在猫棒束孢常规固体培养过程中加入无机硒化合物(亚硒酸钠),可以成功实现无机硒的有机化转化,本方法可用于猫棒束孢的富硒培养。     

让合理、安全用药知识走进千家万户(四十)

正(接上期)科学补硒方法是:A、人工补硒:摄取人工添加的各类补硒产品主要分为无机硒和有机硒两类,无机硒主要为亚硒酸钠,国外多用于饲料使用,有很大的毒素,已处于淘汰的边缘。有机硒与亚硒酸钠等无机硒相比,具有食用安全、无毒副作用、吸收利用率高、营养价值高等优点。有机硒的种类很多,如硒酵母、硒蛋、富硒藻类、富硒蘑菇和硒麦芽等,其中麦芽硒是目前有机硒发展的最高阶段,比     

有机硒富硒麦芽与无机硒亚硝酸钠的毒性比较

目前我国缺硒地区解决硒营养不足问题,是采用口服无机亚硒酸钠片或食用亚硒酸钠强化食盐。然而不少研究表明,有机硒的活性比无机硒高。能更有效地在体内同化,且毒性小。北京市食品工业研究所研制的富硒麦芽,其有机硒的含量达97％以上。与美国研制的硒酵母相比,富硒麦芽还含有一定量的维生素E(V_E)和维生素C(V_C)     

富硒麦芽对阿霉素致小鼠心脏毒性的保护作用

目的：探讨含硒制剂诱导金属硫蛋白在对抗阿霉素心脏毒性中的作用,比较无机硒制剂亚硒酸钠与有机硒制剂富硒麦芽。方法：不同时间给小鼠喂予硒制剂后取血分离血清,按常规查ＧＯＴ和ＣＫ活性,按ＤＴＮＢ法测ＧＳＨ－Ｐｘ活性;取心、肝、肾组织按Ｈｇ－Ｃｈｅｌｅｘ法测金属硫蛋白（）含量并做心脏病理学检查。结果：两种含硒制剂均能减轻阿霉素引起的体重下降,ＧＯＴ与ＣＫ酶升高及心脏病理损害,其中富硒麦芽的效果略优于亚硒酸     

富硒麦芽对阿霉素致小鼠心脏毒性的保护作用

目的:探讨含硒制剂诱导金属硫蛋白在对抗阿霉素心脏毒性中的作用,比较无机硒制剂亚硒酸钠与有机硒制剂富硒麦芽。方法:不同时间给小鼠喂予硒制剂后取血分离血清,按常规查GOT和CK活性,按DTNB法测GSH-Px活性;取心、肝、肾组织按Hg Chelex法测金属硫蛋白(MT)含量并做心脏病理学检查。结果:两种含硒制剂均能减轻阿霉素引起的体重下降、GOT与CK酶升高及心脏病理损害,其中富硒麦芽的效果略优于亚硒酸钠。两者还能增加GSH-Px酶活性,诱导心脏中MT合成增加,连续使用硒制剂的整体效果优于先或后使用该制剂。结论:除升高GSH-Px外,硒制剂诱导合成MT很可能是减轻阿霉素心脏毒性的保护机制之一。两种硒制剂比较使用富硒麦芽较亚硒酸钠更为安全,且不降低原已证实的亚硒酸钠对心肌的保护作用。     

亚硒酸钠诱发大鼠胚胎中脑神经细胞凋亡的观察

目的：研究亚硒酸钠对大鼠胚胎中脑神经细胞凋亡的影响。并探讨其中可能的机制。方法：采用原代培养的大鼠胚胎中脑神经细胞，加入不同浓度的亚硒酸钠（1、5、10、20μmol/L)，观察亚硒酸钠对神经细胞凋亡的影响，用透射电镜观察神经细胞超微结构的变化，流式细胞仪分析法检测DNA含量及凋亡细胞百分率。结果高浓度的亚硒酸钠（≥10μmol/L）会导致神经细胞凋亡，并呈剂量依赖性，10μmol/L的亚硒酸钠作用的神经细胞导现出典型的凋亡形态学改变，且凋亡细胞百分率达13．4％。结论：高浓度的硒可通过激发生氧自由基和调节有关调节基因（P53）的活性等多种途径诱发神经细胞凋亡。     

油酸、亚油酸及硒化合物抗转化活性的研究

油酸、亚油酸及硒化合物抗转化活性的研究曹洁，李瑞珍，龚书明，史永亮，吴端宗利用天然的或合成的具有防癌抗瘤作用的化学物质是目前癌症预防的有效措施之一。１９８８年国内首次合成了新型有机硒化合物──硒化油酸和硒化亚油酸等［１］。我们应用细胞转化试验，观察了...     

富硒益生菌发酵及生物活性研究进展

硒是维持人体正常生理功能必需的元素之一，适量摄入具有抗肿瘤、抗氧化、增强人体免疫等多种功能。很多益生菌能将无机硒转化为有机硒和纳米硒(SeNPs)，可降低硒毒性，并促进人体吸收。富硒益生菌兼具硒和益生菌的双重功效，对人体健康有重要作用，在食品、药品开发方面具有广阔的市场前景。该文综述了近年来富硒益生菌发酵及生物活性的基础研究，并对当前重点研究的一些富硒益生菌进行阐述。     

Selenium compounds modulate the activity of recombinant rat AsIII-methyltransferase and the methylation of arsenite by rat and human hepatocytes

Formation of methylated metabolites is a critical step in the metabolism of inorganic arsenic or selenium. We have previously shown that under conditions of a concurrent exposure sodium selenite inhibits methylation of arsenite by cultured rat hepatocytes. Here, we compare the effects of sodium selenite and mono-, di-, and trimethylated selenium compounds on the methylation of arsenite by purified recombinant rat As(III)-methyltransferase (Cyt19) and by primary rat and human hepatocytes. Among these compounds, sodium selenite was the most potent inhibitor of the methylation of arsenite by the recombinant enzyme (K(i) = 1.4 microM) and by cultured cells. In both systems, methylseleninic acid was an order of magnitude less potent an inhibitor (K(i) = 19.4 microM) than was sodium selenite. Dimethylselenoxide and trimethylselenonium iodide were weak activators of recombinant As(III)-methyltransferase activity but were weak inhibitors of arsenite methylation in hepatocytes. These data suggest that selenite, rather than its methylated metabolites, is responsible for inhibition of arsenite methylation in cultured hepatocytes and that inhibition may involve direct interactions between selenite and As(III)-methyltransferase.     

Inhibition by selenium compounds of catecholamine secretion due to inhibition of Ca2+ influx in cultured bovine adrenal chromaffin cells

Selenium is an essential trace metal element, whereas large doses of selenium exert adverse effects to the human body. We examined the effects of selenium compounds, sodium selenite (Na2SeO3) and sodium selenate (Na2SeO4), on catecholamine secretion from cultured bovine adrenal chromaffin cells. Treatment of chromaffin cells with sodium selenite for 72, 48, and 24 h caused decreases in protein and catecholamine contents, in association with cell damage, at concentrations over 30, 300, and 300 microM, respectively. The cells treated with subtoxic conditions (<100 microM, 48 h) of sodium selenite were used for further experiments. Sodium selenite treatment for 48 h inhibited carbachol (CCh)-induced catecholamine secretion in a concentration-dependent and non-competitive manner, while it did not affect high K+- and veratridine-induced catecholamine secretion. Sodium selenite (100 microM) did not affect CCh- and veratridine-induced 22Na+ influx, while the compound inhibited 45Ca2+ influx induced only by CCh, but not high K+ and veratridine. Sodium selenate even at higher concentrations (1000 microM) did not affect any stimulus-induced catecholamine secretion and 45Ca2+ influx. Thus, sodium selenite may specifically exert adverse effects, such as inhibition of physiological stimulus-induced catecholamine secretion from adrenal chromaffin cells due to inhibition of Ca2+ influx.     

Selenium.

The 4 natural oxidation states of selenium are elemental selenium (0), selenide (-2), selenite (+4), and selenate (+6). Inorganic selenate and selenite predominate in water whereas organic selenium compounds (selenomethionine, selenocysteine) are the major selenium species in cereal and in vegetables. The principal applications of selenium include the manufacture of ceramics, glass, photoelectric cells, pigments, rectifiers, semiconductors, and steel as well as use in photography, pharmaceutical production, and rubber vulcanizing. High concentrations of selenium in surface and in ground water usually occur in farm areas where irrigation water drains from soils with high selenium content (Kesterson Reservoir, California) or in lakes receiving condenser cooling water from coal-fired electric power plants (Belews Lake, North Carolina). For the general population, the primary pathway of exposure to selenium is food, followed by water and air. Both selenite and selenate possess substantial bioavailability. However, plants preferentially absorb selenates and convert them to organic compounds. Aquatic organisms (e.g., bivalves) can accumulate and magnify selenium in the food chain. Selenium is an essential component of glutathione peroxidase, which is an important enzyme for processes that protect lipids in polyunsaturated membranes from oxidative degradation. Inadequate concentrations of selenium in the Chinese diet account, at least in part, for the illness called Keshan disease. Selenium deficiency occurs in the geographic areas where Balkan nephropathy appears, but there is no direct evidence that selenium deficiency contributes to the development of this chronic, progressive kidney disease. Several lines of scientific inquiry suggest that an increased risk of cancer occurs as a result of low concentrations of selenium in the diet; however, insufficient evidence exists at the present time to recommend the use of selenium supplements for the prevention of cancer. The toxicity of most forms of selenium is low and the toxicity depends on the chemical form of selenium. The acute ingestion of selenious acid is almost invariably fatal, preceded by stupor, hypotension, and respiratory depression. Chronic selenium poisoning has been reported in China where changes in the hair and nails resulted from excessive environmental exposures to selenium. Garlic odor on the breath is an indication of excessive selenium exposure as a result of the expiration of dimethyl selenide. The US National Toxicology Program lists selenium sulfide as an animal carcinogen, but there is no evidence that other selenium compounds are carcinogens.     

The Influence of Selenium on Methyl Mercury Toxicity in Rat Hepatoma Cells,Human Embryonic Fibroblasts and Human Lymphocytes in Culture

Abstract The effect of methyl mercury and two selenium compounds have been studied in cell cultures. Methyl mercury in concentrations above 1 μM had a pronounced inhibiting effect on the growth of rat Morris hepatoma cells. Glucose and lactate uptake in relation to cell protein was appreciably stimulated by the organic mercury compound. Selenite in low concentrations (0.5 μM) and seleno-di-N-acetyl glycine in thousandfold higher concentrations offered considerable protection against these effects of methyl mercury. The same selenite concentration (0.5 μM), which did not affect cell growth, caused an appreciable protection against methyl mercury (6 μM), even if it was added 3 days after methyl mercury. The methyl mercury inhibited the growth of human embryonic fibroblasts and the DNA-synthesis in the human lymphocytes. However, no protective effect of selenite were observed in these cell types. These results suggest that selenium compounds exert their protective effects through cell specific processes rather than by a direct chemical reaction between selenite and methyl mercury.     

The role of thioredoxin reductase activity in selenium-induced cytotoxicity

The selenoprotein thioredoxin reductase is a key enzyme in selenium metabolism, reducing selenium compounds and thereby providing selenide to synthesis of all selenoproteins. We evaluated the importance of active TrxR1 in selenium-induced cytotoxicity using transfected TrxR1 over-expressing stable Human Embryo Kidney (HEK-293) cells and modulation of activity by pretreatment with low concentration of selenite. Treatment with sodium selenite induced cytotoxity in a dose-dependent manner in both TrxR1 over-expressing and control cells. However, TrxR1 over-expressing cells, which were preincubated for 72h with 0.1 microM selenite, were significantly more resistant to selenite cytotoxicity than control cells. To demonstrate the early effects of selenite on behaviour of HEK-293 cells, we also investigated the influence of this compound on cell motility. We observed inhibition of cell motility by 50 microM selenite immediately after administration. Moreover, TrxR1 over-expressing cells preincubated with a low concentration of selenite were more resistant to the inhibitory effect of 50 microM selenite than those not preincubated. It was also observed that the TrxR over-expressing cells showed higher TrxR1 activity than control cells and the preincubation of over-expressing cells with 0.1 microM selenite induced further significant increase in the activity of TrxR1. On the other hand, we demonstrated that TrxR1 over-expressing cells showed decreased glutathione peroxidase activity compared to control cells. These data strongly suggest that TrxR1 may be a crucial enzyme responsible for cell resistance against selenium cytotoxicity.     

In vitro enhancement of erythrocyte merucry uptake by spironolactone.

Four groups of male Wistar rats were fed the following regimen for 40 days: (1) 20 ppm methylmercury chloride (MMC); (2) 20 ppm MMC + 3 ppm sodium selenite; (3) 3 ppm sodium selenite; (4) basal diet. The basal diet which contained 0.4 ppm “organic selenium” originating mainly from fish meal and wheat was resumed on day 41. Protective effect of selenite over toxicity of methylmercury was observed in terms of both growth rate and morbidity.Concentrations of total mercury, methylmercury and selenium were determined on Days 0, 20, 41, 47, 54, and 61 in the brain, liver, kidney, and blood. It was noted that methylmercury increased accumulation of selenium in all the organs analyzed while selenium retention varied according to the type of selenium and the organs. Modification by selenite, despite its protective effect, remained equivocal in regard to the organ accumulation of mercury and its retention therein.     

Selenium toxicosis assessment (in vivo and in vitro) and the protective role of vitamin B12 in male quail (Coturnix Coturnix)

The present study was undertaken to elucidate the toxicity induced by sodium selenite in male quail through in vivo and in vitro studies and the role played by vitamin B12 in alleviating selenium toxicity. Administration of selenite orally for 1 month induced hepatic oxidative damage. Selenite decreased body weight gain and increased relative liver weight. Selenite reduced hemoglobin and iron concentrations and elevated total bilirubin concentration. Serum transaminases and alkaline phosphatase activities were increased in selenium-intoxicated quails. Total protein concentration was decreased associated with the appearance of prealbumin fraction, an increased γ-globulin and a decreased α- and β-globulins. The highest level of selenium was found in liver followed by kidney, testis, faeces and blood. Supplementation of vitamin B12 orally for 1 month simultaneously with selenite caused less marked biological alteration in the investigated parameters. In vitro study using isolated quail hepatocytes incubated with sodium selenite showed a dose-dependent response for toxicity markers. These results suggest that selenosis can be reduced by vitamin B12 supplementation.     

利用包合物紫外法进行硒的限量检查

利用β 环糊精和十二烷基硫酸钠在水溶液中形成包合物的性质，实现了直接、快速、简捷地检测微量元素硒，并且与《中华人民共和国药典》（１９９５年版）中的硒检查法相比，具有无需萃取、操作简单、省时省力、协同增敏等优点     

Effects of methylmercury and organic acid mercurials on the disposition of exogenous selenium in rats.

Interaction of methylmercury (MM), an environmental and industrial toxicant, with selenium is well known but incompletely understood. Therefore, the effects of MM (10 micromol/kg i.v.) on the disposition of exogenous selenium were compared with those of other organic mercurials (merbromine, mercuribenzene sulfonic acid, and mercuribenzoic acid) in anesthetized bile duct-cannulated rats injected with sodium [(75)Se]selenite (10 micromol/kg i.v.). The mercurial organic acids (10 micromol/kg i.v.) differed strikingly from MM in their influence on selenium disposition. They promoted renal and hepatic accumulation as well as biliary excretion of selenium but decreased distribution to the muscle, testis, and brain as well as the pulmonary excretion of selenium. In contrast, MM altered selenium distribution in an opposite fashion: it diminished the biliary output of selenium and enhanced selenium exhalation. GC-MS analysis verified that this latter paradoxical effect resulted from increased exhalation of dimethyl selenide. Further studies indicated that the MM-induced increase in pulmonary excretion of dimethyl selenide cannot be due to a diminished conversion of this volatile selenium compound to trimethylselenonium ion (TMSe(+)), because MM influenced neither the urinary excretion nor the hepatic and renal concentration of TMSe(+) in selenite-injected rats. Compared to the selenite-exposed rats, the selenite plus MM-injected animals exhibited a significant rise in the hepatic level of S-adenosylmethionine (SAME), the endogenous methyl donor in selenium methylation, and the ratio of SAME to S-adenosylhomocysteine. Based on these and others' observations, it is hypothesized that MM may increase hepatic availability of SAME in selenite-dosed rats by counteracting selenite-induced inactivation of SAME synthetase, thereby facilitating SAME synthesis, and/or by acting as a methyl donor in formation of dimethyl selenide, thereby sparing SAME. In summary, the toxicologically and ecologically relevant interaction of MM and selenite is not mimicked by organic acid mercurials, possibly because it results in formation of lipophilic Hg- and Se-containing common compound(s) and because it also appears to involve methyl transfer from MM to selenium.