硒多糖的研究进展

多糖和硒对许多疾病都有防治作用 ,近年来对多糖和硒活性的研究已经较为深入 ,但将多糖与硒有机结合成为硒多糖 ,国内外的研究尚处于起步阶段。硒多糖的化学结构有别于普通多糖 ,形成了特殊的硒氧键 ;硒多糖具有多种生理活性 ,可通过提高相关酶的活性来拮抗重金属中毒和抗活性氧损伤的能力 ,可使癌细胞DNA合成受阻而抑制癌细胞生长等。此文综述了硒多糖的研究进展     

硒多糖的化学与药理研究进展

硒多糖以其特有的硒和多糖的生物学活性成为近年来研究的热点,本文就国内外近年来对硒多糖的化学方面的提取、分离、纯化、分析和药理学方面的生物学活性、临床应用进行综述,希望对广大从事此方面研究的工作者有所帮助。     

苯并硒唑酮-多糖衍生物的合成及生物活性研究

目的 研究有机硒-多糖衍生物的人工合成方法及其生物活性。方法 以依布硒（Ebselen）的含硒基团为母核,对苯并硒唑酮-多糖衍生物进行化学合成。结果 合成了4种苯并硒唑酮-多糖衍生物,所用多糖有3种为海洋来源糖类,并测定了其中2种硒多糖对4种肿瘤细胞的增殖抑制活性,抑制率均超过80%。为苯并硒唑酮-多糖衍生物的合成及其活性研究提供了参考。     

灵芝多糖/硒化卡拉胶口服液对免疫抑制小鼠免疫功能的影响

目的:研究灵芝多糖/硒化卡拉胶口服液对环磷酰胺诱导免疫抑制小鼠的非特异性免疫功能、体液免疫功能、细胞免疫功能的影响。方法:小鼠腹腔注射80mg/kg环磷酰胺诱导免疫抑制小鼠模型,灵芝多糖/硒化卡拉胶口服液连续供应30d,每天1次。测定小鼠单核巨噬细胞吞噬功能、腹腔巨噬细胞吞噬鸡红细胞功能、外周血白细胞数目、NK细胞活性、白介素-1(IL-1)活性、白介素-2(IL-2)活性、TNF-α活性、半数血清溶血素、抗体生成细胞、T、B淋巴细胞增殖能力、迟发型变态反应。结果:灵芝多糖/硒化卡拉胶口服液各剂量组(低剂量组:灵芝多糖2.5mg/kg+硒5μg/kg;中剂量组:灵芝多糖5mg/kg+硒10μg/kg;高剂量组:灵芝多糖15mg/kg+硒30μg/kg)均可提高外周血白细胞数目、提高半数溶血素值,低剂量组增强IL-1活性,中剂量组增强IL-2活性,高剂量组和中剂量组增强T、B淋巴细胞的增殖能力、NK细胞活性、TNF-α活性,高剂量组增强腹腔巨噬细胞吞噬功能、碳粒廓清值、提高抗体生成细胞、增强迟发型变态反应。结论:灵芝多糖/硒化卡拉胶口服液对免疫抑制小鼠的免疫功能具有改善作用。     

硒化桑葚多糖及其抗氧化活性研究

目的:通过硒化修饰改变桑葚多糖分子结构,并对比研究其体内抗氧化活性.方法:采用水提醇沉法提取桑葚多糖(FMP),硒化修饰FMP,得到桑葚多糖硒化衍生物(FMPs);考察桑葚多糖的体内抗氧化能力,测定小鼠血清和肝脏中MDA、肝脏T-AOC和CAT;建立高脂血症大鼠抗氧化损伤模型,考察FMP及FMPs的抗氧化能力.结果:FMPs及FMP均可以显著提高正常小鼠肝组织CAT活力及T-AOC,降低小鼠血清及肝脏MDA含量,FMPs抗氧化活性明显优于FMP.此外,FMPs及FMP还可以显著降低四氧嘧啶致高脂大鼠的氧化损伤程度,提高其血清SOD活力及肝脏T-AOC,并降低其血清MDA含量.结论:硒化修饰可显著提高桑葚多糖的抗氧化活性.     

硒化紫球藻胞外多糖毒性及抗氧化活性的研究

目的 研究硒化紫球藻胞外多糖的毒性及抗氧化活性.方法 采用在培养液中添加亚硒酸,制备硒化紫球藻胞外多糖(Se-PSP);在体外培养条件下,测量其对细胞代谢活力的抑制率;建立小鼠动物模型,测量各项抗氧化功能指标.结果 Se-PSP对LO-2的半抑制浓度为80ìg·mL-1;Se-PSP(80,160 mg·kg-1)对小鼠不仅无毒性,而且还有促进其生长、抗氧化等保健功能.结论 Se-PSP在80,160 mg·kg-1低浓度范围内,可以发挥硒多糖的抗氧化等活性.     

云芝多糖对小鼠心、肝、脾、肾和红细胞抗氧化能力的影响

通过测定小鼠心、肝、脾、肾组织和红细胞脂质过氧化物含量和硒谷胱甘肽过氧化物酶活性，观察了云芝多糖对机体各组织及红细胞抗氧化能力的影响。结果表明，云芝多糖能提高机体各组织的硒谷胱甘肽过氧化物酶活性及降低脂质过氧化物含量，提示云芝多糖能有效地提高机体抗氧化能力，为防止或减轻脂质过氧化损伤提供了实验依据。     

箬叶多糖及其衍生物对小鼠艾滋病作用的研究

目的　研究箬叶多糖及其衍生物硫酸酯多糖和硒酸酯多糖对小鼠艾滋病的治疗作用。方法　采用 Ｌ Ｐ Ｂ Ｍ５ 鼠白血病病毒（ Ｍｕ Ｌ Ｖ） 感染 Ｃ５７ Ｂ Ｌ／６ Ｊ 小鼠的方法建立艾滋病模型。结果　硫酸酯多糖５０ ｍｇ·ｋｇ － １·ｄ － １（ｉｐ） 具有较好地抑制小鼠脾肿大、血清 Ｉｇ Ｇ 增高的作用,硒酸酯多糖在两种给药方式中有一定的保护作用。此外,还首次发现感染小鼠出现 Ｇ Ｓ Ｈ Ｐｘ 活力下降,脂质过氧化产物升高,这与 Ｈ Ｉ Ｖ感染的病人的症状是一致的,硒多糖对提高机体的抗氧化功能有较好的作用。多糖经硫酸酯化、硒酸酯化等化学修饰后,活性有不同程度的提高。结论　作为抗氧化剂和免疫增强剂的微量元素硒和多糖类可能对 Ｈ Ｉ Ｖ 感染的病人有一定的治疗作用     

硒多糖、亚砷酸钠对大鼠肝微粒体酶和GSH-Px等的影响

研究了硒多糖、亚砷酸钠在体内、外对大鼠肝微粒体酶细胞色素Ｐ－４５０、ｂ５、ＮＡＤ（Ｐ）Ｈ－细胞色素Ｃ还原酶、谷胱甘肽硫转移酶（ＧＳＴ）的影响;并通过测定硒多糖、亚砷酸钠对肝谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）和脂质过氧化（ＬＰＯ）的影响,探讨了硒、砷相互作用的机理。结果表明：连续７天腹腔注射０．２ｍｇ／ｋｇ硒多糖,细胞色素Ｐ－４５０、ｂ５的含量、ＧＳＴ的活性降低（Ｐ＜０．０５）;硒多糖明显诱导ＧＳＨ－Ｐｘ的活性,降低脂质过氧化,拮抗亚砷酸钠对ＬＰＯ的作用。亚砷酸钠显著增强肝细胞脂质过氧化（Ｐ＜０．０５）,对ＧＳＨ－Ｐｘ和肝微粒体酶无明显影响     

海藻硒多糖抗肿瘤作用机制的研究

目的:对海藻硒多糖抗肿瘤作用以及海藻硒多糖抗肿瘤机制的研究进展进行综述。方法:查阅相关文献资料进行归纳总结。结果:海藻硒多糖通过增强机体的免疫功能、影响肿瘤细胞的细胞周期、诱导肿瘤细胞凋亡、增强机体的抗氧化作用4种机制进行抗肿瘤的作用。结论:海藻硒多糖的开发具有广阔的应用前景。     

海藻硒多糖对小鼠免疫功能的影响

通过动物试验,观察了海藻硒多糖对小鼠免疫功能的影响。结果表明：海落硒多糖对小鼠各项免疫指标的影响均优于同剂量的无机硒和海海藻多糖。证明海藻硒多糖发挥了硒和多糖的彼此协同作用,可作为新型的免疫调节剂应用。     

Thioacetamide-induced cirrhosis in selenium-adequate mice displays rapid and persistent abnormity of hepatic selenoenzymes which are mute to selenium supplementation

Selenium reduction in cirrhosis is frequently reported. The known beneficial effect of selenium supplementation on cirrhosis is probably obtained from nutritionally selenium-deficient subjects. Whether selenium supplementation truly improves cirrhosis in general needs additional experimental investigation. Thioacetamide was used to induce cirrhosis in selenium-adequate and -deficient mice. Selenoenzyme activity and selenium content were measured and the influence of selenium supplementation was evaluated. In Se-adequate mice, thioacetamide-mediated rapid onset of hepatic oxidative stress resulted in an increase in thioredoxin reductase activity and a decrease in both glutathione peroxidase activity and selenium content. The inverse activity of selenoenzymes (i.e. TrxR activity goes up and GPx activity goes down) was persistent and mute to selenium supplementation during the progress of cirrhosis; accordingly, cirrhosis was not improved by selenium supplementation in any period. On the other hand, selenium supplementation to selenium-deficient mice always more efficiently increased hepatic glutathione peroxidase activity and selenium content compared with those treated with thioacetamide, indicating that thioacetamide impairs the liver bioavailability of selenium. Although thioacetamide profoundly affects hepatic selenium status in selenium-adequate mice, selenium supplementation does not modify the changes. Selenium supplementation to cirrhotic subjects with a background of nutritional selenium deficiency can improve selenium status but cannot restore hepatic glutathione peroxidase and selenium to normal levels.     

Section Review Pulmonary-Allergy,Dermatological, Gastrointestinal & Arthritis: The pharmaceutical potential of seleno-organic compounds

Selenium has frequently been used as a less electronegative substitute for sulfur in potential pharmaceuticals. While substitution with selenium can increase the potency of thiol compounds, the reactivity of selenium with sulfhydryl groups often leads to increased toxicity. The discovery of selenium at the active site of glutathione peroxidase (GSH-Px) led to a search for selenium compounds which could affect GSH-Px. The benzisoselenazolone, ebselen, catalyses hydroperoxide breakdown per se, exhibits anti-inflammatory activity and is being developed clinically for the treatment of cerebral ischaemia. Its toxicity is low because of metabolic retention of selenium within the molecule. Other compounds have been synthesised to take advantage of the catalytic activity of selenium substitution, but have either fallen victim to management concerns about toxicity or are still at an early stage of development.     

Influence of selenium supplementation during chelation of lead in rats.

The influence of selenium supplementation during chelation therapy to reduce body burden and toxicity of lead was investigated in rats. Selenium had marginal effects on liver, kidney and blood lead decorporation by calcium disodium ethylenediamine tetra acetic acid (CaNa2EDTA) and activation of inhibited delta- aminolevulinic acid dehydratase (ALAD) activity by calcium trisodium diethylenetriamine penta acetic acid (CaNa3DTPA). Selenium supplementation however, had no influence on lead induced inhibition of renal and hepatic transaminases and alkaline phosphatase. The results suggest that selenium supplementation slightly augments lead mobilization by chelating drugs.     

Effect of certain trace elements on the mutagenicity of N-methyl-N'-nitro-N-nitrosoguanidine

Tests have been carried out to detect inhibitory activity of various trace elements on mutagenesis induced by the carcinogen N-methyl-N'-nitro-N-nitrosoguanidine in Salmonella typhimurium strain TA100. Selenium has been found to be most active in this regard while copper has displayed moderate inhibitory ability. The action of selenium is mediated through an interaction resulting in rapid deactivation of the carcinogen.     

Selenium in water enhances antioxidant defenses and protects against copper-induced DNA damage in the blue mussel Mytilus edulis

Selenium and copper are naturally occurring elements in the environment that have important roles in cellular function. Selenium is known for its role in antioxidant defense, whereas copper is a redox-active metal capable of acting as a pro-oxidant. We investigated the effects of short term selenium (Na₂SeO₃) supplementation (4 μg/L for 3 days) on antioxidant parameters of the blue mussel, Mytilus edulis, and its possible protective effects against a subsequent copper (CuSO₄) exposure (56 μg/L for 3 days). Selenium supplementation caused a 4-fold increase in glutathione levels in gills. The activity of selenium-dependent glutathione peroxidase was modulated by selenium in gills (2-fold increase) and also in cell-free haemolymph (40% increase). Copper exposure produced decreases in protein thiol levels (35%) and in thioredoxin reductase activity (60%) in gills and induced an increase in DNA damage in haemocytes (70% increase in % tail DNA observed using the comet assay). The decrease in thioredoxin reductase activity may constitute a mechanism of copper toxicity in bivalves, warranting further investigation. Pre-treatment with selenium largely prevented these deleterious effects of copper on protein thiols, thioredoxin reductase activity and DNA damage. The results suggest that induction of key antioxidant defenses such as glutathione and selenium-dependent glutathione peroxidase, as a result of selenium supplementation, may play an important role in protection of aquatic organisms against oxidative stress.     

硒和硒化物的药理及药效学研究

硒是人体所必需的微量元素之一，为谷胱甘肽过氧化物酶的重要成分，能消除体内有害自由基，维护正常生理功能。硒及硒化物可防治多种与硒缺乏相关的疾病。本文综述近年来有关硒及硒化物的药理和药效学研究进展。     

In vitro evaluation of selenium genotoxic, cytotoxic, and protective effects: a review

Selenium is an oligoelement with essential biological functions. Diet is the most important selenium source, and intake of this element depends on its concentration in food and amount of food consumed. Among the essential human micronutrients, selenium is peculiar due to its beneficial physiological activity and toxicity. It may have anticarcinogenic effects at low concentrations, whereas at concentrations higher than those necessary for nutrition, it can be genotoxic and carcinogenic. Because of that, selenium is probably the most widely investigated of all the oligonutrients. In the last decades, there has been increasing interest in several nutritional Se compounds because of their environmental, biological, and toxicological properties, particularly for their cancer- and disease-preventing activities. This article gives an overview of the results of in vitro studies on mutagenicity, genotoxicity, cytotoxicity, and DNA repair conducted within the last decades with different organic and inorganic selenium compounds. Results from these studies provide a better knowledge on the selenium activity and help to elucidate the reasons underlying its duality in order to regulate its correct use in nutrition and clinic.     

Modification of Chemical Toxicity by Selenium Deficiency

Modification of Chemical Toxicity by Selenium Deficiency. Burk,R.F. and Lane, J.M. (1983). Fundam. Appl. Toxicol. 3: 218–221.Selenium deficiency causes a number of hepatic metabolic alterationsin the rat which could lead to changes in chemical toxicity.It causes a decrease in glutathione peroxidase activity, anincrease in glutathione S-transferase activity, and an increasein the rate of glutathione synthesis. The hepatotoxicities ofthree compounds which bind to glutathione S-transferase; iodipamide,acetaminophen, and aflatoxin B₁, are decreased by selenium deficiency.The toxicity of redox cycling compounds is generally increasedby selenium deficiency and is accompanied by evidence of lipidperoxidation. Thus, nitrofurantoin (100 mg/kg) causes renaltubular necrosis in selenium-deficient rats but not in controls.Selenium-deficient rats are much more sensitive to diquat toxicitythan are controls. Lethality of diquat in selenium-deficientrats appears to be causally linked to lipid peroxidation. Lethalityof diquat in control rats is not linked to lipid peroxidation.The effect of selenium does not appear to be mediated by glutathioneperoxidase, however, indicating that selenium has another oxidantdefense function. Another interesting observation made was thatincreases in inspired O₂ tension decreased ethane production(lipid peroxidation) in selenium-deficient and in control ratsgiven diquat. Thus, O₂ appears to prevent diquat-induced lipidperoxidation.