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納米硒SCI論文

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1)硒化合物與納米硒粒子的毒性研究

Chapter 44, Handbook of Systems Toxicology(《系統毒理學手冊》第44章),2011年3月

出版社:John Wiley & Sons      主辦:美國食品及藥品管理局(FDA)

2)食品與藥品納米毒性評價:納米硒體外體內生物性質

Chapter 6, NANOTOXICITY: FROM IN VIVO AND VITRO MODELS TO HEALTH RISKS

(《納米毒理體內體外研究模型與健康風險》第六章),2009年8月

出版社:John Wiley & Sons     主辦:美國食品及藥品管理局(FDA)

3)硒納米顆??勺鳛槟c道p53抑制劑,減輕小鼠化療引起的腹瀉Pharmacological Research

(《藥理學研究》), 2019

出版社:Academic Press Inc.    主辦國:英國            影響因子:5.893

4)4)亞硒酸鈉對小鼠腹膜癌抗癌作用的藥理機制Pharmacological Research 147 (2019) 104360

出版社:Academic Press Inc.     主辦國:英國影響因子:5.893

5)硒納米顆粒在產生活性氧方面比亞硒酸鈉更有效,并且硒納米顆粒在癌細胞中的過度積累產生了有效的治療作用 FREE RADICAL BIOLOGY ADN MEDICINE(《自由基生物醫學》), 2018

出版社:Elsevier Science          主辦國:美國   影響因子:6.170

6)腹腔注射硒納米顆粒預防腹膜癌細胞生長的功效和安全性

FREE RADICAL BIOLOGY ADN MEDICINE(《自由基生物醫學》), 2014

出版社:Elsevier Science          主辦國:美國                影響因子:6.170

7)納米尺寸元素硒(納米硒)與甲基硒半胱氨酸比較是一種具有低毒性的潛在防癌劑

TOXICOLOGICAL SCIENCES(《毒理學》), 2008

出版社:Oxford University Press          主辦國:美國           影響因子:3.7034)

8)與硒蛋氨酸比較納米尺寸元素硒具有低毒性并且不削弱調節含硒酶能力

FREE RADICAL BIOLOGY ADN MEDICINE(《自由基生物醫學》), 2007

出版社:Elsevier Science              主辦國:美國           影響因子:6.170

9)超營養水平元素硒納米粒子(納米硒)的硒積累和誘導脫毒酶谷胱甘肽硫轉移酶的尺寸效應

INORGANIC BIOCHEMISTRY(《無機生物化學》), 2007

出版社:Elsevier Science           主辦國:美國   影響因子:3.212

10)硫代乙酰胺誘導硒充足的小鼠肝硬化顯示缺乏硒補充情況下肝臟含硒酶會快速、持續畸形

TOXICOLOGY AND APPLIED PHARMACOLOGY(《毒理學和應用藥理學》),2007

出版社:Academic Press           主辦國:美國   影響因子:3.347

11)元素態納米硒的亞慢毒性研究LIFE SCIENCES(《生命科學》), 2005

出版社:Elsevier Science           主辦國:英國               影響因子:3.647

12)納米硒與亞硒酸鹽短期毒性比較    作者:陳君石等   

LIFE SCIENCES(《生命科學》), 2005

出版社:Elsevier Science           主辦國:英國   影響因子:3.647

13)納米紅色元素硒增加小鼠和細胞中的含硒酶無尺寸效應

LIFE SCIENCES(《生命科學》), 2004

出版社:Elsevier Science          主辦國:英國                影響因子:3.647

14)納米硒體外清除自由基作用

FREE RADICAL BIOLOGY AND MEDICINE(《自由基生物醫學》),2003

出版社:Elsevier Science          主辦國:美國    影響因子:6.170

15)中空球狀硒納米粒子及其體外抗羥自由基作用   作者:高學云等

ADVANCED MATERIALS(《先進材料》), 2003

出版社:Wiley InterScience       主辦國:美國        影響因子:27.398

16)納米紅色元素硒的生物學作用BIOFACTORS(《生物因素》), 2001

出版社:IOS Press                     主辦國:英國     影響因子:4.734

1)Toxicity of Selenium Compounds and Nano-Selenium Particles.

《硒化合物與納米硒粒子毒理研究》

  作者張勁松


[Conclusions]

Selenium is a necessary dietary constituent of at least 25 human selenoproteins and enzymes all containing selenocysteine. Replacement of selenium by sulfur in enzymes diminishes or obfuscates catalytic activity. Replacement of selenium by sulfur in selenium analogues dramatically reduces or totally eliminates toxicity. The reverse is also true. Replacement of catalytic sulfur by selenium in sulfur compounds universally increase catalytic activity and/or toxicity. In excessive amounts, all selenium compounds become toxic is a dose-dependent fashion to cells in vitro and to the primary target tissue of chronic selenium toxicity, the liver. Nanotechnology is a rapidly developing modern technology branch dealing with materials in the nanometer-size range. With their extremely small size nanomaterials can enter cells and with their huge surface area nanomaterials have the potential to interact with intracellular macromolecules exhibiting toxicity or bioactivity. There exist obvious public safety concerns about nanomaterials. Accordingly, a new research discipline known as nanotoxicology has emerged. However, nanotechnology may also hold promise for pharmacology because nanomaterials normally exhibit novel properties different from those of both molecular and bulk materials. Elemental seleniuim has long been considered to be biologically inert. With bovine serum albumin or other dispersant agents such as polysaccharides, biologically active Nano-Se aggregates are formed from sodium selenite and glutathione. Different from the biologically inert black elemental selenium with coarse size, Nano-Se manifests toxicity whcih conforms to the concern of nanotoxicity. However, compared with selenium compounds such as sodium selenite, selenomethionine and Se-methylselenocysteine, Nano-Se is not compromised in increasing the activities of selenoenzyme and phase 2 enzyme, but exhibits much lower toxicity. Nano-Se is thus a potential selenium nutritional source with a prominent characteristic of lower toxicity for supplementation.


[摘要]

硒是人體必需的微量元素,人體中含有至少25種重要的硒蛋白和含硒酶。如果硒元素被硫元素替代,相應生物酶的催化活性就會減少或者發生混淆。同時也會大幅度降低或完全消除毒性。反過來也一樣。用硒元素替代硫化合物中的硫元素,催化活性普遍提高,毒性亦然。過量條件下,所有的硒化合物產生毒性都是有劑量依賴效應的,不論是體外細胞還是主要目標組織的慢性硒毒性,比如肝臟。納米技術是一個飛速發展的當代技術分支,是在納米尺寸范圍對物質進行處理的科學。體積非常微小的納米材料進入細胞,他們具有巨大的表面積,使得納米材料有潛在可能性與細胞內大分子相互作用,顯示出毒性和生物活性。因此對納米材料就存在著明顯的公共安全方面的擔憂。因此,出現了一個新的研究學科——納米毒理學。然而,納米技術也可能給藥理學帶來希望,因為納米材料通常表現出不同于微觀分子或者宏觀物質兩方面的新穎性質。元素硒一直被認為生物惰性。以蛋白或者多糖作為分散劑,亞硒酸鈉還原制備出具有生物活性的納米元素硒Nano-Se。不同于宏觀尺度的生物惰性黑色元素硒,Nano-Se體現出納米毒理學所擔憂的毒性。但是,與其它硒化合物相比,如亞硒酸鈉、蛋氨酸和甲基硒半胱氨酸等,Nano-Se在同等調節含硒酶以及二相酶活性上升時顯示出更低的毒性。因此,Nano-Se具有的明顯低毒性表明它可以作為營養補充劑的硒源。

2)Evaluation of Nanotoxicity of Foods and Drugs: Biological Properties

of Red Elemental Selenium at Nano Size (Nano-Se) In Vitro and In Vivo

《食品與藥品納米毒理評價:納米硒體外體內生物性質》   

  作者:張勁松


[Summary]

Nanotechnology holds promise for medication and nutrition because material at nanometer dimensions exhibits novel properties different from those of both isolated atoms and bulk material. Elemental selenium in the redox state of zero in general is considered to be biologically inert. With a certain protein as a disperser, neonatal elemental selenium atoms generated via reducing sodium selenite with glutathione can aggregate into Nano-Se. In contrast to biologically inert black elemental selenium at micrometer size, Nano-Se indeed manifests toxicity, which conforms to the notion that nanoparticles increase health risks. On the other hand, selenium is an essential trace element with a narrow margin between necessary intake amount and toxicity, whereas cancer-preventive effects of selenium were mostly observed at high doses in animals. For nutritional supplementation and cancer prevention, the optimal selenium form is expected to possess high biological activity and low toxicity. Compared with sodium selenite, selenomethionine or Se-methylselenocysteine, Nano-Se possesses equal efficacy in increasing the activities of selenoenzymes, but has much lower toxicity. These results suggest that Nano-Se can be considered as a novel selenium source with a reduced risk of selenium toxicity.

[摘要]

納米技術為醫學和營養學發展帶來新的前景,因為納米尺寸顆粒既不同于獨立的原子又不同于塊體材料,會出現新特性。通常情況下,零價態硒被認為沒有生物學性質。使用特定的蛋白質作為分散劑,谷胱甘肽還原亞硒酸鈉生成的新生零價態硒原子聚集成為納米顆粒,即納米硒。與沒有生物活性的微米尺寸黑色元素硒相比,納米硒確實產生了毒性,這與廣泛的共識相一致,即納米粒子可能具有健康風險。另一方面,硒作為人體必需的微量元素,它的毒性劑量和所需的營養劑量之間范圍很窄,而動物實驗發現,高劑量硒在癌癥預防時效果更確切。對于營養補充和癌癥預防,最理想的硒形式是具有高活性的同時毒性較低。與亞硒酸鈉、硒蛋氨酸、硒甲基半胱氨酸這些國內外廣泛使用的無機硒或有機硒相比,納米硒擁有與他們相同的增強含硒酶的能力,但是,納米硒的毒性最低。這些結果表明納米硒可以作為一種安全性高的新型硒源。

3)Selenium nanoparticles act as an intestinal p53 inhibitor mitigating

chemotherapy-induced diarrhea in mice. Pharmacological Research 149 (2019) 104475

論文標題:硒納米顆??勺鳛槟c道p53抑制劑,減輕小鼠化療引起的腹瀉


[ABSTRACT]

Selenium, at high-dose levels approaching its toxicity, protects tissues from dose-limiting toxicities of many cancer chemotherapeutics without compromising their therapeutic effects on tumors, there by allowing the delivery of higher chemotherapeutic doses to achieve increased cure rate. In this regard, selenium nanoparticles (SeNPs), which show the lowest toxicity among extensively investigated selenium compounds including methylselenocysteine and selenomethionine, are more promising for application. The key issue remains to be resolved is whether low-toxicity SeNPs possess a selective protective mechanism. p53 or p53-regulated thrombospondin-1 has each been confirmed to be an appropriate target for therapeutic suppression to reduce side effects of anticancer therapy. The present study demonstrated that SeNPs transiently suppressed the expression of many intestinal p53-associated genes in healthy mice. SeNPs did not interfere with tumor-suppressive effect of nedaplatin, a cisplatin analogue; however, effectively reduced nedaplatin-evoked diarrhea. Nedaplatin-induced diarrhea was associated with activation of intestinal p53 and high expression of intestinal thrombospondin-1. The preventive effect of SeNPs on nedaplatin-induced diarrhea was correlated with a powerful concomitant suppression of p53 and thrombospondin-1. Moreover, the high-dose SeNPs used in the present study did not suppress growth nor caused liver and kidney injuries as well as alterations of hematological parameters in healthy mice. Overall, the present study reveals that chemotherapeutic selectivity conferred by SeNPs involves a dual suppression of two well-documented targets, the p53 and thrombospondin-1, providing mechanistic and pharmacologic insights on low-toxicity SeNPs as a potential chemoprotectant for mitigating chemotherapy-induced diarrhea.

4)Pharmacological mechanisms of the anticancer action of sodium selenite against peritoneal cancer in mice. Pharmacological Research 147 (2019) 104360

論文標題:亞硒酸鈉對小鼠腹膜癌抗癌作用的藥理機制


[ABSTRACT]

Peritoneal carcinomatosis has an extremely poor overall prognosis and remains one of the greatest oncologic challenges. Prior studies in mice show that sodium selenite administered intraperitoneally is highly effective in inhibiting cancer cells implanted in the peritoneal cavity. However, the pharmacological mechanism remains unclear. The present study revisited the therapeutic effect of selenite and elucidated its mechanism of action. We found that intraperitoneal delivery of selenite to cancer cells in the peritoneal cavity of mice rapidly and robustly killed the cancer cells, with a therapeutic efficacy higher than that of cisplatin. The action of selenite was associated with the following pharmacological mechanisms. 1) Favorable drug distribution: selenite increased selenium levels in the cancer cells by 250-fold, while in normal tissues only by 7-fold. 2) Optimal selenium form: selenite was converted in the cancer cells mainly into selenium nanoparticles (SeNPs), which are more efficient than selenite in producing reactive oxygen species (ROS). 3) Persistent hijacking of two pro-survival systems to generate ROS: selenite did not impair thioredoxin- and glutaredoxin-coupled glutathione systems, which facilitate SeNPs to generate ROS and caused severe organelle injury and apoptotic response in the cancer cells. Overall, these mechanisms tend to maximize the potential of selenite in producing ROS in cancer cells and underlie selenite as a candidate therapeutic agent for peritoneal carcinomatosis.

5)Selenium nanoparticles are more efficient than sodium selenite in producing reactive oxygen species and hyper-accumulation of selenium nanoparticles in cancer cells generates potent therapeutic effects. Free Radical Biology and Medicine 126 (2018) 55–66

論文標題:硒納米顆粒在產生活性氧方面比亞硒酸鈉更有效,并且硒納米顆粒在癌細胞中的過度積累產生了有效的治療作用


[ABSTRACT]

We have previously demonstrated that selenium nanoparticles (SeNPs) administered via oral route possess similar capacities of increasing selenoenzyme activities as the extensively examined sodium selenite, selenomethionine and methylselenocysteine, and yet display the lowest toxicity among these selenium compounds in mouse models. However, the low toxicity of SeNPs found in mammalian systems would lead to the interpretation that the punctate distribution of elemental selenium found in cultured cancer cells subjected to selenite treatment that triggers marked cytotoxicity represents a detoxifying mechanism. The present study found that SeNPs could be reduced by the thioredoxin- or glutaredoxin-coupled glutathione system to generate ROS. Importantly, ROS production by SeNPs in these systems was more efficient than by selenite, which has been recognized as the most redox-active selenium compound for ROS production. This is because multiple steps of reduction from selenite to selenide anion are required; whereas only a single step reduction from the elemental selenium atom to selenide anion is needed to trigger redox cycling with oxygen to produce ROS. We thus speculated that accumulation of SeNPs in cancer cells would result in a strong therapeutic effect, rather than serves a detoxification function. Indeed, we showed herein that preformed SeNPs generated a potent therapeutic effect in a mouse model due to rapid, massive and selective accumulation of SeNPs in cancer cells. Overall, for the first time, we demonstrate that SeNPs have a stronger pro-oxidant property than selenite and hyper-accumulation of SeNPs in cancer cells can generate potent therapeutic effects.


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