Aflatoxin B2 is metabolized in the liver by microsomal monooxygenases to the less toxic reactive metabolite alfatoxin M2. Aflatoxin B2 is also proposed to be metabolized to B1, which in turn is transformed to M1. (A705, L1956)
Aflatoxins produce singlet oxygen upon their exposure to UV (365-nm) light. Singlet oxygen in turn activates them to mutagens and DNA binding species. Aflatoxin metabolites can intercalate into DNA and alkylate the bases through their epoxide moiety, binding particularity to N7-guanine bases. In addition to randomly mutating DNA, this is thought to cause mutations in the p53 gene, an important gene in preventing cell cycle progression when there are DNA mutations, or signaling apoptosis. (L1877, A2859, A2972) The mechanism of action many furocoumarins is based on their ability to form photoadducts with DNA and other cellular components such as RNA, proteins, and several proteins found in the membrane such as phospholipases A2 and C, Ca-dependent and cAMPdependent protein-kinase and epidermal growth factor. Furocoumarins intercalate between base pairs of DNA and after ultraviolet-A irradiation, giving cycloadducts. (L579)
The main target organ in mammals is the liver so aflatoxicosis is primarily a hepatic disease. Protracted exposure to aflatoxins may cause liver damage and necrosis, cholestasis, and hepatomas. Moreover, protracted exposure to aflatoxins has been associated with hepatocellular carcinoma, acute hepatitis, Reye's syndrome, bile duct cell proliferation, periportal fibrosis, hemorrhages, mucous membrane jaundice, fatty liver changes, cirrhosis in malnourished children, and kwashiorkor. However, aflatoxins accumulate in the presence of liver disease, and the association with hepatic cancer is confounded by the occurrence of hepatitis-B. Thus, it is not clear in these various instances whether aflatoxin is a primary cause of the disease, is an innocent bystander which accumulates secondary to the disease process, or is a contributing cause in conjunction with other factors. It is also mutagenic and teratogenic. Inhaled aflatoxins may produce pulmonary adenomatosis. Aflatoxins modify the immune system by affecting antibody formation, complement, cell-mediated immunity, and phagocytosis. (A704, L1956) Furocoumarins can cause photosensitization dermatitis especially if these compounds come into contact with the skin. Some furocoumarins, especially bifunctional furocoumarins, are known to be carcinogenic (A15105). Furocoumarin photochemotherapy is known to induce a number of side-effects including erythema, edema, hyperpigmentation, and premature aging of skin. All photobiological effects of furocoumarins result from their photochemical reactions. Because many dietary or water soluble furocoumarins are strong inhibitors of cytochrome P450s, they will also cause adverse drug reactions when taken with other drugs. Limited evidence of carcinogenic effect. (L579)
来源:Toxin and Toxin Target Database (T3DB)
毒理性
暴露途径
口服、皮肤、吸入和 parenteral（被污染的药物）。 (A3101)
Oral, dermal, inhalation, and parenteral (contaminated drugs). (A3101)
The present disclosure relates generally to heterobifunctional linkers.
本公开涉及异双功能连接剂。
Mykotoxinbindendes Gemisch
申请人：Sagmeister, Franz, Dr.
公开号：EP0038792A1
公开（公告）日：1981-10-28
Ein Gemisch mit Mykotoxine bindenden Eigenschaften enthaltend eine anorganische Substanz mit großer innerer Oberfläche, z.B. Kieselgur, in Kombination mit einem kreuzvernetzten Homopolymer des N-Vinyl-2-pyrrolidon.
An affinity matrix and a method for the detection of low molecular weight compositions such as aflatoxins are provided utilizing specific monoclonal IgM antibody having an affinity constant not less than about 1 x 109 liters per mole. Methods for the preparation and use of such affinity matrices are also given. The detection is rapid, accurate, reproducible, and allows for quantitative recovery of the composition of interest.
本发明提供了一种亲和基质和一种检测黄曲霉毒素等低分子量成分的方法，该方法利用了亲和力常数不小于约 1 x 109 升/摩尔的特异性单克隆 IgM 抗体，还提供了制备和使用这种亲和基质的方法。 该检测方法快速、准确、可重复，并可定量回收相关成分。
Threshold ligand-receptor assay
申请人：BIOSITE DIAGNOSTICS INC.
公开号：EP0378391A2
公开（公告）日：1990-07-18
This invention is directed to a ligand-receptor assay for determining the presence or amount of at least one target ligand, capable of competing with a ligand analogue conjugate for binding sites available on a ligand receptor, said ligand analogue conjugate comprising at least one ligand analogue coupled to a signal development element capable of emitting a detectable signal, in a fluid sample suspected of containing said target ligand, comprising the steps of:
a. contacting said fluid sample with ligand analogue conjugate and ligand receptor to form a reaction mixture, the relative amounts of ligand analogue conjugate and ligand receptor being such that in the absence of target ligand, and subsequent to substantially equilibrium binding, substantially all of the ligand analogue conjugate is bound to ligand receptor;
b. detecting the unbound ligand analogue conjugate;
c. relating the detectable signal to the presence or amount of target ligand in the fluid sample.
In one embodiment an optional means also is employed for removing receptor from the reaction mixture. In related claimed assay formats the analyte of interest may be either ligand receptor or ligand.
本发明涉及一种配体-受体检测方法，用于确定至少一种目标配体的存在或数量，该目标配体能够与配体类似物共轭物竞争配体受体上可用的结合位点，所述配体类似物共轭物包括至少一种配体类似物，在疑似含有所述目标配体的流体样品中，该配体类似物与能够发射可检测信号的信号发射元件耦合，包括以下步骤：
a. 将所述流体样品与配体类似物共轭物和配体受体接触，形成反应混合物，配体类似物共轭物和配体受体的相对含量为：在没有目标配体的情况下，基本上平衡结合后，配体类似物共轭物基本上全部与配体受体结合；
b. 检测未结合的配体类似物共轭物；
c. 将检测到的信号与流体样品中目标配体的存在或数量联系起来。
在一个实施方案中，还采用了一种可选的方法从反应混合物中去除受体。在相关的检测方法中，相关分析物可以是配体受体或配体。
Präparat zur Wirkstoffapplikation in Kleinsttröpfchenform
申请人：Cevc, Gregor, Prof. Dr.
公开号：EP0475160A1
公开（公告）日：1992-03-18
Die Erfindung betrifft ein Präparat zur Applikation von Wirkstoffen in Form kleinster, insbesondere mit einer membranartigen Hülle aus einer oder wenigen Lagen amphiphiler Moleküle bzw. mit einer amphiphilen Trägersubstanz versehenen Flüssigkeitströpfchen, insbesondere zum Transport des Wirkstoffes in und durch natürliche Barrieren und Konstriktionen wie Häute und dergleichen. Das Präparat weist einen Gehalt einer randaktiven Substanz auf, der bis zu 99 Mol.-% des Gehaltes dieser Substanz entspricht, durch den der Solubilisierungspunkt der Tröpfchen erreicht wird. Das Präparat eignet sich zur nichtinvasiven Verabreichung von Antidiabetica, insbesondere von Insulin. Die Erfindung betrifft außerdem ein Verfahren zur Herstellung solcher Präparate.
